IDJSR Issue 2

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(ISSN 2278‐3784)

VOLUME 1 ISSUE 2

Currently indexed in:

Index Copernicus Genamics Journal Seek Ulrichsweb Global Serial Dictionary

Editorial Board

Kumar Anshul, Editor In Chief – Manipal College of Dental Sciences, India Harsh Rajvanshi, Executive Editor – I.T.S Centre for Dental Studies and Research, India Ayesha Zaka, Executive Editor‐ Hamdard Medical and Dental College, Pakistan

Cover art by:

Ebadullah Shafi, Design and Graphics Incharge‐ RAK College of Dental Sciences, UAE

“Covert art illustration shows a chip about the size of a grain of rice that stores a person's unique identification number linked to his or her entire medical history. The chip is implanted in a tooth where it can neither be felt nor

rejected by the body.”

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INTERNATIONAL DENTAL JOURNAL OF STUDENT’S RESEARCH| June‐Sep 2012| Volume 1| Issue 2

FOREWORD

Prof. Mohamed A.K. El Massry (MBBCh., MSc ., BDS., Ph.D) Professor of Oral & Maxillo facial Surgery, Alexandria, UN, Egypt. Consultant, MOH Kuwait.

It is a great pleasure to contribute to the IDJSR, which in fact came out as a result of great efforts of young Dental Students. I was really thrilled by the idea and I have to admit that I was surprised by the efforts and the professional attitude of the editorial board. Using the available tools of technology to build up such a network of ambassadors and contributors was an amazing and fantastic work. It is the spirit of those enthusiastic young men and women that will lead our profession in the future and I am sure that through your hard work you will be able to achieve a lot. The first volume came out with great success and it contained good articles and was really impressive. The aim of our profession is to deliver the best effort to our patients and this comes through acquiring knowledge, developing research and exchange of opinions in topics of mutual interest. I believe through your journal, site and face book page you will be able to globalize your efforts in a very short time. I wish you all the best.

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EDITORIAL

Kumar Anshul Editor‐in‐Chief Manipal College of Dental Sciences, Manipal India

Three months ago in May 2012, when we released the 1st issue of IDJSR, we saw a dream. A dream of recognizing students’ work, a dream to create a forum for students across the globe to present their research. In a nutshell, to give a chance and platform to the students to publish. Getting indexed in Index Copernicus, Genamics Journal Seek and Ulrichsweb Global Series Directory was another feat which IDJSR achieved after the release of 1st issue. 2nd issue contains some amazing research/review/case report articles from undergraduate as well as postgraduate students of India, Pakistan, China, Croatia and Canada. We are proud that we are following our policy of IDJSR as a “STUDENT ONLY” journal successfully. Signing off, with the words of Mr. Richard Branson “ SCREW IT, LET’S DO IT “

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Harsh Rajvanshi Executive Editor I.T.S Centre for Dental Studies and Research India Welcome in the second issue of the journal. The editorial team is overwhelmed by the tremendous response the first issue has received from all quarters. We are deeply touched by sincere gestures of experts, seniors, colleagues, juniors, professionals. Frankly we never anticipated that our immature effort will cultivate such a generous interest amongst all concerned, far and near, above and below, juniors and seniors. Thank you all for the belief you have shown in our humble beginning. It is very interesting seeing a dream grow. Dream being realized. Taking shape. Evolving into reality. The second issue is coming after London Olympics. USA achieving the medal dominance from China which she lost in Beijing, a remarkable comeback. We watched with bated breath Saina Nehwal achieving the till now unachievable, M.C. Marycom, a proud mother of two, sweating it out to win, Indian Archers battling against unfamiliar hostile London winds, Virtually unknown Vijay Kumar earning glory for the nation. In the same spirit our team tried to identify themselves with the same spirit, holding our heads high with proud researches of students in the global Dental Community. We believe that this time’s selection of articles will be palatable to the hungry minds of our readers, we shall be too happy to receive the free and frank opinions of our valued readers. We understand that the data being presented are for the interest of readers and it is our duty that we correct our self to the satisfaction of the end user, i.e. the reader. This issue has been kept small so that the readers are able to finish through the journal in 2‐3 of sittings. We have however restricted ourselves too much because with such a great response from our contributors, it is quite a task what to include and what to leave. We would request our readers to apprise whether increase in volume is welcome in future issues. Once again, we at the editorial desk, express our thanks and gratitude for the warm response received from all quarters. We shall try our best to be worthy of your belief in our efforts. With best wishes

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Ayesha Zaka Executive Editor Hamdard Medical & Dental College Pakistan After the huge success of first issue we are back again with the second issue of IDJSR. The response we received from first issue was over whelming and beyond our expectations. In the previous issue we had representation from four countries, now in this one we have representation from *five* different countries . We plan to cover as many countries as we can in the coming issues and with the rate your articles are pooling in our inbox and we are very eager to release many more issues in the coming months. Sometimes you send your research but it gets rejected due to multiple factors, don't ever let that stop you, its] is done for your correction, to make you the best among others out there. To those who’s researches get published, don't stop either, work on something else, the hunger of research must be inside you at a very early level, so you can have a stable career from the very beginning. I hope that you'll go through each article with utmost interest and will strive to do your bit in dental research as well. Research is ever changing, what your predecessors have done might be changed by you someday, so keep struggling hard and move forward. Thank you to our Ambassadors for efficiently spreading a word about International Dental Journal of Students Research in their respective college and to our Respected Reviewer Panel for taking their time out and going through each article so carefully. Happy reading!

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REVIEW ARTICLE

ORAL MUCOSITIS –MANAGEMENT PROTOCOL BY ORAL PHYSICIAN

Dr. Suresh Ludhwani1

1Post Graduate Student, Department of Oral Medicine and Radiology, Ahmedabad Dental College and Hospital

Corresponding Author

Dr. Suresh Ludhwani Post Graduate Student, Department of Oral Medicine and Radiology, Ahmedabad Dental College and Hospital Email: [email protected]

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AbstractOral mucositis also called stomatitis, is one of the most common and troublesome forms in individual

undergoing cancer treatment. Oncology treatment does not distinguish between the malignant cells

and normal epithelial cells of mucosa because of their high proliferative capacity. Thus, the mucosa

becomes atrophic, and more susceptible to trauma, allowing the development of inflammation and

installation of secondary infection, which aggravates the patient’s clinical conditions and reduce the

quality of life. The clinical management of mucositis includes preventive and palliative strategies.

The role of the oral physician in prevention and management of chemotherapy and radiotherapy

induced mucositis is critical.

Introduction Oral mucositis may be defined as inflammation of oral mucosa with extensive ulceration and painful irritation (1).It is considered an acute inflammation caused by the necrosis of the basal layer of the oral mucosa. The more important clinical features are erythema and/or ulceration (6), which may extend from the mouth to the rectum (2). It

can induce several life-threatening complications, such as intestinal obstruction and perforation (3), reducing the patient’s quality of life and leading to severe infections, which may require the interruption of the antineoplasic treatment (6). Oral and throat pain caused by the mucosa ulceration, abdominal pain, vomits and diarrhea are characteristics that compromise the patient’s nutritional status because of a decrease of

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food intake, leading to weight loss (5). The progression of oral lesions and its impact on general conditions of the patient may require parenteral nutrition or temporary interruption of the antineoplasic treatment (7). It is a complex biological process divided into four phases, which are interdependent and can occur due to action of cytokines on epithelium. These phases are 1. Inflammatory or vascular phase: day 0 2. Epithelial phase: days 4-5 3. Ulcerative or bacteriologic phase: days 6-12 4. Healing phase: days 12-162 Epidemiology Mucositis has received significant attention from the physician community in the last two decades of life. It is estimated that oral mucositis affects 40% of the patients undergoing chemotherapy, 75% of the patient undergoing chemotherapy and bone marrow transplantation and more than 90% patient undergoing radiotherapy for head and neck cancer. According to chiappelli, 40% of the patient undergoing radiotherapy develop mucositis. (12) Pathophysiology Firstly, the chemotherapy drugs induce the death of the basal epithelial cells, which may occur by the generation of free radicals. These free radicals activate second messengers that transmit signals from receptors on the cellular surface to the inner cell environment, leading to up-regulation of pro-inflammatory cytokines, tissue injury, and cell death. The pro-inflammatory cytokines produced by macrophages, such as TNF-α, amplify the mucosal injury; the production of these pro-inflammatory cytokines can also be stimulated by a superimposed infection of the ulcerated areas of the mucosa. Later, epithelial

proliferation and cellular differentiation occur, restoring the integrity of the mucosa (12). The anti cancer drug most commonly associated with oral mucositis include bleomycin, doxorubicin, fluorouracil and methotrexate. The cancer therapy agents vincristine and daunorubicin have a toxic effect on the mucosa [Köstler et al., 2001]. Either the use of these drugs or the cancer itself leads to neutropenia, which predisposes the mucosa to mucostitic lesions and also enables bacterial invasion of the submucosa and vascular walls, leading to bacteraemia and septicaemia [Sonis, 2004; Brown and Wingard, 2004]. The patient in the case described here initially exhibited bacteraemia, the remission of which occurred following haematological recovery associated to the use of meropenem and vancomycin. In radiotherapy, an inflammatory response is influenced by the depth and volume of radiation, total gray delivered and the number and frequency of treatments. The onset, duration and intensity vary with the individual but most often the onset starts with second week of therapy or after a dose of about 2000cGy.radiation therapy causes loss of taste by damaging the microvilli and outer surface of taste cells, the onset is rapid and progressive with ageusia or mouth blindness occurring after 3000 cGy. Clinical Manifestation The first symptoms reported by patients with oral mucositis are burning mouth and color changes in the mucosa, which becomes white because of insufficient keratin desquamation. Then, this epithelium is replaced by atrophic, edematous, erythematous, and friable mucosa, allowing the development of ulcerated areas with the formation of a pseudomembrane, characterized by the presence of a fibrinopurulent, yellow, and outstanding layer (6,9). The ulcerated lesions are painful and compromise the patient nutrition and oral

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hygiene, and also are considered sites for the development of local and systemic infections. In the oral mucosa, this condition involves the ventral portion of tongue, floor of the mouth and soft palate (scully et al;2004). According to the World Health Organization, oral mucositis is classified into the following grades: Grade 0 – absence of mucositis; Grade I – presence of painful ulcerations and erythema; Grade II – presence of painful, erythema, edema or ulcerations that do not affect the patient food intake; Grade III – confluent ulcerations that affect the food intake; Grade IV – the patient requires parenteral nutrition (13).

Oral Hygiene Assessment Prior to cancer therapy, the patient was submitted to an assessment of the oral cavity. Dental caries or periodontal disease associated with inadequate oral hygiene may lead to a greater risk for oral complications during the course of cytotoxic therapy. Odontogenic and gingival infections are a considerable source of bacteria, which aggravate oral mucositis lesions. These risk factors underscore the importance of an inspection of the oral environment before and during treatment that has a potentially toxic effect on the mucosa, as prior assessment allows differentiating oral mucositis from other pre-existing lesions as well as the elimination of potential sources of infection and sites of chronic irritation [Stevenson-Moore, 1990; Pajari et al., 1995; Brown and Wingard, 2004]. This conduct is part of the protocol for patients at the Oncology Clinic at which the present case was treated. Regarding the indices used for the assessment of mucositis, the first study employed the Daily Mucositis Index (DMI) [Tardieu et al., 1996], the gradation of which ranges from 0 to 3 and assesses different aspects in the lips, gums, oral mucosa and tongue. In the present case, the WHO scale [1979] was employed, which ranges from 0 to 4 and does not measure different aspects in the different sites analysed. Moreover, the aforementioned study assessed the lesions only on the first and last days of treatment, whereas the assessment was performed on a daily basis in the present case.

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CATEGORY RATING 1 2 3 4 LIPS 1 2 3 4 Smooth,pink,moist

and intact Slightly wrinkled and dry; one or more isolated reddened areas

Dry and somewhat swollen, may have one or two isolated blisters; inflammatory line or demarcation

Very dry and edematous ;entire lip inflamed; generalized blisters or ulcerations

Gingiva and oral mucosa

1 2 3 4 Smooth,pink,moist and intact

Pale and slightly dry; one or two isolated lesions, blisters or reddened areas.

Dry and somewhat swollen, generalized redness; more than two isolated lesions, blisters or reddened areas.

Very dry and edematous; thick and engorged; entire tongue very inflamed; tip very red and demarcated with coating; multiple blisters or ulcers.

Tongue 1 2 3 4 Smooth,pink,moist and intact

Slightly dry; one or two isolated reddened areas; papillae prominent , particularly at base.

Dry and somewhat swollen,; generalized redness but tip and papillae are redder; one or two isolated lesions or blisters.

Very dry and edematous; thick and engorged; entire tongue very inflamed; tip very red and demarcated with coating; multiple blisters or ulcers.

Teeth 1 2 3 4 Clean; No debris Minimal debris; mostly between teeth

Moderate debris clinging to one-half of visible enamel

Teeth covered with debris

Saliva 1 2 3 4 Thin, watery, plenty Increase in amount Saliva scanty and maybe somewhat thicker than normal

Saliva thick and ropy, viscid or mucid

Oral dysfunction

No dysfunction Mild dysfunction Moderate dysfunction

Severe dysfunction

Score 5 6-10 11-15 16-20 Treatment modalities Antioxidants Antioxidants may he particularly important since cancer treatment is an oxidative process. Radiotherapy and chemotherapy generate free radical species, which require anfioxidants to be neutralized

Beta-carotene This has been proven to be useful in chemotherapy-induced mucositis. In one trial, chemotherapy patients were given 400,000 IU per day for 3 weeks and then 125,000 IU for an additional 4 weeks.

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Vitamin E in combination with vitamin C Both act on a cellular level by protecting the cell membrane and preventing peroxidation. Glutamine A precursor of glutathione, this is very important for stress periods. It is the most abundant amino acid in the human body, and it is now considered a conditionally essential amino acid during periods of catabolism. Early studies show that glutamine has a positive effect through three mechanisms: (1) as a cellular fuel; (2) as a precursor for nucleotides needed for cell regeneration; and (3) as a source of glutathione, which is a potent antioxidant's The use of 4 grams of powdered glutamine in oral rinse in a swish and swallow suspension, twice per day, decreases the intensity and duration of the mucositis Lysofylline A protectant that reduces lipid peroxidation also decreases oxidative injury. It is presently being tested in chemoradiation trials of head and neck cancer Mucosal barriers Clobetasol (0.05% ointment 1:1 with Orábase). As a topical corticosteroid, it plays a role in inflammation and immunosuppression. It is contraindicated in infection. Mouthwashes Benzydamine hydrochloride As an oral rinse, this has been shown to be effective, safe, and well tolerated in ameliorating the symptoms of cancer treatment induced mucositis. Rinsing then expectorating 15 mL of 0.15% solution every 2 hours will help with the painful inflammation of the mouth and throat. Benzydamine base local analgesic, antimicrobial, and anti-inflammatory properties. It prevents the

release of the arachidonic acid cycle, which is an initiator of the inflammatory process. Corticosteroid mouthwashes These may be beneficial and are contraindicated if the patient bas a bacterial or viral infection. Triamcinolone acetonide 0.2% aqueous suspension can be used as a rinse for 1 minute twice a day and expectorated. Chamomile mouthwashes These have been used to improve mucosal healing. With controversial results. However, rinsing with 15 drops in 10 mL of warm water, three times a day, has reduced the incidence and severity of mucositis in cancer patients. Local anesthetic mouthwashes These may help to relieve pain on a temporary basis. Analgesics Capsaicin This is found in chili peppers and acts upon nerve endings to provide temporary pain relief. The exact mechanism of action is unknown Morphine A central nervous system analgesic, it depresses pain impulse transmission. It is effective for managing mucositis pain in cancer patients, but dry mouth is one of its adverse reactions. (13)It does not improve the health of the mucosa. Fentanyl (transdermal patch) A very potent short acting opioid, it is used primarily as an anesthetic. It is available in a sustained-release transdermal delivery system (duragesic) with a half-life of 22 hours.

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Immunomodulators Thalidomide An immunomodulatory and antiangiogenic agent, it inhibits tumor necrosis factor-alpha (TNF-o;), which is associated with oropharyngeal ulcers. In multiple studies, the efficacy of this medication against oral and esophageal ulcers bas been demonstrated. In one trial, 92% of patients had complete healing after 4 weeks by taking 200 mg by mouth at bedtime. Nonpharmacologic approach Cryotherapy This produces vasoconstriction, which reduces blood flow and diminishes the distribution of the chemotherapeutic agent to the oral mucosa. Ice swishing for 30 minutes following cancer therapy has been shown to be beneficial for these patients Low-intensity laser therapy This may improve wound healing and accelerate replication of the cells. Low-energy helium-neon (He-Ne) laser seems to be a safe, simple, atraumatic, and efficient method for the prevention and treatment of chemotherapy/radiotherapy- induced mucositis. Management protocol Grade 1 Brush with soft bristled nylon brush and floss daily Rinse with salt and soda or 15% hydrogen peroxide Apply a moisturizer. Promote oral hydration and nutritional intake Remove and clean denture

Grade 2 & 3 Increase frequency of oral hygiene to every 2-3 hours Use foam oral wash if brushing is too painful Use agent to protect mucosa Apply topical agent for pain control Supplement oral intake with enteral or parental support. Provide proper analgesics and/or antibiotics if indicated Cultural suspect areas Grade 4 Continue frequent oral hygiene I.V antibiotics Laser therapy Cryotherapy Conclusion Mucositis is a common side effect of radio and/or chemotherapy anticancer treatments, but it has a complex pathophysiology and requires management strategies that have not been standardized yet. To identify patients at high risk to develop this condition is essential to reduce the costs of the anticancer treatment and to avoid its interruption after the installation of mucositis. There are many agents used for the treatment of mucositis with different mechanisms of action. However, there are no conclusive evidences on their effectiveness to establish protocols for patients undergoing radio and/or chemotherapy References 1. Implications for evidence-based research in alternative and complementary palliative treatments. Evid Based Complement Alternat Med 2005;2:489-94. 2. Epstein JB, Schubert MM. Oral mucositis in myelosuppressive cancer therapy. Oral

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Surg Oral Med Oral Pathol Oral Radiol Endod 1999;88:273-6. 3. Gibson RJ, Bowen JM, Keef DM. Technological advances in mucositis research: new insights and new issues. Cancer Treat Rev 2008;34:476-82. 4. Rubenstein EB, Peterson DE, Schubert M, Keefe D, McGuire D, Epstein J et al. Clinical practice guidelines for the prevention and treatment of cancer therapy-induced oral and gastrointestinal mucositis. Cancer 2004;100:2026-46. 5. Volpato LE, Silva TC, Oliveira, TM, Sakai VT, Machado MA. Radiation therapy and chemotherapy-induced oral mucositis. Rev Bras Otorrinolaringol 2007;73:562-568. 6. Keefe DM, Schubert MM, Elting LS, Sonis ST, Epstein JB, Raber- Durlacher JE et al. Updated clinical practice guidelines for the prevention and treatment of mucositis. Cancer 2007;109: 820-31. 7. Arora H, Pai KM, Maiya A, Vidyasagr MS, Rajeev A. Efficacy of He- Ne Laser in the prevention and treatment of radiotherapy-induced oral mucositis in oral cancer patients. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2008;105:180 8. Lionel D, Christophe L, Marc A, Jean-Luc C. Oral mucositis induced by anticancer treatments: physiopathology and treatments. The Clin Risk Manag 2006;2:159-68. ___________End of Article__________

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REVIEW ARTICLE

IMPORTANCE OF INFORMED CONSENT IN DENTISTRY

1Dr. Annie Mehnaz Mirza

1BDS, SVS Institute of Dental Sciences, India


Dr. Annie Mehnaz Mirza E-Mail: [email protected]


AbstractThe aim of this article is to provide fundamental information regarding consent when providing dental care. The change in attitude of patients with emphasis on being involved and informed of every aspect of care is not only apparent in adults but also when providing care for children and young adults. It is important for the dentist to be well informed of the fundamental process of consent, which exists under the law affecting both adults and minors in order to provide care within the legal framework. 2

Introduction Patients’ informed consent is a legal regulation and a moral principle. It represents patients’ rights to take part in the clinical decisions concerning their treatment. In order to practice in a professionally responsible manner, dentists must assist patients to make well-informed decisions about treatment procedures. The importance of obtaining informed consent in dentistry is increasingly recognized for moral and legal arguments which are explored. Morally, patients have the right to self-determination and respect for it underpins the relationship of trust deemed so important for clinical success.3 Legally, this right is reinforced through the risk of dentists being sued for negligence if they do not adequately respect it. The practical implications of the doctrine of informed

consent are sometimes unclear in clinical work - the reasons for this are assessed and illustrated. Standards of good practice in obtaining informed consent are suggested. How it is done Dentists have a duty to explain clearly about the pros and cons of a treatment. That does not mean that he must engage in an explanation equal to the depth of three hours of dental continuing education! It does mean, however, that a dentist must inform, in layman’s terms, the condition or disease present and the treatments available to the patient, whether or not the practitioner performs all of the treatments discussed. For example, a general dentist must discuss the option of implants as well as bridges and partial dentures, even if that dentist does not place or restore implants, if he plans to

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remove a tooth or two on the lower right quadrant. The patient must understand not only the importance of replacing the extracted teeth but all of the available options to do so as well. There are three essential components to valid consent:

• Competence: It means that the patient has sufficient ability to understand the nature of the treatment and the consequences of receiving or declining that treatment.

• Voluntariness: It means that the patient has fully agreed to have the treatment and there has been no coercion or undue influence to accept or decline the treatment.

• Information and knowledge: It means that sufficient comprehensible information is disclosed to the patient regarding the nature and consequences of the proposed and alternative treatments.

All these three elements are interdependent but must be present for consent to be ethically and legally valid. Types of Informed Consent

Informed Consent is of three types:

1. Implied Consent: Implied consent refers to when a patient passively cooperates in a process without discussion or formal consent. The principles of good communication apply in these circumstances and health professionals need to provide the patient with enough information to understand the procedure and why it is being done. Implied consent does not need to be documented in the clinical record.

2. Verbal Consent: A verbal Consent is where a patient states their consent to a procedure verbally but does not sign any written form. This is adequate for routine treatment such for diagnostic

procedures and prophylaxis, provided that full records are documented.

3. Written Consent: A written consent is necessary in case of extensive intervention involving risks where anesthesia or sedation is used, restorative procedures, any invasive or surgical procedures, administering of medications with known high risks etc.

When the Patient disagrees

As is often the case in the dental office, patients arrive in pain and simply want the pain to stop no matter what the consequences. In such cases, it is best to alleviate the pain with local anesthetic to allow a less clouded judgment and normal thought process to emerge. In the eyes of the law, a person cannot consent to anything if his or her judgment is impaired in any way. This was often meant to include drugs and alcohol, which remove the ability to make sound decisions, yet pain should also be included in this category since it too often impairs the ability to think in a rational manner. Patients have the ultimate say when it comes to treatment, but it is the practitioner’s duty to make sure all options for treatment are explored. In this case, a signed refusal protects the doctor by documenting the conditions found and the treatment options presented. This is called an Informed Refusal.4 A competent patient has a right to refuse medical treatment for any reason. It has been established that it does not matter if the decision is not what others would consider to be reasonable, nor does it matter if it leads to fatality as a result of the decision. What exactly is needed in the Informed Consent? It is not sufficient that a dentist simply document in the chart that he or she “went over all risks of treatment and the patient understands.” Specific risks must be written down, and patients must be given the opportunity to discuss with the doctor and question those issues which they do not understand. It should consist of a well formed questionnaire including but not limiting to:

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• The proposed treatment plan (indicating to what extent it depends upon established versus relatively new or controversial procedures) and its cost.

• Likely prognosis, outcomes and benefits.

• Possible complications, side-effects and material risks inherent in the treatment.

• Possible alternative treatments and cost options.

• Likely consequences of no treatment. • Any other aspects requested by the

patient.5

This should be immediately followed by the patient’s signature/date, doctor’s signature/date and witness’s signature/date. Make sure that the patient’s name is legibly printed somewhere on the form since some signatures are illegible. In most cases, a consent form need be little more than one page for most dental procedures if it is organized well. When is Consent not required?

• In case of an emergency the treatment is a necessity and there is no written advance directive by the patient to the contrary.

• Treatments authorised by statute are medical treatments/interventions identified in law, including compulsory drug screening and certain procedures relating to mental health patients.

• Any medical treatment/intervention to be carried out or ceased as a result of a direction/order of the court. Valid informed consent by the patient is not required.

Consent for Children or minors Obtaining consent for children is a difficult task. The primary responsibility for providing

care and consent for the child or young person should lay with his/her parents. Patients under the age of majority or adults with diminished mental capacity should have treatment consent obtained from a parent or legal guardian. The adult accompanying the pediatric patient may not be a legal guardian allowed by law to consent to medical procedures. Examples of this include a grandparent, stepparent, noncustodial parent or friend of the family. 6

Where a child requires treatment without a parent or legal guardian present:

• Telephone consent may be obtained. • Where the child or minor is assessed

as competent they may provide consent.

• Where a responsible adult (i.e. teacher, Grandparent) is with the child, evidence of parental consent to treatment must be sighted or parental consent obtained.

When problem arise with the child and parents with different opinions then, according to law a person with parental responsibility can always override decisions made by children. In case of an emergency, the health practitioner has a right to treat the patient without the consent. Consent to Disclose/Release of Information During the general consent to treatment process patients need to be made aware that their health information will be shared with the treating team within the hospital / health care facility and also to their General Practitioner (GP) as part of that treating team. And health information may also be released to third parties to ensure the provision of appropriate and continuing care. This should only occur with the specific consent of the patient without which there are

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chances of the practitioner being sued for releasing the information. Conclusion However, in dentistry, just as in medicine, unforeseen mishaps occur despite our best efforts. Therefore, it is just as important for dentists to obtain informed consent prior to every invasive and/or irreversible procedure. At first glance, most patients appear friendly and most dental procedures appear routine, but once a procedure goes wrong, an unhappy patient with a skilful attorney can become a dentist’s worst nightmare. A signed, written informed consent may be the only evidence that the mishap that occurred was a foreseeable risk acknowledged by the dentist and accepted by the patient. Although obtaining informed consent may at first seem awkward, cumbersome, and time-consuming, it may very well save a practitioner countless hours in the courtroom and thousands of rupees in legal fees should some mishap occur.

References

1. Lewis Laska, Nashville, TN -Medical Malpractice Verdicts, Settlements and Experts.

2. Seema Lal, Consent in Dentistry, Pacific Health Dialog, Volume 10, 2003.

3. Dr. Jay Baxley, A Peer Reviewed article,“Informed Consent”

4. ACT - Consent to treatment, Patient safety and Quality Unit.

5. Australian Dental Association, Guidelines for good Dentistry, Consent for Care in Dentistry by Federal Council, 1999.

6. American Academy of Pediatric Dentistry- Guidelines of Informed Consent, 2005. ___________End of article____________

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REVIEW ARTICLE

MICRO‐ENDODONTICS: AGGRANDIZEMENT OF ROOT CANAL TREATMENT

Sameer D Jain1

1BDS, M.G.V’s K.B.H Dental College and Hospital [Mahatashtra University of Health Sciences (M.U.H.S)], Mumbai –Agra Highway, Panchavati, Nashik, Maharashtra, India


Sameer D Jain A-1 Kaustubh Park, SVP Road, Borivali-W, Mumbai-400103, Maharashtra, India Contact no. 022 28944364 +91 9892490644 +91 9029297516 Fax – 022 28954657 E-Mail: [email protected] Access this Article Online

AbstractThis article presents a review of the history of the dental-operating microscope and how it experienced slow acceptance. Following its introduction in 1982, it wasn’t until 1997 that microscopy training became mandatory for Advanced Specialty Education Programs in Endodontics. Undoubtedly, microscopic enhanced endodontics ultimately reshaped clinical practice and created a potential for a higher standard of care.

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Introduction It may seem surprising that the microscope is not a high-tech instrument. It has been used in the medical field for over 50 years. According to the Zeiss Company, the microscope was first introduced to otolaryngology around 1950, and then to neurosurgery in the 1960s, and to endodontics in the early1990s (1). Dentistry, therefore, is about 40 years behind medicine in this respect. As in medicine, the incorporation of the microscope in clinical endodontics has had profound effects on the way endodontics is done and has changed the field fundamentally. For this reason, the 1998 American Dental Association accreditation requirement change states that all accredited United States postgraduate programs must teach the use of the microscope in nonsurgical and surgical endodontics (2). This was a giant step forward in the advancement of endodontics. This article outlines the key prerequisites for the use of the microscope in nonsurgical endodontic procedures. There are many microscopes on the market; the three most popular ones are presented in Fig. 1.

Fig. 1: The three most popular microscopes in endodontics Methods Prerequisites for the use of the microscope in nonsurgical endodontics:

Rubber dam placement The placement of a rubber dam prior to any endodontic procedure is an absolute requirement for sterility purposes. This technique is taught at all dental schools. In endodontics, however, the purpose is greater. Here, the rubber dam placement is necessary because direct viewing through the canal with the microscope is difficult, if not impossible. A mirror is needed to reflect the canal view that is illuminated by the focused light and magnified by the lens of the microscope. If the mirror were used for this purpose without a rubber dam, then the mirror would fog immediately from the exhalation of the patient. Thus, the powerful microscope magnification and illumination would be rendered totally useless for the necessary visualization of the chamber floor and the canal anatomy. To absorb reflected bright light and to accentuate the tooth structure, it is recommended to use blue or green rubber dams (Fig. 2).

Fig. 2: The use of a rubber dam is essential for effective microscope use Indirect view and patient head position. As mentioned previously, it is nearly impossible to view the pulp chamber directly under the microscope. Instead, the view seen through the microscope lens is a view reflected by way of a mirror. To maximize the access and quality of the view by this indirect means, the

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position of the patient (especially the head position) is important (Fig. 3). The optimum angle between the microscope and the mirror is 450, and the clinician should be able to obtain this angle without requiring the patient to assume an uncomfortable position. The maxillary arch is rather easy for indirect viewing. Basically, the patient’s head is adjusted to create a 900 between the maxillary arch and the binocular (Fig. 4). In this position, the mirror placement will be close to 450 for best viewing (3).

Fig. 3: Patients should wear protective dark glasses and have support for the neck, such as a moldable pillow

Fig. 4: Positioning the microscope. Notice the ergonomics of the clinician and comfortable patient position Mouth mirror placement It is always a good idea to use the best mirror for this purpose. If a rubber dam has been placed, then the mirror must be placed away from the tooth within the confines of the rubber dam. If the mirror is placed close to the tooth, then it will be difficult to use other

endodontic instruments. Readjusting the mirror will necessitate refocusing of the microscope, making the entire operation time-consuming and, at times, frustrating. This is especially true during a lengthy perforation repair. With practice, however, the ‘‘correct’’ placement of the mirror will become automatic. Some key instruments The ability to locate hidden canals is the most important and significant benefit gained from using the microscope. To do this effectively and efficiently, clinicians must use specially designed microinstruments. An explorer can pick the entrance of a canal under the microscope, but negotiating the canal with a file can be challenging because there is only a tiny space between the mirror and the tooth for a finger with a file to move around. Files specially designed by Maileffer, called microopeners, have with different sized tips and can be extremely useful (Fig. 5). These hand-held files allow the clinician to initially negotiate the canal, verifying that the ‘‘catch’’ is truly a canal. After the canal is located in this manner, clinicians can instrument the canal normally without the microscope. The use of Gates–Glidden burs to enlarge the canal entrance prior to full instrumentation, however, can be easily achieved under the microscope, facilitating the subsequent steps of canal instrumentation.

Fig. 5: Micro-openers by Maillefer are ideal instruments for exploration of hidden canals at high magnification

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For what procedures is the microscope really essential? Some enthusiasts claim that the microscope must be used for all steps of nonsurgical endodontic procedures. This may a noble idea, but in reality, it is not needed or desired. A clinician must consider the benefit/risk ratio when using the microscope. The following procedures are those that benefit from the use of the microscope. Diagnosis The microscope is an excellent instrument to detect microfractures that cannot be seen by the naked eye or by loupes. Under 16_ to 24_ magnification and focused light, any micro fracture can be easily detected (Fig. 6). Methylene blue staining of the microfracture area assists this effort greatly. A persistently painful tooth after endodontic therapy may be due to an untreated missing canal (eg, MB2 in a maxillary molar). Re-examination of the chamber at high magnification under the microscope may locate the missing canal (see the article by Kim elsewhere in this issue [Fig. 5]). Locating hidden canals The most important utility of the microscope in nonsurgical endodontics is locating hidden canals. The canal anatomy is extremely complex. All endodontic textbooks have information on molar teeth with three canals, premolars with two canals, and anterior teeth with one canal. Often, dental anatomy is not that predictable.

Fig. 6: Microfracture detected under the microscope (A) and the same tooth after extraction (B) Arrows identify the fracture line.

It has been found that nearly an astounding 50% of all molars (maxillary and mandibular) have a fourth canal, more than 30% of all premolars have a third canal, and close to 25% of all anterior teeth have two canals. What was considered a rare exception in the past has become a routine finding when using the microscope. Considering this as the benefit of using the microscope for endodontic procedures is obvious. There are teeth where the canal bifurcates at 3 to 5 mm into the canal and in the maxillary second molar, where the MB and DB are in very close proximity of each other; the microscope is an invaluable tool in clearly detecting the bifurcation and the two separate canals (4). Management of calcified canals With normal vision or low-power loupes, calcified canal in the pulp chamber is not detectable. When the calcified canal is looked at through the microscope at high magnification, however, the difference in the color and texture between the calcified canal and the remaining dentin can be easily seen. Careful probing and use of ultrasonics with CPR or Buc tips (Obtura/Spartan, Fenton, Missouri) will allow clinicians to detect and negotiate the calcified canal easily (Fig. 7). Sometimes in these cases, the ultrasonic preparation of the canal or canals has to go as far as a couple of millimeters short of the apex. Again, the microscope allows the clinician to detect and prepare conservatively, and not to gouge the healthy dentin structures (Fig. 8). Perforation repair Perforation does occasionally occur no matter how carefully the tooth is accessed for endodontic therapy. When a perforation occurs, the microscope is the key instrument to identify and evaluate the damaged site.

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Fig. 7: Buc tips (Obtura/Spartan) are ideal ultrasonic instruments for cleaning the pulp chamber and floor for clear viewing of the canals.

Fig. 8: Access preparation and management of calcified canals at a high magnification under the microscope (A–F) The results of a careful inspection will be the basis for which the preparation of the perforation repair will be made. Briefly, the microscopic procedure is to place a matrix precisely, just outside of the perforation site (i.e. just exterior of the root substance). The matrix can be calcium sulfate or resorbable collagen. After the matrix is placed, mineral trioxide aggregate is packed against the matrix. This procedure requires delicate and careful handling of the materials so as not to extrude, overfill, or underfill. The microscope is essential for this procedure.

Retrieval of broken files With the more frequent use of nickel-titanium rotary files in general dentistry, the incidence of file separation within the canals has increased. When the file is broken at the apex, the microscope cannot be of help. If the file breaks within the coronal half of the canal, however, then the microscope is essential to guide the clinician to retrieve the broken files. In this manner, the broken file can be removed while minimizing the damage to the surrounding dentin. Final examination of the canal preparation It takes a simple step to see whether a canal is completely cleaned. Under the microscope, a small amount of sodium hypochlorite, a popular irrigation solution, is deposited into the canal and observed carefully at high magnification. If there are bubbles coming from the prepared canal, then there is still remnant pulp tissue in the canal. In short, the canal needs more cleaning. Discussion & Conclusion Cost versus patient benefit

Many of the practitioners who perform endodontic procedures and do not yet own a dental microscope are still evaluating the benefits of its use. Practicality is the key concern. How does one recoup the cost of the capital expenditure and the cost and time associated with training? Are the clinical benefits worth the expenditure of time and money? To address the critical cost and efficiency issue, clinicians should take an intensive training course at the very beginning to make them comfortable with handling the microscope and with working underneath it. Clinicians should also become totally committed to using the microscope in each of their treatment cases, not just selected ones. This practice is the fastest route toward proficiency and the best way to maximize the return on investment. In addition to clinical benefits associated with the use of the microscope in endodontics, after the initial learning

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curve, endodontic procedures can be done in less time because of the greater visibility of the root canal anatomy. Procedural errors can be greatly reduced (5), if not eliminated, and complicated cases become less so under the microscope. Another benefit of the microscope is the flexibility with documentation. Compared with intraoral video cameras, microdental images can be captured on computer or digital camera. The information can then be shared with referring dentists or patients and the images are, of course, also required information for the patient record.

References

1. Syngcuk Kim. Modern Endodontic Practice: Instrumentsand Techniques, Dent Clin N Am 2004; 48: 1–9.

2. Syngcuk Kim, Seungho Baek. The microscope and endodontics. Dent Clin N Am 2004; 48: 11–18.

3. Branson BG, Bray KK, Gadbury-Amyot C, et al. Effect of magnification lenses on student operator posture. J Dent Educ. 2004;68:384-389. Valachi B. Vision quest: finding your best working distance when using loupes. Dental Practice Report. 2006;4:49-50.

4. Spear FM. One clinician’s journey through the use of magnification in dentistry. Advanced Esthetics and Interdisciplinary Dentistry. 2006; 2:30-32.

5. Cuomo GM. Posture-directed vs. image-directed dentistry: ergonomic and economic advantages through dental microscope use. http://www. heryschein.com/usen/dental/services/cehp/HomeStudy.aspx. Published April 27, 2006. Accessed November 14, 2008.

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CASE REPORT

ENDODONTIC THERAPY IN A 3‐ROOTED MANDIBULAR SECOND MOLAR: A CASE REPORT

Dr. Saurabh S. Chandra1, Dr. Supriya

Chandra 2, Dr. Nilofer Hussain3, Dr. Anurag

Ahuja4

1 MDS, Assistant Professor, Dept. Of Conservative Dentistry & Endodontics, School Of Dental Sciences, Sharda University, Greater Noida, India 2 MDS, Senior Lecturer, Dept. Of Periodontology, Sree Bankey Bihari Dental College, Ghaziabad, India

3 Intern, School of Dental Sciences, Sharda University, Greater Noida, India 4 Intern, School of Dental Sciences, Sharda University, Greater Noida, India


Dr. Saurabh S. Chandra MDS, Assistant Professor, Dept. Of Conservative Dentistry & Endodontics, School Of Dental Sciences, Sharda University, Greater Noida, India Email: [email protected] Access this Article Online

AbstractA rare case of a three-rooted mandibular permanent second molar in a 21-year-old male patient is reported. After clinical and radiographic examination, four separate root canal orifices were detected. A mesial shift radiograph confirmed the presence of an additional disto-lingual root. The tooth was treated by orthograde endodontic treatment in two visits. The case report underlines the importance of complete knowledge about root canal morphology and possible variations that exist in mandibular molars; coupled with full clinical and radiographic examination, in order to increase the ability of clinicians to treat root canal aberrancies. Aim: Clinicians should be aware of these unusual root morphologies in the mandibular second molars. The initial diagnosis of a third root before root canal treatment is important to facilitate the endodontic procedure, and to avoid ‘missed’ canals. Keywords: Dental Anomalies, Mandibular molars, Radix Entomolaris, Three rooted mandibularmolar

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Introduction Orthograde endodontic treatment comprises of meticulous cleaning & shaping, disinfection of the entire root canal space followed by a three dimensional obturation. Root canals may be left untreated during endodontic therapy if the clinician fails to identify their presence, particularly in teeth with anatomical variations or extra root canals.1,2 Comprehensive knowledge of the presence of unusual root canal anatomy and morphology is important for successful dental practice and for identifying features of anthropological significance. It is commonly acknowledged that both deciduous and permanent mandibular molars display several anatomical variations. The majority of mandibular second molars are two-rooted with two mesial and one distal canal.3 However, the number of roots and root canals may vary. An additional third root, first mentioned in the literature by Carabelli, is called the Radix Entomolaris (RE).4 This supernumerary root is located distolingually in mandibular molars, mainly first molars. An additional root at the mesiobuccal side is called the radix paramolaris (RP).1,4-6 The identification and external morphology of these root complexes, containing a lingual or buccal supernumerary root, are described by Carlsen and Alexandersen.6

This supernumerary root (RE) has a frequency of less than 4% in Caucasians, 2.8% in African populations, whereas in populations with Mongoloid traits (Chinese, Indians and Eskimos) this macrostructure occurs with a frequency between 5% and 30%.1,2,6 In these populations, RE is considered to be a normal morphological variant and can be seen as an Asiatic trait.1 The aim of this paper is to report a mandibular second molar featuring

with three roots, which is a rare clinical entity. Case Report A 21-year-old southeast-Asian male patient reported to the Department of Conservative Dentistry and Endodontics, Ragas Dental college & Hospital, Chennai with the chief complaint of spontaneous dull pain in the lower right region for the preceding few months. His medical history was noncontributory. An intraoral clinical examination revealed a deep carious lesion in the right mandibular second molar (tooth #31) with tenderness on percussion. Radiographic and sensitivity tests were performed that led to a diagnosis of irreversible pulpitis with apical periodontitis, necessitating endodontic treatment (Fig. 1). The tooth was anesthetized using 2% lignocaine with 1:100,000 adrenalin (Lignox; Indoco Remedies, Mumbai, India) and isolated under rubber dam (Hygenic Dental Dam, Colténe Whaledent, Germany). Caries was excavated, and an adequate endodontic access cavity was made using an Endo Access bur (Dentsply Maillefer, Ballaigues, Switzerland). The chamber was flushed with 3% sodium hypochlorite (Dentpro, Chandigarh, India) to remove the debris. Observation via a conventional access cavity revealed the presence of 3 canal orifices, 2 mesial and 1 distal. The dentinal map on the floor of the chamber was traced and explored using a DG 16 endodontic explorer (Hu-Friedy, Chicago, IL) following which the pulp tissue was extirpated using barbed broaches (Dentsply Maillefer, Tulsa, OK). On inspection with 2.5 magnification prismatic loupes (Seiler, St. Louis, MO), a dark line was observed between the distal canal orifice and the distolingual corner of the pulp chamber floor. At this corner overlying dentin was removed with a diamond bur with

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a noncutting tip (Diamendo, Dentsply Maillefer) and a second distal canal orifice was detected (Fig.2). Canal patency was established using a #10 K file (Mani, Tochigi, Japan). The canal length was determined electronically using an electronic apex locator (Root ZX II; J. Morita, Tokyo, Japan) and subsequently verified with an intraoral periapical radiograph. Root canal instrumentation was performed with ProTaper Ni-Ti rotary files (Dentsply Maillefer, Tulsa, OK) using a crown-down technique. During preparation, EDTA (Glyde File Prep, Dentsply Maillefer, Tulsa, OK) was used as a lubricant and the root canals were disinfected with 3% sodium hypochlorite solution (Dentpro, Chandigarh, India). The canals were finally rinsed with saline (Marck Biosciences, Gujrat, India), dried with sterile absorbent paper points (Dentsply Maillefer), and an intra canal medicament of calcium hydroxide was place. Initially, the distolingual root canal was thought to be a second canal in one distal root. Radiographically the outlines of the distal root(s) were unclear; however, the unusual location of the orifice far to the disto-lingual indicated a supernumerary root, and the presence of an RE was confirmed on the postoperative radiograph. The patient was recalled after a week and the canals were obturated with cold laterally condensed gutta-percha (Dentsply Maillefer) using AH Plus resin sealer (Dentsply Maillefer). A postoperative radiograph (Fig. 3) was taken; the opening cavity was sealed with posterior composite (Solare, GC Fuji, Japan) and the patient was scheduled for a permanent coronal restoration. Discussion Anatomical variations of mandibular molars are documented in the literature. Nonetheless, variations of the anatomy of the root canal system in molars are not appreciated by a great number of general practitioners. A

supernumerary root can be found on the first, second and third mandibular molar, occurring least frequently on the second molar.1 There are various case reports of mandibular first molars featuring an RE. On the contrary, RE in the mandibular second molars has been seldom reported. Poorni et al. reported a case of mandibular second molar featuring an RE confirmed using spiral CT.7 The RE is located distolingually, with its coronal third completely or partially fixed to the distal root. The dimensions of the RE can vary from a short conical extension to a ‘mature’ root with normal length and root canal.1 In most cases the pulpal extension is radiographically visible. In general, the RE is smaller than the distobuccal and mesial roots and can be separate from, or partially fused with, the other roots. A classification by Carlsen and Alexandersen describes four different types of RE according to the location of the cervical part of the RE: types A, B, C and AC.6 Types A and B refer to a distally located cervical part of the RE with two normal and one normal distal root components, respectively. Type C refers to a mesially located cervical part, while type AC refers to a central location, between the distal and mesial root components. This classification allows for the identification of separate and nonseparate RE. The etiology behind the formation of the RE is still unclear.1 In dysmorphic, supernumerary roots, its formation could be related to external factors during odontogenesis, or to penetrance of an atavistic gene or polygenetic system (atavism is the reappearance of a trait after several generations of absence). In eumorphic roots, racial genetic factors influence the more profound expression of a particular gene that results in the more pronounced phenotypic manifestation.5,6 Curzon suggested that the ‘three-rooted molar’ trait has a high degree of genetic penetrance as its dominance was reflected in the fact that

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the prevalence of the trait was similar in both pure Eskimo and Eskimo/ Caucasian mixes. The location of the orifice of the root canal of an RE has implications for the opening cavity. The orifice of the RE is located disto- to mesiolingually from the main canal or canals in the distal root.1 An extension of the triangular opening cavity to the (disto) lingual results in a more rectangular or trapezoidal outline form. If the RE canal entrance is not clearly visible after removal of the pulp chamber roof, a more thorough inspection of the pulp chamber floor and wall, especially in the distolingual region, is necessary. Visual aids such as a surgical loupes, or dental microscope can be useful. A dark line on the pulp chamber floor can indicate the precise location of the RE canal orifice. The distal and lingual pulp chamber wall can be explored with an angled probe to reveal overlying dentin or pulp roof remnants masking the root canal entrance. The calcification, which is often situated above the orifice of the RE, has to be removed for a better view and access to the RE. An initial relocation of the orifice to the lingual is indicated to achieve straight-line access. 8 These anatomic variations in distal root anatomy may be identified through careful reading of angled radiographs. Slowley has demonstrated how difficult it is to detect extra roots, let alone extra canals.9 On the contrary, completing a thorough radiographic study of the involved tooth with exposure from three different horizontal projections, the standard buccal-to-lingual projection, 20° from the mesial, and 20° from the distal reveals the basic information regarding the anatomy of the tooth in order to perform endodontic treatment.8,9 However, using the buccal object rule with two radiographs with different horizontal angulations may suffice to determine the position of a lingual root. One of these radiographs is taken in the orthoradial

position and the other taken either 30° mesially or distally. This buccal object rule has also been called Clark’s rule, the same lingual, opposite buccal (SLOB rule) and Walton’s projection. It is imperative that a comprehensive pre-operative radiographic evaluation is done prior to initiation of endodontic therapy. Conclusion Knowledge of both normal and abnormal anatomy of the mandibular molars dictates the parameters for execution of root canal therapy and can directly affect the probability of success. Therefore, practitioners must be familiar with all molar abnormalities, as well as their prevalence. References

1. Calberson FL, De Moor RJ, Deroose CA. The radix entomolaris and paramolaris: clinical approach in endodontics. J Endod 2007;33:58–63.

2. De Moor RJ, Deroose CA, Calberson FL. The radix entomolaris in mandibular first molars: an endodontic challenge. Int Endod J 2004;37:789 –99.

3. Skidmore AE, Bjorndal AM. Root canal morphology of the human mandibular first molar. Oral Surg Oral Med Oral Pathol 1971;32:778-784

4. Carabelli G. Systematisches Handbuch der Zahnheilkunde. 2nd ed. Vienna: Braumüller and Seidel 1844; 114.

5. Bolk L. Bemerkungen über Wuzelvariationen am menschlichen unteren Molaren. Zeitschrift für Morphologie Anthropologie 1915;17:605–10.

6. Carlsen O, Alexandersen V. Radix entomolaris: identification and

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7. morphology. Scan J Dent Res. 1990;98:163–73.

8. Poorni S, Senthilkumar A, Indira R. Radix entomolaris in mandibular molars confirmed using spiral CT: a case report. Endond Prac Today 2010;4

9. Ingle JI, Heithersay GS, Hartwell GR et al. Endodontic diagnostic procedures. In: Ingle JI, Bakland LF,

eds. Endodontics, 5th edn. Hamilton, London, UK: BC Decker Inc., 2002;203–58.

10. Slowley RR. Radiographic aids in the detection of extra root canals. Oral Surgery, Oral Medicine and Oral Pathology 1974;37, 762–72.

Legends Fig. 1 Pre-operative radiograph Fig. 2 View of Pulp chamber Fig. 3 Post operative radiograph

Fig. 1

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Fig. 2

Fig. 3

_____________End of article______________

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ORIGINAL ARTICLE

SEM EVALUATION OF EFFECT OF 37% PHOSPHORIC ACID GEL, 24% EDTA GEL AND 10% MALEIC ACID GEL ON THE ENAMEL AND DENTIN FOR 15 AND 60 SECONDS: AN IN‐VITRO STUDY

Narendra Parihar1, Manish Pilania 2

1BDS, Jodhpur Dental College General Hospital, Jodhpur 2Intern, Department of Conservative Dentistry and Endodontics, Jodhpur Dental College General Hospital, Jodhpur, Rajasthan, India

Corresponding Authors

1. Narendra Parehar Khanda Falsa, Jalori Gate, Jodhpur. Contact no. (+91)9799108142 Email: [email protected]

2. Manish Pilania G-43, Shastri Nagar, Jodhpur Contact no. (+91)9461055068 Email: [email protected] Access this Article Online

AbstractBackground: The purpose of this study was to investigate the relationship between etching of enamel and dentin with different acids: 37% phosphoric acid, 10% maleic acid and 24% EDTA, at different etch durations of 15 and 60 seconds; so as to analyze the surface characteristics of etched enamel, diameter of the dentinal tubules and the depth of demineralization in the tubules under scanning electron microscope (SEM). Method: Thirty freshly extracted maxillary and mandibular premolars, indicated for orthodontic extraction were selected from patients in the age group of 14 to 21 years. The teeth were randomly divided into 3 groups of 10 teeth each and were etched with 37% phosphoric acid, 24% EDTA gel and 10% maleic acid gel respectively for 15 and 60 seconds. The samples were then split along their long axes, dehydrated and sputtered with palladium gold. The sputtered specimens were examined under scanning electron microscope. Results: Acid etching causes various types of etching patterns in enamel indicating preferential dissolution of the enamel prisms. With 37% phosphoric acid, type 2 etching pattern is seen; with 10% maleic acid, type 1 etching pattern is predominant and etching with 24% EDTA leads to type 4 etching pattern. In dentin, etchants widen the dentinal tubule orifices due to demineralization of peritubular dentin and this demineralization extends deep into the dentinal tubules for varying depths depending upon the type of acid used and time of its application. No statistically significant difference exists in the widening of the dentinal tubule orifices between the group I (37% phosphoric acid) and group III (10% maleic acid) specimens. Conclusion: It can be suggested that 15 seconds etching with a milder acid like 10% maleic acid instead of 37% phosphoric acid is sufficient to obtain adequate bond strength because there is no significant difference within the observational parameters, except for the depth of demineralization in tubules. Additional depth is unnecessary because the adhesive systems cannot penetrate completely into the dentinal tubules, leading to nanoleakage.

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Introduction An ideal restorative material would be the one which chemically bonds to the tooth and has strength comparable to that of the tooth structure. In 1955, Buonocore instituted the use of 85% phosphoric acid solution to cause selective decalcification of tooth structure. This produced microporosities in the enamel, increased the surface area, as well as enhanced wettability of the surface providing an intimate contact between tooth and restoration thereby changing the retention form from mechanical to micromechanical. In 1979, Fusayama introduced and popularized the concept of etching of dentin.3 Stronger acids like phosphoric acid not only decalcify the enamel and dentin

surfaces but also demineralize in depth to a greater extent. The increased depth of demineralization is not essentially required because the adhesive systems are not able to penetrate till the complete depth, leading to nanoleakage and incessant degradation.6 Dentin being a vital tissue and containing more organic content than enamel, requires use of milder acids (10% maleic acid and 24% EDTA) so as to prevent damage to micromorphological structure and preserve the integrity of the collagenous mass as they do not denature it.2

Materials and Methods Thirty intact, caries free maxillary and mandibular premolars extracted due to orthodontic reasons were used. These were extracted in the Department of Orthodontics, Jodhpur Dental College General Hospital, Jodhpur, from patients in the age group of 14 to 21 years. After extraction, the teeth were thoroughly cleaned using pumice slurry, and the roots were sheared off from the crown at the labial cementoenamel junction with a diamond abrasives coated safe sided disc. The teeth were then stored in normal saline at 4ºC. At the start of the study, the buccal surfaces of the premolars were ground wet on 320 grit and 600 grit silicon carbide paper till the dentin was exposed to create a flat surface on the enamel and dentin. The samples were then sectioned in the middle along their long axis through the lingual surface with a diamond abrasive coated safe sided disc 1 – 1.5 mm short of the buccal flat surface. The samples were rinsed thoroughly in normal saline to clear off any debris.

The following materials were used for etching of the specimens:-

* 37% phosphoric acid gel.

* 24% Ethylenediamine tetracetic acid (EDTA) gel.

* 10% maleic acid gel.

The prepared samples were randomly divided into three groups:-

Group I, Group II and Group III.

The group I, II and III were further divided into two subgroups of 5 teeth each.

Ia - 5 specimens to be etched with 37% phosphoric acid gel for 15 seconds.

Ib - 5 specimen to be etched with 37% phosphoric acid gel for 60 seconds.

IIa - 5 specimens to be etched with 24% EDTA gel for 15 seconds.

IIb - 5 specimens to be etched with 24% EDTA gel for 60 seconds.

IIIa - 5 specimens to be etched with 10% maleic acid gel for 15 seconds.

IIIb - 5 specimens to be etched with 10% maleic acid gel for 60 seconds.

The etchant gels were applied on the flat buccal surfaces with the help of a brush, the gel was rinsed off from the teeth with 10ml distilled water for 20 seconds. The specimens were then sectioned into two halves with a sharp chisel and mallet by placing the chisel into the groove which had been prepared along the long axis of the samples. The sectioned specimens were utilized for analyzing the depth of demineralization in dentin by the etchants.

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Photograph 1: Armamentarium used for the study

Photograph 2: Materials used in the study

The samples were transferred to small bottles containing graded concentrations of ethyl alcohol (60% to100%). The samples remained in each alcohol concentration for two hours. The dehydrated samples were removed from 100% ethyl alcohol and were mounted on aluminium stubs and placed in vacuum chamber to desiccate them completely.

Samples were viewed under scanning electron microscope (LEO) at various magnifications.

The magnifications selected were:-

- For enamel - x 3,000

- For dentin - x 2,000

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Photograph 3: Scanning Electron Microscope

The parameters to be observed were:- * The etching patterns on enamel surface. The etching patterns were categorized

according to Galil & Wright’s classification4: Type 1 Preferential dissolution of the

prism cores resulting in a ‘honeycomb’ appearance

Type 2 Etch pattern showing preferential

dissolution of the prism peripheries giving a ‘cobblestone’ appearance leaving prism cores relatively unaffected.

Type 3 A more random etch pattern, areas

of which corresponded to type 1 and

2 pattern together with regions in which the pattern of etching could not be related to prism morphology.

Type 4 Pitted enamel surface. Type 5 Flat smooth surface of enamel

without microirregularities. * Diameter of the widened dentinal tubules * Depth of demineralization in the dentinal

tubules. The diameter of the tubules and the depth of demineralization were measured in µm (µ)

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Statistical Analysis

Using the standard deviation, the student t-test was applied

The probability value (p value) was kept constant at 5% significance

STATISTICAL ANALYSIS FOR THE WIDTH OF LOSS OF

ENAMEL PRISM CORE / PERIPHERY

Intragroup comparison

Mean StandardDeviation

Standard Error

T-value Status p<0.05 significant p> 0.05 insignificant

I Ia 0.39µ 0.0554 0.0248

1.65 Insignificant Ib 0.54µ 0.2040 0.0912

II IIa 0.00 0.00 -- IIb 0.00 0.00

III IIIa 3.30µ 0.9758 0.4364

1.195 Insignificant IIIb 4.29µ 1.5614 0.6983

STATISTICAL ANALYSIS FOR DIAMETER OF THE OPENED DENTINAL TUBULES

Intragroup comparison

Mean StandardDeviation

Standard Error


I Ia 2.99 0.8450 0.3779

1.208 Insignificant Ib 3.87 1.3881 0.6208

II IIa 1.94 0.3837 0.1716

3.543 Significant IIb 2.68 0.2663 0.1191

III IIIa 2.93 0.4168 0.1864 1.626 Insignificant IIIb 3.33 0.3671 0.1642

STATISTICAL ANALYSIS FOR DEPTH OF DEMINERALIZATION IN THE TUBULES

Intragroup comparison Mean

StandardDeviation

Standard Error


I Ia 8.87 1.0405 0.4653 2.532 Significant Ib 11.48 2.0587 0.9207

II IIa 0.00 0.00

10.894 Significant IIb 3.92 0.8050 0.3600

III IIIa 7.09 0.5575 0.2493 2.375 Significant IIIb 8.83 1.5382 0.6879

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Results

All etchants changed the micromorphological appearance of enamel and dentin surfaces. Etching of enamel with 37% phosphoric acid gel resulted in a 'cobblestone' appearance of the etched surfaces due to preferential dissolution of the peripheries of enamel prisms (photographs no. 4 and 5). This type of etching is classified as type 2 etching pattern.4 On dentinal surface, phosphoric acid gel removed the smear layer and caused widening of the dentinal

tubules (photograph no. 6). The widening of the tubule orifices occurs due to demineralization of peritubular dentin. The demineralization extends into the depth of tubules giving a 'funneled' effect (photographs no. 8 and 9). The dentinal surfaces treated for 15 and 60 seconds showed particulate residue. This surface residue is possibly silica which is used to thicken the etching gel (photographs no. 6 and 7).

Effect of 37% Phosphoric Acid Gel on Prepared Specimens for 15 Seconds.

Sample

No. Width of loss of enamel prisms periphery

Diameter of opened dentinal tubules

Depth of demineralization in tubules

1. 0.33µ 2.56µ 7.67µ2. 0.34µ 2.9 µ 8.58µ3. 0.44µ 4.3µ 10.43µ4. 0.38µ 2.03µ 9.26µ 5. 0.45µ 3.15µ 8.4µ

Mean 0.39µ 2.99µ 8.86µ Table: 1

Effect of 37% Phosphoric Acid Gel on Prepared Specimens for 60 Seconds.

Sample

No. Width of

loss of enamel prisms

periphery


Depth of demineralization

in tubules

1. 0.44µ 2.67µ 9.64µ 2. 0.36µ 3.90µ 9.31µ 3. 0.50µ 6.22µ 11.96µ4. 0.89µ 3.16µ 14.34µ5. 0.53µ 3.38µ 12.15µ

Mean 0.54µ 3.87µ 11.48µTable: 2

ETCHING OF ENAMEL WITH 37% PHOSPHORIC ACID

(Type 2 Etching Pattern)

Photograph 4: Etching Time-15 Seconds

Photograph 5: Etching Time- 60 Seconds

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ETCHING OF DENTIN WITH 37% PHOSPHORIC ACID

(Widened Dentinal Tubule Orifices)

(Particulate Residue on Surface)

Photograph 6: Etching Time- 15 Seconds

Photograph 7: Etching Time- 60Seconds

ETCHING OF DENTIN WITH 37% PHOSPHORIC ACID GEL

(Depth of Demineralization in Tubules)

Photograph 8: Etching time - 15 seconds


Effect of 24% EDTA gel on enamel after 15 and 60 seconds etching was comparatively insufficient. The surface micromorphology depicted pitted enamel surface which falls into the category of type 4 etching pattern (photographs no. 10 and 11). The dentinal surfaces after 15 seconds and 60 seconds etching were smooth and debris free. The dentinal micrmorphology showed presence of peritubular dentin around the tubule openings in both the subgroups etched with EDTA, indicating its partial

or selective demineralization (photographs no. 12 and 13).

However no discernible depth of demineralization was observed in the specimens.

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Effect Of 24% EDTA Gel for 15 Seconds Application on Prepared Specimens.

Sample

No. Width of

loss of enamel prisms core /

periphery



in tubules

1. 0.00 1.73µ 0.00 2. 0.00 2.54µ 0.003. 0.00 1.52µ 0.004. 0.00 2.01µ 0.005. 0.00 1.88µ 0.00

Mean 0.00 1.94µ 0.00Table : 3

Effect Of 24% EDTA Gel for 60 Seconds Application

on Prepared Specimens

Sample No.

Width of loss of enamel prisms core /

periphery



in tubules

1. 0.00 2.76µ 3.7µ2. 0.00 2.59µ 5.14µ3. 0.00 2.29µ 3.85µ 4. 0.00 3.02µ 2.9µ 5. 0.00 2.72µ 4.02µ

Mean 0.00 2.67µ 3.92µTable : 4

ETCHING OF ENAMEL WITH 24% EDTA GEL (Type 4 Etching Pattern)



ETCHING OF DENTIN WITH 24% EDTA GEL

(Open Dentinal Tubules)



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ETCHING OF DENTIN WITH 24% EDTA GEL (Depth of Demineralization in Tubules)



With 10% maleic acid gel, preferential loss of the prism cores was evident. The surface topography of the etched enamel resembled that of a 'honeycomb' (photographs no. 16 and 17) and is categorized as type 1 etching pattern (according to Galil and Wright's Classification). This study also showed that acid etching with 10% maleic acid for 15 and 60 seconds removed the smear layer and widened the

dentinal tubule orifices. The surface morphology was that of a smooth, debris free surface (photographs no. 18 and 19)

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EFFECT OF 10% MALEIC ACID GEL APPLIED FOR

15 SECONDS ON PREPARED SPECIMENS.

Sample No.

Width of loss of enamel prisms core.



in tubules

1. 3.56µ 2.62µ 7.32µ2. 3.67µ 3.41µ 6.78µ3. 2.19µ 2.57µ 7.04µ 4. 4.61µ 3.35µ 7.90µ 5. 2.49µ 2.68µ 6.43µ

Mean 3.30µ 2.93µ 7.09µTable: 5

EFFECT OF 10% MALEIC ACID GEL APPLIED FOR

60 SECONDS ON PREPARED SPECIMENS

Sample No.

Width of loss of enamel

rods periphery



in tubules

1. 2.45µ 3.52µ 6.91µ2. 5.2µ 2.99µ 11.02µ3. 4.76µ 3.8µ 8.02µ4. 6.13µ 2.93µ 9.4µ5. 2.9µ 3.41µ 8.81µ

Mean 4.29µ 3.33µ 8.83µ Table: 6

ETCHING OF ENAMEL WITH 10 % MALEIC

ACID GEL (Type 1 Etching Pattern)



ETCHING OF DENTIN WITH 10 % MALEIC ACID GEL

(Widened Dentinal Tubule Orifices)


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ETCHING OF DENTIN WITH 10% MALEIC ACID GEL

(Depth of Demineralization in Tubules)



Discussion

The objective of etching enamel is to create microporosities for resin penetration. Dentinal etching removes the smear layer and smear plugs along with demineralization of the surface. It also exposes both intertubular and peritubular collagen.5 Etching of dentin is comparatively a complex phenomenon. This can be attributed to the heterogenous structure of dentin and the dentinal fluid flow in an outward direction that make reliable

bonding to dentin remarkably problematic. The higher organic content of dentin predisposes it to denaturation and weakening of the collagenous mass. Phosphoric acid gel is a strong acid with pH = 1 and dissociation constant, pKa = 2.1. Maleic acid gel is an organic acid with higher molecular weight, pH = 2.9 and dissociation constant pKa = 1.8. EDTA is a powerful organic chelating agent. It is odorless, crystalline white powder with pKa = 6.1 and neutral pH. The results of the study indicate that in group I, in which the prepared surfaces of the specimens were etched with 37% phosphoric acid for 15 and 60 seconds had no significant difference on the etching

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effect and subsequent bond strength values on enamel. On etching of enamel with 10% maleic acid for 15 seconds etching time, the dissolution of the prism cores was lesser, amounting to 3.3µ and with 60 seconds etching time, there was greater dissolution of the prism cores (4.29µ). However, there was no significant difference (p>0.05) in the width of loss of prism core when the teeth were etched for 15 and 60 seconds.24% EDTA etchant gave relatively smooth appearance on enamel and did not alter the intact enamel surface significantly with non-uniform shallow pittings being visible. Photomicrographs of the dentinal surfaces treated with 37% phosphoric acid gel showed that the tubule orifices were open. With 24% EDTA gel, the mean diameter of the tubule orifices was 1.94µ and 2.67µ with 15 seconds and 60 seconds etching respectively. There was no significant difference (p>0.05) in widening of the tubuli when the etching time was extended from 15 seconds to 60 seconds.

Etching with 10% maleic acid gel showed enhanced widening of the dentinal tubules. The mean diameter of opened tubules was 2.93µ when the specimens were etched for 15 seconds and 3.33µ with 60 seconds etching time. No statistically significant difference (p>0.05) was observed. The dentinal surface appeared smooth and free of debris in contrast to the samples etched with 37% phosphoric acid which showed evidence of particulate residue (Silica dioxide) on surface. Intergroup comparison of different acids showed that there exists no significant difference in tubule diameter whether the teeth were etched with 37% phosphoric acid gel or 10% maleic acid gel (p>0.05). However, significant variation exists when the tabulated results were compared between phosphoric acid and EDTA, and maleic acid & EDTA (p<0.05) with EDTA showing less widening of the tubule orifices as compared to the effect of the other two acids. Maximum penetration of the acid into the tubules was seen with 37% phosphoric acid. Phosphoric acid not only dissolves the mineral phase of dentin but also results in denaturation of the collagenous matrix1, 2 which may interfere with hybrid layer. For better retention of the restorative materials, the number of resin tags into dentin is more important than the depth of the tags.

The depth of demineralized dentin to the extent of 11.96µ, 12.15µ and 14.34µ in group etched with 37% phosphoric acid for 60 seconds is not desirable.

Moreover, the adhesive resins may not be able to infiltrate demineralized dentin completely till the depth of demineralization. The incomplete penetration of the demineralized collagen network could result in a delicate zone inside the hybrid layer and, between the hybrid layer and the unaltered dentin that could be susceptible to continuous degradation and a pathway for nanoleakage causing failure of the restoration.6 Further, as the resin penetrates deeper into dentin, the more difficult it will be for them to polymerize if they rely on light activation. In addition, dentinal fluid may interfere with polymerization of the resin tags.7Intergroup comparison between 37% phosphoric acid, 24% EDTA and 10% maleic acid shows comparable results of phosphoric acid and maleic acid apart from the depth of demineralized dentin which is significantly higher (p<0.05) for the 37% phosphoric acid gel group. Considering that 10% maleic acid gel provides clinically acceptable depth of demineralized dentin, 7.09µ (15 seconds) and 8.83µ (60 seconds etch time) it can be inferred that milder acid like 10% maleic acid can replace stronger, more destructive, 37% phosphoric acid for etching of teeth so as to enhance retention of the adhesive restorations.Although acid etching is more than 57 years old, answers to some of the basic questions concerning it are still being sought.

Conclusion With this study we conclude that:-

1. Acid etching causes various types of etching patterns in enamel indicating preferential dissolution of the enamel prisms. With 37% phosphoric acid, type 2 etching pattern is seen; with 10% maleic acid, type 1 etching pattern is predominant and etching with 24% EDTA leads to type 4 etching pattern.

2. In dentin, etchants widen the dentinal tubule orifices due to demineralization of peritubular dentin and this demineralization extends deep into the dentinal tubules for varying depths depending upon the type of acid used and time of its application. No statistically significant difference exists in the widening of the dentinal tubule orifices between the group I (37% phosphoric acid) and group III (10% maleic acid) specimens.

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37% phosphoric acid causes maximum demineralization in the tubules with mean depth of demineralization being more pronounced in 60 seconds subgroup (11.48µ). 10% maleic acid also causes demineralization in tubules but the mean depth is significantly less (8.83µ) than that seen with 37% phosphoric acid. With 24% EDTA etching for 15 seconds, no discernible demineralization is seen in tubules and for 60 seconds.

3. Milder acids like 10% maleic acid can be effectively used for etching of teeth instead of 37% phosphoric acid.

However, a larger sample size is required before deriving any definite conclusions.

Acknowledgement We place on records our deep gratitude towards our mentor, an eminent academician, Dr. (Mrs.) Sumita Kaswan, MDS, Professor, Department of Conservative Dentistry & Endodontics, Jodhpur Dental College General Hospital, Jodhpur, who prudently provided us the impetus for the present study. Photomicrograph Courtesy- Scanning Electron Microscopy Department, AIIMS.

References 1. Blomlof JPS et al. Acid conditioning

combined with single component and two component dentin bonding agents. Q.I. 2001; 32: 711 – 715.

2. Blomlof JPS, Cederlund AL, Blomlof LB et al. A new concept for etching in restorative dentistry. Int J Perio Rest Dent 1999; 19: 31 – 35.

3. Fusayama T, Nakamura M et al. Non pressure adhesion of a new adhesive restorative resin. J Dent Res 1979; 58 (4) : 1364 – 1370.

4. Galil KA and Wright GZ. Acid etching patterns on buccal surfaces of permanent teeth. Paediatric Dent 1979; 1: 230-234.

5. Matos AB, Palma RG et al. Effects of acid etching on dentin surface : SEM morphological study. Braz Dent J 1997; 8(1) : 35 – 41.

6. Perdigao J, Lopes M. The effect of etching time on dentin demineralization. Q.I. 2001; 32 : 19 –

7. Sidhu GK. The effect of acid etched dentin on marginal seal. Q.I. 1994; 25 : 797 – 800.

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ORIGINAL ARTICLE

AMSA (ANTERIOR MIDDLE SUPERIOR ALVEOLAR): ALTERNATE TO MULTIPLE INFILTRATIONS IN MAXILLARY ANAESTHESIA

Dr Amit Sangle1 Dr. Ritika Tambuwala2

Dr. Ritika Agrawal3

1 MDS, Professor and Guide, Department of Oral and Maxillofacial Surgery, M.A. Rangoonwala College of Dental Sciences and Research Centre. 2MDS, Professor and HOD, Department of Oral and Maxillofacial Surgery, M.A. Rangoonwala College of Dental Sciences and Research Centre. 3 Post Graduate Student, Department of Oral and Maxillofacial Surgery, M.A. Rangoonwala College of Dental Sciences and Research Centre.


Dr. Ritika Agrawal Address: M.A. Rangoonwala College Of Dental Sciences And Research Centre, Hidayatullah Road, Azam Campus, Camp, Pune- 1 Tel No: 02026452288, 02026452040 Contact number: 09604646209 E-Mail: [email protected] [email protected] Access this Article Online

AbstractThis article describes an alternate technique of anaesthesia of single injection for the maxillary arch, pulpal anaesthesia from the central incisor to the second premolar without requiring collateral anesthesia of the face and muscles of facial expression. The importance of this review was to bring about awareness among the general clinician who have to use multiple injection for any treatment to be performed in the maxillary arch. The non compliance of the treatment on the maxillary arch is usually due to these factors. Hence introducing this technique can help patient compliance as well ease for the clinician. Also the duration of treatment is reduced. In our study we have introduced a modification of administration of injection using a disposable syringe and needle instead of computer controlled local anaesthetic delivery system (CCLAD); which makes this technique a very useful technique for various multiple extractions, anterior maxillary cysts and other procedures like flap surgeries for dentists as well as oral surgeons. Keywords: Pulpal Anaesthesia, Disposable Syringe and Needle, Single Injection

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Introduction Maxillary mucogingival or flap surgery usually requires up to five injections to obtain anesthesia of the hard and soft tissues. Posterior superior alveolar, middle superior alveolar, and anterior superior alveolar block injections are used to anesthetize buccal tissues whereas greater palatine and nasopalatine blocks are used for palatal anesthesia. Although this series of injections effectively anesthetizes maxillary tissues, it may also inadvertently affect facial structures such as the upper lip, lateral aspect of the nose, and lower eyelid [1,2]. The palatal soft tissue anesthesia is achieved without numbness to the lips and face or interference with the muscles of facial expression. A bilateral AMSA injection supposedly anesthetizes 10 maxillary teeth extending from the second premolar on one side to the second premolar on the opposite side [3].The AMSA injection derives its name from the injection’s ability to supposedly anesthetize both the anterior and middle superior alveolar nerves [4]. The middle superior alveolar (MSA) and anterior superior alveolar (ASA) nerves branch from the infraorbital nerve before they exit from the infraorbital foramen. This technique anterior middle superior alveolar block was first reported by FREIDMAN & HOCHMAN in 1997[5] with the development of CCLAD system; it provides pulpal anaesthesia to multiple teeth from a single injection site. Method Inclusion Criteria In our study we used AMSA on patients requiring multiple maxillary extractions and/ or anterior maxillary cysts, unilateral or bilateral as per the requirements. Anatomy (Figure1 and 2) a) The middle superior alveolar (MSA) and anterior superior alveolar (ASA) nerves branch from the infraorbital nerve before they exit from the infraorbital foramen. The middle superior alveolar nerve is thought to innervate the maxillary premolars and plays some role in pulpal innervation of the

mesiobuccal root of the first molar. The anterior superior alveolar nerve provides pulpal innervation to the central and lateral incisors and canines [5]. The plexus where both nerves join is the target site for the AMSA injection [6].

Figure 1

Figure 2 Clinical Case Presentation Patient aged 55/male was advised extraction with 11,12,13,14 and 15 due to grade 3 mobility and gingival recession Modification We used of a 27 guage disposable syringe and needle (Fig 3) instead of CCLAD system (Fig 4) .0.6 to 0.9 ml Lignocaine hydrochloride in

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the conc of 1:100000 dilution of vasodepressor was used as the local anaesthetic agent.

Figure 3

Figure 4 Technique a) Malamed [1, 4] described the injection site to be on the hard palate about halfway along an imaginary line connecting the mid-palatal suture to the free gingival margin. Another description of the injection site is that it is located on the hard palate at the intersection of a vertical line bisecting the premolars and a horizontal line halfway between the mid-palatine raphe and the crest of the free gingival margin [20].(fig 5) b) To avoid patient discomfort due to the tightly bound nature of the palatal tissue, the anesthetic agent should be injected into the

site at a methodic rate of 0.5 ml per minute [3]. Slow deposition of the anesthetic agent, the bound nature of the palatal tissue promotes diffusion of the anesthetic agent through the palatal bone via numerous nutrient canals [3]. A successful AMSA injection typically blanches the palatal tissue in a unilateral fashion that does not cross the midline [21]. Anesthesia of structures typically innervated by the greater palatine nerve, nasopalatine nerve, anterior superior alveolar nerve and middle superior alveolar nerve is achieved [22, 23].

Figure 5: point of insertion of the needle. c) Within 2 minutes of this block ,pulpal anesthesia anesthetizing from central incisor to 2nd premolar along with the pulpal anesthesia, palatal tissues from the midpalatal region to the free gingiva of the same region are also considerably anaesthetized. d) The duration of anaesthesia is about 60 minutes to 90 minutes. The needle during injection is oriented at a bevel of 45 degree with constant and controlled pressure. e) The classical blanching of the palatal tissues is seen in AMSA block clinically indicating proper point of insertion and anaesthesia of the associated tissues along

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with the other clinical subjective signs. (Figure 6)

Figure 6: Blanching of the tissues on the anaesthetized side is shown. Results 1. Most of the patients reacted well to the technique. Adequate anaesthesia for an accepted duration is achieved and it reducesthe cumulative reduction of the number of injections reducing patient discomfort.

2. In certain patients short lived central incisor anaesthesia was observed 3. In some other patients an additional buccal vestibular infiltration was required.

Discussion Advantages 1. The ability of the AMSA injection to cover large maxillary surgical fields provides multiple benefits because it reduces the cumulative number of necessary injections.

2. The elimination of repetitive transmucosal punctures, the elimination of multiple injections reduces the total amount of delivered vasoconstrictor and may prove useful for cardiovascular-compromised patients requiring maxillary anesthesia. 3. For maxillary anterior esthetic procedures, the AMSA’s maintenance of upper lip function allows for continuous evaluation of gingival contours unimpeded by the ‘‘lip drooping’’ that

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Disadvantages 1) The long administration time: Some patients may find it disconcerting to have an injection last 4 minutes, and attempts to speed up the AMSA injection may lead to increased patient discomfort at the injection site.

2) The reduction of cumulative anesthetic vasoconstrictor may also prove to be problematic for certain surgical procedures. 3) The reduction in vasoconstrictor proves beneficial for cardiovascular- compromised patients, it may lead to less than desirable hemostatic control. 4) The AMSA eliminates the need for multiple injections, less vasoconstrictor enters the buccal tissues and a subsequent decline in hemostasis may obscure portions of the surgical field. 5) Several cases of short-lived anesthesia in the maxillary central incisor is observed. Conclusion This technique has the advantage to anaesthetize multiple teeth with a single injection covering large surgical area in the maxillary region; thus can be used in day-to-day practice by oral surgeons and general dentists.

References [1] Malamed SF. Handbook of Local Anesthesia, 5th ed. St. Louis: Mosby; 2004;213-216. [2] Gomolka KA. The AMSA block: Local anesthesia without collateral numbness. CDS Rev 2000;93:34. [3] Friedman MJ, Hochman MN. Using AMSA and P-ASA nerve blocks for esthetic restorative dentistry. Gen Dent 2001;49:506-511. [4] Malamed SF. Handbook of local anesthesia. 4th ed. St. Louis: Mosby; 1997; p. 149, 150, 160. [5] Friedman M, Hochman M. A 21st century computerized injection system for local pain control. Compendium 1997;18:995-1003. [6] Friedman M, Hochman M. The AMSA injection: a new concept for local anesthesia of maxillary teeth using a computer-controlled injection system. Quintessence Inter 1998;29:297-303. [7] Blanton PC, Roda RS, The anatomy of local anesthesia. J Cal Dent Assoc 1995;23(4):55-69.

[8] Donaldson D, James-Perdok L, et al, A comparison of Ultracaine, DS (articaine Hcl) and Citanest, Forte (prilocaine Hcl) in maxillary infiltration and mandibular nerve block. J Can Dent Assoc 1987;1:38-42. [9] Gibson RS, Allen K, et al, The Wand vs. traditional injection: a comparison of pain related behaviors. Pediatric Dent 2000;22(6):458-62. [10] Saloum FS, Baumgartner JC, et al, A clinical comparison of pain perception to the Wand and a traditional syringe. Oral Surg Oral Med Oral Pathol 2000; 89(6):691-5. [11] Goodell GG, Gallagher FJ, Nicoll BK, Comparison of a controlled injection pressure system with a conventional technique. Oral Surg Oral Med Oral Pathol 2000;90(1):88-94. [12] Carter RB, Keen EN, The intramandibular course of the inferior alveolar nerve. J Anat 1971;108:433-40. [13] Rood JP, The nerve supply of the mandibular incisor region. Br Dent J 1977;143:227-30. [14] Frommer J, Mele FA, Monroe CW, The possible role of the mylohyoid nerve in mandibular posterior tooth innervation. J Am Dent Assoc 1972;85(1):113-7.

typically occurs with traditional anesthetic techniques. 4. Maxillay mucogingival procedures, the AMSA’s palatal delivery of a full carpule of anesthetic with vasoconstrictor provides outstanding hemostasis and reduces the need for multiple re-injections to attain hemostatic control during graft harvest if indicated. 5. As we used a modified technique to the original one using CCLAD system, cost factor was decreased making it an affordable technique.

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[15] Madeira MC, Percinoto C, Silva MGM, Clinical significance of supplementary innervation of the lower incisor teeth: a dissection study of the mylohyoid nerve. O Surg O Med O Pathol 1978;46:608-14. [16] Sutton RN, The practical significance of mandibular accessory foramina. Aust Dent J 1974;19:167-73. [17] Haveman CW, Tebo HG, Posterior accessory foramina of the human mandible. J Prosthet Dent 1978;35:462-8. [18] Wilson S, Johns P, Fuller PM, The inferior alveolar and mylohyoid nerves: an anatomic study and relationship to local anesthesia of the anterior mandibular teeth. J Am Dent Assoc 1984;108:350-2. [19] Chapnick L, Nerve supply to the mandibular dentition: a review. J Can Dent Assoc 46:446-8, 1980. [20] Holtzclaw D, Toscano N. Alternative anesthetic technique for maxillary periodontal surgery. J Periodontol 2008;79:1769-1772. [21] Lee S, Reader A, Nusstein J, Beck M, Weaver J. Anesthetic efficacy

of the anterior middle superior alveolar (AMSA) injection. Anesth Prog 2004;51:80-89. [22] Perry DA, Loomer PM. Maximizing pain control: The AMSA injection can provide anesthesia with fewer injections and less pain. Dimens Dent Hyg 2003;1: 28-33. [23] Nusstein J, Lee S, Reader A, Beck M, Weaver J. Injection pain and postinjection pain of the anterior middle superior alveolar injection administered with the Wand or conventional syringe. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2004;98:124-131. [24] Holtzclaw D, Toscano N. Alternative anesthetic technique for maxillary periodontal surgery. J Periodontol 2008;79:1769-1772. [25] Allen KD, Kotil D, Larzelere RE, Hutfless S, Beiraghi S. Comparison of a computerized anesthesia device with a traditional syringe in preschool children. Pediatr Dent. 2002;24:315-20.

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REVIEW ARTICLE

ENDOTHELIAL CELL BASED ENGINEERING OF CAPILLARIES‐LIKE NETWORK IN A TISSUE‐ENGINEERED SKIN SUBSTITUTE

Dr. Mohammad Ahmad Javaid1

1BDS, MSc Dental Sciences Candidate, Faculty of Dentistry, McGill University Canada Corresponding Author Dr. Mohammad Ahmad Javaid Faculty of Dentistry 3640 University Street, Room B/15 Montreal, QC H3A 0C7 Canada Telephone: 438 401 8150 Email: [email protected]


AbstractTreatment of patients with burns, surgeries and accidents involving extensive skin replacement has long been a challenge for reconstructive surgery. Classical approaches like cadaver skin or xenografts have failed to provide a permanent solution to this ever increasing problem. Different tissue engineering techniques have been tried in the past but, clinically none has lived up to the early promise that in vitro studies showed mostly, due to limited vascular supply leading to cell death when grafts comprising of epidermis and dermis were used in deep wounds. More recently scientists have developed a new approach using endothelial cells for construction of pre vascularised tissue engineered skin grafts constituting epidermis and dermis. In this mini review we look at a few experiments and animal studies which have been conducted so far and have yielded promising results, both in vitro and in vivo. This new approach involving endothelial cells for engineering of capillary like network in tissue engineered skin substitute is the way forward and can potentially provide a solution to this problem which scientists and surgeons have been trying to address for the last half century. Acknowledgment I am immensely grateful to my supervisor, Dr. Mari Kaartinen, Associate Professor at Faculty of Dentistry and Medicine McGill University and Director Biomedical Sciences, Faculty of Dentistry and Faculty of Medicine at McGill University for her continuous support, encouragement, guidance and advice. I would also like to extend my gratitude to Dr. Satya Prakash, Professor of Biomedical Engineering Department at McGill University for his guidance in writing this mini review.

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Introduction Treatment of burn victims or patients with surgeries involving extensive skin removal is a complex procedure. The classic therapeutic options which have been tried like cadaver skin or xenografts have proved to be temporary solution[1, 2] [3]. In recent times tissue engineered skin has offered a therapeutic alternative [4-6]. Although human epidermis has already been developed in large quantities from skin biopsy by using techniques developed in tissue engineering [7, 8] [9]but if dermis is destroyed due to trauma, replacement by epidermis alone does not lead to optimal healing [3, 8]. In such instances, a bilayered tissue engineered substitute is sought [10]. Drawbacks for replacement of skin wounds with epidermal substitutes alone are many and include high sensitivity of mechanical damage and variable percentage of graft take which may be attributed to absence of underlying dermis. With engineered constructs consisting of both epidermis and dermis, many of these drawbacks will be potentially overcome [3, 11] Researchers have tried to transplant skin substitutes with increasing thickness to accommodate for increased tissue loss in different clinical scenarios. Although there have not been many such transplantation experiments but, there have been studies which, show unfavourable results which may be due to insufficient vascularisation in dermis which in turn leads to deleterious effects on epidermis survival as this layer is dependent on diffusion of nutrients from dermis[4, 12, 13]. In most of the cases the graft failure is due to inadequacy of vascularisation which leads to hypo perfusion and ischemic injury [4, 9, 14-16]. The graft cells are dependent on diffusion of nutrients and oxygen from underlying wound which is generally insufficient for sustained survival of graft [9]. Cell located within 100-200 micro meter of a vessel can

derive nutrients via diffusion [17-21]. As the distance increases, diffusion alone cannot sustain cells and so cell death increases. Inosculation has been explained as the anastomoses or connection of capillaries present in graft with vessels in the host’s wounds [4, 22, 23]. In some studies it was demonstrated when human skin was grafted onto mouse, initial vascularisation was due to anastomoses between severed ends of human capillaries with mouse micro vasculature[16, 19]. Later mice endothelial cells replaced the human endothelial cells. This demonstrated that grafts with intrinsic blood supply may have a better long term prognosis and survival. Hence it was proposed that methods should be sought to replace skin with grafts containing intrinsic microvasculature [13]. This observation found the basis of idea to develop a tissue engineered skin substitute with intrinsic vascular component [4]. Many approaches are currently being investigated to increase vascularisation in tissue engineered skin substitutes to promote inosculation and hence survival of the transplanted engineered skin substitute [19] One approach is to incorporate growth factors into scaffold biomaterial. [24]. A different approach is to pre-encapsulate the growth factors in microspheres which are then transferred to the scaffold leading to steady and sustained released of growth factor [25]. This has been proven by studies like [26]who demonstrated that various biodegradable polymers can be developed and used for transplantation of isolated or encapsulated cells which would allow to form an engineered tissue with intrinsic vasculature [26]. Many studies have been carried out to promote vascularisation in engineered tissues through use of growth factors including Vascular Endothelial Growth Factor [5, 6, 27-30], Fibroblast Growth Factor [29] and Transforming Growth Factors [31]. But it has been shown in previous studies that systemic delivery can cause unwanted tissue growth and subcutaneous injections yield a very

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limited promotion in neovascularisation [26]. Another approach is utilization of stem cells for creation of tissue engineered vascular grafts [24, 32, 33]. Studies involving genetic modification of cells have also been carried out. For instance study by [34]. In this study it was demonstrated that over expression of platelet derived growth factor A in tissue engineered skin substitutes by genetically modified keratinocytes and fibroblasts was not statistically significant compared to unmodified keratinocytes and fibroblast. It was also observed that Tissue Engineered Skin substitute was devoid of intrinsic micro vasculature and this limitation can hypothetically be overcome by over expression of certain cytokines [35]. Lastly a different approach is to engineer micro vessels in vitro in scaffold using endothelial cells. After transplantation, the endothelial cells form blood vessels which develop interconnections with host blood vessels leading to adequate perfusion of the graft. However one issue needs to be addressed which is homogenous distribution of endothelial cells and resulting blood vessels [24]. This issue has been addressed in a few studies like [26].Their paper hypothesizes that endothelial cells if seeded in tissue engineered scaffold would form capillary like tubular structures which can form the basis of intrinsic graft microvasculature which would increase the long term survival of graft by anastomoses between graft and host micro vasculature [26].Human endothelial cells have also been shown in previous studies to spontaneously sprout capillary like structures and form microvasculature when co cultured with fibroblasts and seeded on tissue engineered skin substitutes in vitro. For instance in a study by [36] conditions for HUVEC (Human Umbilical Vein Endothelial Cells) to form capillary like tubular structures with in a 3D scaffold were demonstrated which would allow HUVEC to form in vitro capillary like tubular structures within tissue engineered scaffold

which can then be transplanted onto graft site on host. In this mini review, we look at different studies which used endothelial cells in different models to increase the development of microvasculature in the engineered skin substitutes so as to promote inosculation and hence survival of the tissue engineered skin substitute. In Vitro Experiment, First of its Kind In a study by [4], the objective was to develop Endothlialized Skin Equivalent (ESE) in which capillary like structures could be reproduced in vitro. For this purpose Human Keratinocytes and Dermal Fibroblasts were isolated. As it has been shown by [37]] that human dermal fibroblasts and keratinocytes produce a more well organised tissue engineered construct in comparison to bovine cells which results in the production of auto or self produced tissue engineered skin construct which would increase the tendency for ‘take’ of the graft. Human Umbilical Vein Endothelial Cells (HUVECs) were taken as endothelial cells. Three dermal equivalents were produced with seeding fibroblasts on top of biopolymer in one; HEVEC on biopolymer in second and endothelial-fibroblast dermal equivalent was prepared seeding both fibroblasts and HUVEC on biopolymer in third. Keratinocytes were seeded in all three dermal equivalents [4]. It was observed that HUVEC when cultured alone although expressed on the biopolymer scaffold but mostly showed features attributed to dying cells and produced very limited extracellular matrix. On the other hand fibroblast cultured alone attached to the biopolymer scaffold, proliferated and laid down extracellular matrix in appreciable amount. In equivalents with both cells, proliferation of fibroblasts with deposition of extracellular matrix was observed in which HUVEC migrated and formed new capillary like tubular structures. The capillary like tubular structures observed in

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Endothelialized Dermis Equivalent (EDE) and Endothelialized Skin Equivalent (ESE) was not observed in case of absence of HUVEC. Taking in vitro results to in vivo experiments In another study by Tremblay et al. HUVEC seeded in dermis were used to develop microvasculature with in engineered skin substitute and transplanted onto mice to take the in vitro technique developed by [4]to in vivo stage. This was compared with dermis without HUVEC. Two different tissues were prepared. One the standard reconstructed dermis without endothelial cells and second reconstructed dermis with human umbilical vein endothelial cells (HUVEC). Adult male athymic mice were selected for graft transplantation. Excisions were made and deep wounds were created in three groups of mice. In one group human skin was transplanted, in other reconstructed skin without endothelial cells and in third endothlialized reconstructed skin was transplanted. Four mice in all three groups were sacrificed at day 4, 7 and 14 post-grafting for analysis. [16] Capillary like Structures (CLS) were observed under epidermis in ERS before placement of graft while no such structures was observed in RS. Also red blood cells were detected in capillaries on fourth day after placement of skin graft. These red cells came from mice as no red cells were observed in capillaries of human skin before transplantation. In ERS, after four days, blood containing vessels were seen underneath the epidermis. These vessels were identified via double staining which showed that vessels beneath epidermis contained human Endothelial Cells (ECs). It was also shown that mouse EC were only present in the lower compartment of graft and not in epidermis as seen with RS. At 14 days after graft placement, a co-localization between human and mouse endothelial cells was seen in the graft through use of confocal microscopy. Presence of red

blood cells in their lumen was a clear evidence of inosculation between graft capillary like structures and mouse capillaries. Lastly total number of capillaries human and mouse were evaluated per tissue section for each type of grafts i.e. Human Skin, Reconstructed Skin without endothelial cells and Endothelialized Reconstructed Skin. There was a twofold decrease in number of human capillaries in Human Skin graft. This could be attributed to degeneration of supernumerary vessels that did not anastomose with the mouse capillaries. This type of decrease was not observed in Endothelialized Reconstructed Skin, in fact a statistically significant increase in number of mouse capillaries was observed in ERS [[16] In another study by Laschke et al., microvascular network was formed in the PLGA scaffold by placing the scaffold onto flank of donor mice. After 20 days when blood vessels had grown into the scaffold, forming a network of micro vasculature within the scaffold, the engineered scaffold was excised and transplanted onto the recipient mice. The results showed that preformed microvessels within tissue engineered skin substitute developed interconnections with host micro vasculature which resulted in accelerated vascularisation of cells in the graft compared to avascular grafts [25] In 2010, a study was carried out by Gibot et al in which two substitutes were prepared. Endothelialized Reconstructed Skin (ERS) and RS (Reconstructed Skin) serving as control. The dermal layer in these models comprised of three layers of fibroblasts with inferior two plated with Human Umbilical Vein Endothelial Cells (HUVECs) in ERS and without HUVEC in RS. Graft site were prepared on athymic mice by removal of back skin and then tissue engineered skin was grafted onto the mice. [19] After 30 days of in vitro culture, the Endothelialized Reconstucted Skin showed well developed and fully differentiated human

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epidermis. In this model, human endothelial cells formed Capillary like Structures which has also been shown in previous studies. The lumens of micro vessels were well defined. Reconstructed skin endothelialized with either Human Umbilical Vein Endothelial Cells (HUVEC) demonstrated an organised network of Capillary like Structures (CLS) with a branching morphology. The Endothelialized Reconstructed Skin developed its own intrinsic microvasculature where as Reconstructed Skin which was considered a negative control did not show development of such microvasculature. All the grafts showed a complete take at day. Both grafts, RS and ERS adhered completely with underlying hosts tissues at day but more vascularisation was observed in ERS compared to RS. It was also revealed that the human endothelial lined vessels transported mice red blood cells which demonstrated that functional anastomoses was established between graft microvasculature and hosts capillaries at. The human vessels formed were homogenously distributed in superficial and deeper layers ensuring complete perfusion of the entire graft [19]. Discussion One of the main obstacles in wide spread use of Reconstructed Skin for wound coverage is delayed vascularisation due to thickness of dermis. But this thick dermis is important because it protects the reconstructed epidermis against mechanical, chemical and bacterial accumulations and also results in better healing. This however delays the complete vascularisation of the graft which ultimately culminates in necrosis of epidermis [16] It took years to fully understand and appreciate the phenomenon of neovascularisation which is a key step in increasing take of graft and keeping it viable. It has been shown in previous studies that split thickness skin graft survives by

diffusion, followed by inosculation and finally by neovascularisation. Composite skin substitutes without intrinsic blood supply cannot vascularise as the natural split thickness graft. Diffusion is responsible for supply of nutrients to the epidermis which is not sufficient to ensure the permanent implantation of grafted skin substitute until process of neovascularisation takes over. In study carried out by [4]which was the first study of its kind the aim was to develop capillary like network within the skin substitute in vitro, which may prove to be a cornerstone in tissue engineered skin substitutes [4] The aim of the Black ET AL study was to develop in vitro endothlialized tissue engineered skin substitute which would demonstrate vascular like tube formation developed from human cells without the use of specific growth factors or carcinogenic agent like PMA. Their results were very promising and formed the basis of further trial of endothelial cells for formation of blood vessels within the Tissue Engineered Skin Substitute which could be tried in vivo. The results of [4] study strongly suggest that HUVEC can organise and give rise to network of capillary-like structures when cocultured with dermal fibroblasts and keratinocytes. On the other hand these structures do not develop when each cell type is cultured independently. The results showed strong evidence that fibroblasts when present in conjunction with endothelial cells in a 3D culture medium lay down the extracellular matrix in which capillary like structures formed [4] The study Black et al formed the basis of taking in vitro results to in vivo experiments carried out by Tremblay et al in which it was hypothesized that a reconstructed skin containing capillary like structures would promote faster vascularisation by anastomoses between graft vessels and hosts capillaries as had been shown by

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transplantation of full thickness human skin on wounds in previous studies. In this study it was demonstrated that Human Umbilical Vein Endothelial Cells when added to the Reconstructed Skin accelerated the process of vascularisation as compared to conventional Reconstructed Skin. Human capillaries filled with red blood cells were observed near the epidermis. These findings were in coherence with the previous work done by other groups of researchers. Same results were observed with ERS. Human capillaries containing mouse red blood cells were observed beneath epidermis after 4 days of graft placement and no mouse blood vessel was observed in the area in that time. The filling of human capillary with mouse blood pointed to the fact that there were anastomoses or inosculations between the human and mouse vasculature. It was also observed that blood circulation establishment beneath epidermis was faster in ERS compared to RS and was as fast as seen in Human Skin. The results showed that initial vascularisation observed at 4 days was due to inosculation of human capillary like structures with mouse vessels. Mouse capillaries extended by process of neovascularisation were not detected beneath epidermis of ERS until day 14. According to authors of study this was the first study which demonstrated inosculation process between human capillaries reconstructed in vitro through tissue engineering with wound bed vasculature [16] The latest study in this regard using Endothelial Cells was carried out Gibot et al which was again based on the initial work done by Black et al. In this study, the aim was to develop an easy to handle ERS model, which could demonstrate in vitro formation of capillary like network by co culture of fibroblasts, endothelial cells (HUVEC) without use of external growth factors. This model could also be completely autologuos for future

clinical applications. In this model, cell secreted extra cellular matrix and there was also cell-cell and cell-extracellular matrix interaction which created a physiological micro environment allowing endothelial cells to express capillary like structures. Also the thickness of model could be compared with human skin slit thickness graft generally used in clinical arena which is categorized as thin (130-300), intermediate (300-460) or thick (460-760) micro meter. The human microvasculature created in vitro anastamosed with host capillaries and became functional in less than 96 hours. Mouse red blood cells were found in lumen of human endothelial capillaries which demonstrated efficacious blood circulation. These anastomoses could only be established if hosts micro vessels grow in the graft and then establish inosculation with graft vessels. Complete replacement of graft vasculature endothelial cells by host cells is key for skin graft revascularization and long term survival and acceptance of graft. In this study the graft was remodelled completely with host’s endothelial cells. [19] Conclusion From use of Split thickness skin grafts, to grafts from cadavers and xenografts, the science of development of perfect Tissue Engineered Skin Substitute has come a long way. With in vitro development of microvasculature in Tissue Engineered Skin, the first steps towards perfect skin substitutes were taken. “Although many studies have been conducted but it is safe to say that Tissue Engineering of Skin and its application in clinical practise is the beginning of a long journey. Now with improvement in cell culture techniques and advancement in knowledge, epidermis and dermis are being prepared separately from small biopsies taken from the recipient, in vitro. This is just the beginning, with final

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aim of generating a full transplantable replica of skin with adnexa and vasculature” [38]. References 1. Gallico, G.G., 3rd, Biologic skin

substitutes. Clin Plast Surg, 1990. 17(3): p. 519-26.

2. Pham, C., et al., Bioengineered skin substitutes for the management of burns: a systematic review. Burns, 2007. 33(8): p. 946-57.

3. Berthod, F. and O. Damour, In vitro reconstructed skin models for wound coverage in deep burns. Br J Dermatol, 1997. 136(6): p. 809-16.

4. Black, A.F., et al., In vitro reconstruction of a human capillary-like network in a tissue-engineered skin equivalent. FASEB J, 1998. 12(13): p. 1331-40.

5. Sheridan, M.H., et al., Bioabsorbable polymer scaffolds for tissue engineering capable of sustained growth factor delivery. J Control Release, 2000. 64(1-3): p. 91-102.

6. Langer, R. and J.P. Vacanti, Tissue engineering. Science, 1993. 260(5110): p. 920-6.

7. Rheinwald, J.G. and H. Green, Formation of a keratinizing epithelium in culture by a cloned cell line derived from a teratoma. Cell, 1975. 6(3): p. 317-30.

8. Bello, Y.M., A.F. Falabella, and W.H. Eaglstein, Tissue-engineered skin. Current status in wound healing. Am J Clin Dermatol, 2001. 2(5): p. 305-13.

9. Shepherd, B.R., et al., Vascularization and engraftment of a human skin substitute using circulating progenitor cell-derived endothelial cells. FASEB J, 2006. 20(10): p. 1739-41.

10. Cuono, C.B., et al., Composite autologous-allogeneic skin replacement: development and clinical

application. Plast Reconstr Surg, 1987. 80(4): p. 626-37.

11. MacNeil, S., Progress and opportunities for tissue-engineered skin. Nature, 2007. 445(7130): p. 874-80.

12. Boyce, S.T., et al., Topical nutrients promote engraftment and inhibit wound contraction of cultured skin substitutes in athymic mice. J Invest Dermatol, 1995. 104(3): p. 345-9.

13. Young, D.M., K.M. Greulich, and H.G. Weier, Species-specific in situ hybridization with fluorochrome-labeled DNA probes to study vascularization of human skin grafts on athymic mice. J Burn Care Rehabil, 1996. 17(4): p. 305-10.

14. Boyce, S.T., et al., Comparative assessment of cultured skin substitutes and native skin autograft for treatment of full-thickness burns. Ann Surg, 1995. 222(6): p. 743-52.

15. Curran, M.P. and G.L. Plosker, Bilayered bioengineered skin substitute (Apligraf): a review of its use in the treatment of venous leg ulcers and diabetic foot ulcers. BioDrugs, 2002. 16(6): p. 439-55.

16. Tremblay, P.L., et al., Inosculation of tissue-engineered capillaries with the host's vasculature in a reconstructed skin transplanted on mice. Am J Transplant, 2005. 5(5): p. 1002-10.

17. Folkman, J. and M. Hochberg, Self-regulation of growth in three dimensions. J Exp Med, 1973. 138(4): p. 745-53.

18. Colton, C.K., Implantable biohybrid artificial organs. Cell Transplant, 1995. 4(4): p. 415-36.

19. Gibot, L., et al., A preexisting microvascular network benefits in vivo revascularization of a microvascularized tissue-engineered skin substitute. Tissue Eng Part A, 2010. 16(10): p. 3199-206.

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20. Jain, R.K., et al., Engineering

vascularized tissue. Nat Biotechnol, 2005. 23(7): p. 821-3.

21. Rouwkema, J., N.C. Rivron, and C.A. van Blitterswijk, Vascularization in tissue engineering. Trends Biotechnol, 2008. 26(8): p. 434-41.

22. Converse, J.M., et al., Inosculation of vessels of skin graft and host bed: a fortuitous encounter. Br J Plast Surg, 1975. 28(4): p. 274-82.

23. Laschke, M.W., B. Vollmar, and M.D. Menger, Inosculation: connecting the life-sustaining pipelines. Tissue Eng Part B Rev, 2009. 15(4): p. 455-65.

24. Laschke, M.W., et al., Angiogenesis in tissue engineering: breathing life into constructed tissue substitutes. Tissue Eng, 2006. 12(8): p. 2093-104.

25. Laschke, M.W., et al., Improvement of vascularization of PLGA scaffolds by inosculation of in situ-preformed functional blood vessels with the host microvasculature. Ann Surg, 2008. 248(6): p. 939-48.

26. Mikos, A.G., et al., Prevascularization of porous biodegradable polymers. Biotechnol Bioeng, 1993. 42(6): p. 716-23.

27. Mooney, D.J., et al., Localized delivery of epidermal growth factor improves the survival of transplanted hepatocytes. Biotechnol Bioeng, 1996. 50(4): p. 422-9.

28. Peters, M.C., et al., Release from alginate enhances the biological activity of vascular endothelial growth factor. J Biomater Sci Polym Ed, 1998. 9(12): p. 1267-78.

29. Griffith, L.G. and G. Naughton, Tissue engineering--current challenges and expanding opportunities. Science, 2002. 295(5557): p. 1009-14.

30. Levenberg, S., et al., Engineering vascularized skeletal muscle tissue. Nat Biotechnol, 2005. 23(7): p. 879-84.

31. Chen, R.R. and D.J. Mooney, Polymeric growth factor delivery strategies for tissue engineering. Pharm Res, 2003. 20(8): p. 1103-12.

32. Riha, G.M., et al., Review: application of stem cells for vascular tissue engineering. Tissue Eng, 2005. 11(9-10): p. 1535-52.

33. Zhang, J., et al., Engineering of vascular grafts with genetically modified bone marrow mesenchymal stem cells on poly (propylene carbonate) graft. Artif Organs, 2006. 30(12): p. 898-905.

34. Supp, D.M., et al., Genetic modification of cultured skin substitutes by transduction of human keratinocytes and fibroblasts with platelet-derived growth factor-A. Wound Repair Regen, 2000. 8(1): p. 26-35.

35. Supp, D.M., K. Wilson-Landy, and S.T. Boyce, Human dermal microvascular endothelial cells form vascular analogs in cultured skin substitutes after grafting to athymic mice. FASEB J, 2002. 16(8): p. 797-804.

36. Schechner, J.S., et al., In vivo formation of complex microvessels lined by human endothelial cells in an immunodeficient mouse. Proc Natl Acad Sci U S A, 2000. 97(16): p. 9191-6.

37. Auger, F.A., et al., Skin equivalent produced with human collagen. In Vitro Cell Dev Biol Anim, 1995. 31(6): p. 432-9.

38. Dieckmann, C., et al., Regenerative medicine in dermatology: biomaterials, tissue engineering, stem cells, gene transfer and beyond. Exp Dermatol, 2010. 19(8): p. 697-706.

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REVIEW ARTICLE

BENIGN FIBRO‐OSSEOUS LESIONS OF JAWS‐ A REVIEW

Rashi Bahl1, Sumeet Sandhu 2, Mohita Gupta3

1Reader, Department of Oral and Maxillofacial Surgery, Genesis Institute Of Dental Sciences & Research, Ferozepur, Punjab, India

2Prof. & Head, Department of Oral and Maxillofacial Surgery, Sri Guru Ramdas Institute of Dental Sciences & Research, Amritsar, Punjab, India

3Genesis Institute of Dental Sciences and Research, Ferozepur, Punjab, India


Mohita Gupta (BDS) Address: 302, Green Avenue, Amritsar, Punjab. PIN 143001 Contact number: 08146182200 E-Mail: [email protected] Access this Article Online

AbstractBenign Fibro-osseous Lesions is a group of lesions in which normal bone is replaced initially by fibrous connective tissue and over a period of time, the lesion is infiltrated by osteoid and cementoid tissue. This is a benign and idiopathic process. Fibro-osseous lesions of the maxillofacial bones comprise a diverse group of pathologic conditions that include developmental lesions, reactive or dysplastic diseases, and neoplasms. The concept of fibro-osseous lesions has evolved over the last several decades and now includes two major entities: fibrous dysplasia and ossifying fibroma. The less common lesions include florid osseous dysplasia, periapical dysplasia, focal sclerosing osteomyelitis, proliferative periostitis of Garre, and osteitis deformans. It represents a diverse group of pathological conditions that includes developmental lesions, reactive or dysplastic diseases, and neoplasms. Owing to substantial overlap of the histopathologic findings, sub classification of Benign Fibro-osseous Lesions may be problematic. Despite the advances in the understanding of these conditions, f ibro-osseous lesions continue to present problems in classification, diagnosis, and management due to multiple histological and radiographic similarities. The objective of this article is to review the most current clinic pathologic, radiographic, and molecular studies of Benign Fibro-osseous Lesions to aid the surgical pathologist in the recognition and diagnosis of this diverse group of maxillofacial lesions.

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Introduction The fibro-osseous lesions represent a large group of disorders that may have common characteristics including clinical , radiographic and microscopic features. Although most are of unknown etiology, some are believed to be neoplastic and others are related to metabolic imbalances. It is not unusual to see these lesions presenting with a range of radiographic appearances, causing considerable diagnostic confusion1. Benign fibro-osseous lesion is a well-known, descriptive term that encompasses a wide range of conditions, the diagnoses of which may be challenging. In part, the challenge arises because the histopathological appearances of all f ibro-osseous lesions are very similar, if not identical , making cl inical diagnosis dif ficult based on microscopic features alone. The maxillofacial f ibro-osseous lesions are the lesions that are different (except fibrous dysplasia) to those found in the rest of the skeleton. Charles Waldron wrote “In absence of good clinical and radiologic information a pathologist can only state that a given biopsy is consistent

with f ibro osseous lesions. With adequate clinical & radiologic information, most lesions can be assigned with reasonable certainty into one of the several categories2 owing to their similar histology. Radiographically, f ibro-osseous lesions vary considerably from a simple radiolucent lesion to mixed radiolucent/ radiopaque or radiopaque lesion. These can be well defined or il l -defined blending imperceptibly into the surrounding bone. There may or may not be expansion of bone, with or without displacement of tooth. Histologically, the f ibro-osseous lesions mainly consist of two components - hard tissue and soft t issue component. The treatment of f ibro-osseous lesions varies depending on the nature of the lesion. It may vary from simple surgical excision or curettage in cemento ossifying fibroma to a surgical excision and resection of the involved jaw in cases of juvenile ossifying fibroma, osteogenic sarcoma and chondrosarcoma.

Classification Charles A Waldron in 1985 classified fibro osseous lesions into main groups on the basis of clinical behavior, histopathology and radiographic findings:

1) Fibrous Dysplasia 2) Reactive (dysplastic) lesions

arising in the tooth bearing area: Periapical cemento osseous dysplasia

Focal cemento osseous dysplasia Florid cemento osseous dysplasia 3) Fibro – osseous neoplasms Cementifying fibroma Ossifying fibroma Cemento ossifying fibroma

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FIBROUS DYSPLASIA It is one of the most perplexing diseases of osseous tissues & has been described as a lesion of unknown etiology, uncertain pathogenesis and diverse histopathology. It is a congenital, metabolic, non-familial disturbance that produces 2.5% of all bony tumors and over 7% of all non malignant tumors of bone3. It is a benign fibro osseous lesion characterized by formation of f ibrous connective tissue within the spongiosa of the affected bone and often by the painless expansion of that bone to cause deformity4. There is the replacement of normal bony architecture with fibrous and osteoid tissue5. It may also contain islands of calcified tissue, the appearance of which is dependent on the age of the lesion. There is proliferation of f ibroblast l ike cells that have features of osteoblasts in some areas and those

of chondroblasts in others. It occurs because of maturation arrest of bone formation at the stage of woven/fibre bone6. The resultant fibro osseous tissue is poorly formed, elastic and structurally inadequate. It can impair cosmetic & structural function of bone leading to osteolytic lesions, fractures, & deformations. It may involve one or more bones of the cranial or extra cranial skeleton. It has two basic clinical forms: monostotic and polyostotic4 . It may also be associated with endocrine dysfunction, abnormal pigmentation,

and precocious puberty in girls7.

It was first reported by Von Recklinghausen in 1891. Fibrous dysplasia is defined as a disease of bone, characterized by localized areas, usually in a unilateral distribution showing a maturation arrest of bone formation at the stage of woven bone8.

Etiology and Pathogenesis

Fibrous dysplasia is postulated to occur as a result of a lack of stress alignment and insufficient mineralization results in substantial loss of mechanical strength, leading to the development of pain, deformity, and pathologic fractures6.Marie et al showed that an activating mutation of Gsα in osteoblastic cells of patients with McCune-Albright syndrome and monostotic disease leads to constitutive activation of adenylate cyclase, increased cell proliferation, and inappropriate cell dif ferentiation, resulting in overproduction of a disorganized f ibrotic bone matrix in polyostotic and monostotic fibrous dysplasia6 , 3 . Pregnancy has been implicated in exacerbation of f ibrous

dysplasia perhaps because of estrogen receptors in the fibrous tissue3.

Clinical Features

It occurs most commonly in second or third decade of l i fe9 . The average age of occurrence is ten years. Some studies revealed no gender predilection1 0 .Male to female ratio in some studies is 2:1.Some studies also show that sex predilection is almost equal. Among the jaw bones, maxilla is more commonly affected than the mandible.

The most common sign is painless expansion of the affected area and deformity of the affected site. The foramina of cranial nerves, may be encroached upon producing nerve palsies, the disfigurement may be

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extreme justifying the term “leontiasis ossea”. Diffuse polyostotic lesions in large weight-bearing bones are prone to lead to bowing deformities that increase with age and skeletal growth. Unlike deformities in patients with monostotic disease, deformities in patients with polyostotic disease may continue to progress after skeletal maturity1 0 . Oral Manifestations Pain or paraesthesia is an unusual complaint. Displacement of the teeth with resultant malocclusion and interference with normal eruption patterns may occur. In children teeth in the affected part may fail to erupt. Dentinal dysplasia is a disorder that occurs in patients with inherited fibrous dysplasia. Pathologically, f ibrous tissue that is firm, rubbery, and gritty7. Histologically, f ibrous dysplasia consists of varying amounts of spindle cell bundles and trabeculae of immature woven bone. The fibrous tissue in fibrous dysplasia is well vascularized and often show numerous small vessels in the centre and large peripheral sinusoids7. Three site specific patterns of histopathology have been identified. Chinese writing type; sclerotic/pagetoid type; and sclerotic/ hypercellular type. Radiographic Picture

The lesions of f ibrous dysplasia are usually poorly circumscribed, with the lesions demonstrating a blending margin and are radiopaque (ground glass appearance) although early lesions may be largely radiolucent. According to Akintoye, it can present

as a spectrum of four patterns in a panoramic radiograph: ground glass (condensed/granular) , radiolucent (lytic) , mixed radiolucent/radiopaque (mixed density) and radiopaque (sclerotic) . Variations in the cortical thickness are caused by slow resorption of the endosteal surface, commonly referred to as "endosteal scalloping." The periosteal surface remains smooth1 0. Three varieties of appearances are seen on CT scan: ground glass pattern, homogeneously dense pattern, and cystic variety6. Magnetic resonance imaging in addition can help distinguish f ibrous dysplasia from meningioma, osteoma, or mucocele and define the extent of soft tissue involvement, particularly if central nervous system structures are impinged on7. Single photon emission computed tomography has been reported to be more sensitive in detecting the areas involved in cases of f ibrous dysplasia6. A slight elevation of serum alkaline phosphatase may be seen in some cases but may not always be raised. Calcium, phosphate and various other hormones are seen in normal range4. I) Polyostotic Fibrous Dysplasia

Involvement of two or more bones is called as polyostotic f ibrous dysplasia. Two apparent types of polyostotic f ibrous dysplasia are described:

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a) Jaffe – Lichtenstein syndrome b) Mc Cune –Albright syndrome

It most commonly occurs in childhood. Median age of onset of symptoms is 8-10 years, with most occurring before the age of ten1 1. The disease apparently has a distinct tendency to occur in women with a male: female ratio of 1:31 1 . Long bones of extremity are most often affected in following order of frequency: femur, tibia, humerus & radius. Next in order of frequency are bones of the skull (cranial vault & jaw bones)1 1 .

Clinical Presentation

A l imp, pain in leg and fracture is the initial symptom. It pursues a protracted clinical course characterized by pain, deformity & a tendency to pathological fracture of the affected bones1 1 . Leg length discrepancy is very common as a result of involvement of the upper portion of the femur1 2 . Frequently identified deformities include coxa vara, the shepherd's crook deformity, bowing of the tibia etc1 0 . The objective features seen in roentgenograms of bones affected by polyostotic fibrous dysplasia include: broadening or expansion of bone, thinning of cortex, characteristic rarefied & apparently trabeculated appearance, secondary deformities of affected bones1 1 . Premature secretion of pituitary follicle stimulating hormone has been reported as well as moderately elevated basal metabolic rate. Most surgical tissue is obtained by curettage. The specimen has a distinct gritty feeling reflecting the

osteoid trabeculae inherent in the lesion.

The typical microscopic f indings of fibrous dysplasia show irregularly shaped trabeculae of immature bone in a cellular, loosely arranged fibrous stroma. The bony trabeculae are not connected to each other1 2 . Stellate osteoblasts are seen particularly in active lesions and appear to arise from fibroblasts. II) Monostotic Fibrous Dysplasia It is more common than the polyostotic type. It most commonly occurs at the age of 20 to 30 years with some cases becoming dormant by the third decade and hormonal changes l ike in pregnancy reactivating a dormant lesion7. It can also occur in infancy5, occurs with apparently equal predilection for males and females. Ribs and craniofacial bones are most commonly affected7. Other bones affected include, clavicle, t ibia, femur etc. The patient may be asymptomatic and lesion discovered incidentally or patient may present with a painless swell ing caused by a slow growing lesion causing expansion of the jaw and producing a non tender facial asymmetry1 3 .In children the teeth may fail to erupt1 3 . Fibrous dysplasia of the maxilla is an especially serious form of the disease since it has a marked predilection for occurrence in children. Severe malocclusion and bulging of the canine fossa or extreme prominence of the zygomatic process, producing a marked facial deformity, are typical sequlae of this disease in maxilla. Serum alkaline phosphatase and urinary hydroxypoline are examples of

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useful markers and are used to monitor response in the non surgical treatment of disease rather than for diagnosis1 3 . A ground glass or orange peel appearance is seen when there are areas of condensation interspersed with areas of radiolucency. The lesion causes resorption of roots of erupted teeth1 3.It may show focus of gritty tissue in the bone5.

The trabeculae may be devoid of osteoblastic rimming, thereby appearing to be formed by fibroblastic osseous metaplasia 1 3 .

Syndromes Associated with Fibrous Dysplasia McCune-Albright syndrome is an endocrinopathy occurring mainly in girls, consisting of the triad of precocious puberty, polyostotic f ibrous dysplasia and characteristic cutaneous pigmentation. The cutaneous lesions are flat pigmented

macules, often referred to as "café au lait" spots Mazabraud syndrome is the rare combination of f ibrous dysplasia

and soft-tissue myxomas. There are three modes of treatment i .e . observation, medical therapy & surgical treatment. Cortisone has been reported to produce some relief in pain of bone lesions. Important l ine of medical treatment is with bisphosphonates which inhibit osteoclastic activity6. Young patients receiving pamidronate should be monitored with serial radiographs to check for a transient mineralization defect, which presents as increased growth plate thickness, thickening of cortices and/or ossification of radiolucent areas1 0 .

Surgical Treatment According to El Deeb M, the treatment of choice is surgical , depending upon the size of the lesion as ascertained by the radiographic picture and by biopsy. In the osteolytic type radical curettage is indicated, whereas in the more mature, solid type surgical shaving and recontouring is indicated. Fibrous dysplasia is treated by curettage and packing with cancellous chip grafts, by subperiosteal excision and cancellous bone graft, by extraperiosteal excision and cancellous bone graft, cortical graft or both. In maxillofacial area, a common procedure is to delay surgery until bone growth ceases and to contour the bulged portion of the bone for an esthetic appearance. In case of visual disturbance caused by compression of optic nerve, immediate surgery is needed5. According to Edgerton the surgical techniques used are:

1) Simple bone contouring

2) Resection and acrylic implant

3) Resection, remodeling and replantation

Recurrence of f ibrous dysplasia following curettage is more common in children than in adults. This “remove, reshape, and replant” technique has excellent bone healing, good postoperative contours, and no clinical evidence of recurrence of bone enlargement. Malignant transformation of fibrous dysplasia occurs very infrequently, with reported prevalence’s ranging from 0.4% to 4% with average incidence being 1%1 0. The most common

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malignant tumors were osteosarcoma, fibrosarcoma, and chondrosarcoma.

Diffferential Diagnosis Other entities which may be confused with fibrous dysplasia are ossifying fibroma, cemento osseus dysplasia, Pagets disease, cementoma, cherubism, hyperparathyroidism, chronic sclerosing osteomyelitis, osteogenic sarcoma etc. Lesions that may suggest f ibrous dysplasia include simple bone cysts, nonossifying fibromas, osteofibrous dysplasia, adamantinoma, low-grade intramedullary osteosarcoma, and Paget disease1 0 . CEMENTO-OSSEOUS DYSPLASIA (COD) Cemento-osseous dysplasia is the most common fibro-osseous lesion occurring in the tooth bearing areas of the jaws. COD is a group of non neoplastic processes usually confined to the tooth bearing areas of the jaws or edentulous alveolar processes1 4 . Many terms have been used to refer to cement-osseus dysplasia: Periapical cement-osseous dysplasia (PCD), Florid osseus dysplasia (FOD), Florid cemento osseus dysplasia (FLCOD), Focal cemento osseus dysplasia (FCOD).

Robinson attributed the cause as injured bone reacts in an abnormal way to low-grade or chronic injury by resorbing formed bone trabeculae and replacing it with cellular f ibrous connective tissue, in which immature bone and a cementum-like substance are deposited.

Periapical Cemento–Osseous Dysplasia also known as cementoma, osseous dysplasia and periapical cemental dysplasia. The first comprehensive clinical, radiographic, and histopathologic study was reported by Stafne in 1933. Blum in 1930 and Thoma in 1937and 1944 defined its histopathology. PCD is not a true neoplasm but a dysplastic condition in which multiple focal areas of bone and marrow are replaced by cellular connective tissue lesions with limited growth potential. The lesion attains a f ixed size and later undergoes a maturation process that culminates in the formation of multiple dense calcified intraosseous nodules1 2 . PCD is an asymptomatic lesion often discovered on routine radiographic examination .Multiple lesions are often present. Buccal and l ingual expansion of the cortices is often absent.

The age of occurrence has been variably reported by various authors from 3r d to 5t h decade with a range of 14-82 years and mean of 42.5 years with cases rarely occurring before 20 years of age1 2 . Mandible (68.15%)5 is more commonly affected than maxilla1 4 .The lesion principally involves the apical area of one or more vital mandibular teeth, particularly the incisors. Female to male ratio has been variably reported between10:1 to 14:1. Most lesions are less than 0.5 cm in size. Maximum size rarely exceeds 1.5 cm. Periapical cemento-osseous dysplasia has been classically described as progressing through 3 radiographic stages.

1) Osteoloytic stage

2) Cementoblastic stage.

3) The third or mature stage

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Differential diagnosis Radiolucent stage

Apical periodontal granuloma or a radicular cyst

Primordial odontogenic cyst

Early phase of ossifying fibroma

Chronic osteomyelitis( i f 4 to 6 anterior teeth are involved)

Mixed stage and radiopaque stage

Odontoma

Chronic osteomyelitis

Ossifying fibroma

Osteoblastoma

Treatment Only periodic observation is necessary during which one would expect to see the radiographic changes associated with maturation of the lesion.

Focal Cemento-Osseous Dysplasia This condition derives histogenetically from elements of the periodontal l igament. Other etiological theories consider it to be a reactive lesion and it is more common in women2.

Clinical Features

FCOD is almost invariably an asymptomatic discovered lesion on a radiographic examination and occurs in periapical areas of teeth with vital pulps or in regions of extractions. The condition rarely produces expansion of the bone. Larger lesions may however cause sl ight jaw enlargement. FCOD

usually occurs between 3r d to 6t h decades, female: male ratio being 8:1to 10:1. Mandible is more commonly the site of occurrence with around 77% of lesions being in mandible; particularly tooth bearing areas of posterior mandible, and 11-23% of lesions occurring in maxilla. The size range varies from 0.2 -11 cm with average of 1.8 cm2. Regardless of stage, an important diagnostic feature is its close association with the periapex or previous extraction site. Focal cemento-osseous dysplasia tends to be well demarcated with or without cortication. There is no bowing of inferior mandibular border.

At the time of surgical exploration, the surgeon usually finds gritty hemorrhagic material. These gross findings contrast sharply with those of cemento-ossifying fibromas, which share many features histologically. The latter neoplasms tend to enucleate in one piece and are often white, gl istening and homogeneous on cut surface. Radiology was of central importance to the detection of at least 64% of focal cement-osseous dysplasias found incidentally to radiography1 5. On the basis of histopathologic study 3 progressive stages can be identified: The early (osteolytic) , the intermediary (fibro-osseous), the late (Osteosclerotic) .

Because focal cemento-osseous dysplasia generally exhibits l ittle or no tendency to enlarge even after partial removal of the lesion, these lesions do not require any treatment.

Florid Cemento-Osseous Dysplasia

Cemento-osseous dysplasia has a pattern of expression that is often multifocal and commonly affects all

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quadrants of the maxilla and mandible. This multifocal expression is known as f lorid cemento-osseous dysplasia. It is cl inically the most extensive form of cemento-osseous dysplasia and hence the term florid. Melrose et al initially reported FLCOD as florid osseous dysplasia. The disease appears to have a familial distribution; it is more common in women2. The disorder is strictly localized to the tooth bearing areas and not associated with any other skeletal deformity. When the lesions are large, jaw expansion may be noted, particularly of the mandible leading sometimes to facial deformity, symptoms such as dull pain, discharging sinuses or sequestrations. Occasionally, patients without signs of infection complain of an intermittent, dull , aching sensation in the mandibular molar area. All Teeth have normal spontaneous pain and are vital . It is seen more commonly in females2. They have striking tendency towards bilateral, often quite symmetrical, location, and it is not unusual to f ind extensive lesions in all four quadrants, particularly the posterior region (molar-premolar region). They affect only the alveolar processes and seem to be independent of teeth. Lesions have been found more commonly in mandible and sometimes in the maxil la.

Radiographically, a wide spectrum is seen. Radiographs usually display diffuse distribution of lobular, irregularly shaped radiopacities throughout the alveolar process. The lobular densities are often enmeshed in poorly defined areas of decreased radiodensity, often having a ground-glass appearance. The lesions appear as multiple sclerotic masses, located

in two or more quadrants usually in the tooth bearing areas. Biopsy is not necessary.

Management of FLCOD is often difficult and not very satisfactory. In the asymptomatic patient, it is probably wise to keep the patient under observation without surgical intervention because the radiologic features are diagnostic. Management of the symptomatic patient is more difficult . Sequestration of the cementum-like masses will occur slowly and healing will follow this. Saucerization or surgical excision of the sclerotic masses is often not successful and may make matters worse1 2 .

Differential Diagnosis

These include chronic diffuse sclerosing osteomyelitis, Paget’s disease of bone, the osteomas of Gardner’s syndrome, Gigantiform cementoma, osteogenesis imperfecta and polyostotic f ibrous dysplasia.

Malignant Potential Development of malignant spindle cell tumor has been reported in a patient with FLCOD but it is a rare occurrence.

Hereditary Cemnto Osseous Dysplasia/Gigantiform Cementoma In 1953, Agazzi & Belloni reported a condition that was clinically and radiographically similar to florid cemento-osseous dysplasia but was inherited as an autosomal dominant trait. They proposed the name Gigantiform cementoma. This condition is rare. The gnathic

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enlargement in most patients results in significant facial deformity, as well as impaction, malposition and malocclusion of the involved dentition. If not treated the osseous enlargement eventually ceases during the 5t h decade1 2. Usually develop during 1s t decade of l i fe and by adolescent typical obvious lesions are noted and followed by a rapid and expansive growth pattern. It demonstrates multifocal involvement of both maxilla and mandible1 2 . The initial features resemble those seen in cemento-osseous dysplasia, appearing as multiple radiolucencies, in the periapical regions. With progression, the affected sites expand to replace much of the normal bone within the involved quadrant and develop a mixed radiolucent and radiopaque pattern. With further maturation, the lesion becomes predominantly radioopaque but often maintain a thin radiolucent rim. Extensive resection of the altered bone and reconstruction of the facial skeleton and associated soft tissue is recommended can produce acceptable functional and aesthetic result1 2 .

Differential Diagnosis

Osteitis deformans or Paget’s disease of bone, chronic sclerosing osteomyelitis, Scelerotic cemental masses, chronic productive osteitis, osseous dysplasia, multiple enostoses.

OSSIFYING FIBROMA (OF) Ossifying fibroma is a benign odontogenic tumor of mesenchymal origin. OF behaves like a benign bone neoplasm 1 6 . The tumor is demarcated and occasionally encapsulated lesion consisting of fibrous tissue containing

variable amounts of mineralized material resembling bone and/or cementum.

Montgomery was first to coin the term “ossifying fibromatissue within which the bone is formed1 7. It accounts for only 0.1% of the bony lesions. Ossifying fibroma belongs to the poorly defined group of f ibro-osseous lesions involving the jaws and craniofacial bones that result in replacement of the bone by fibrous tissue and subsequent mineralization1 8 , 1 9 . The cause of the ossifying fibroma remains unknown. OF usually occurs between the 3r d and 4t h decade of l ife with the average age being 30 yrs1 2 .Marked predilection for occurrence is reported to be seen in females with female to male ratio varying from 1.56:1 to 5:1. Goaz and White reported that when OF occurs in the maxilla, it is most commonly located in the canine fossae and zygomatic arch. It may grow to completely fi l l the maxillary sinus. It can effect both maxilla and mandible but the preferred site of occurrence is reported to be mandible varying from 70%-89% of cases and maxilla in 11%-26% with affinity for premolar & molar area. The maxillary lesions were found to be more aggressive. Ossifying Fibromas are associated with a slowly progressing enlargement of the affected bone. Lesion is asymptomatic until the growth produces a notable swelling and mild deformity and facial asymmetry. Displacement of teeth is an early clinical feature. When rapid growth does occur, the symptoms are related to the lesion site and may include painless cheek swelling, unilateral proptosis, diplopia and

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epistaxis. Death is a rare occurrence secondary to intracranial extension. These lesions may occasionally have il l -defined border, i f relatively rapid growth occurs. As the lesion matures, mixed radiolucent and radiopaque appearance may be seen. The characteristic features of OF in radiographs are expansion and lesion margination, demarcation, or cortication. Cortical expansion is present, often with an eggshell- thin cortex. Large ossifying fibromas of mandible often demonstrate a characteristic downward bowing of inferior cortex of mandible. On surgical exploration, the tumor is found to be relatively hypovascular and well demarcated from the surrounding tissue, permitting relatively easy separation from the surrounding bone. Some lesions will have a definite capsule. This demarcation from the surrounding tissue is an important feature in distinguishing OF from FD . The vascular spaces resemble arterioles or capillaries displaying a continuous endothelial layer with plump endothelial cells protruding into the capillary lumen .The calcif ied component consists of rounded or lobulated basophilic cementum-like masses, trabeculae of osteoid or bone or combinations of both, the majority of bony trabeculae in cemento-ossifying fibroma are thin, single, and separate with osteoblastic rimming.

Treatment of ossifying fibroma involves the complete removal of lesion by curettage, enucleation, or excision. Complete excision of the tumor has become a necessity since it is notorious for recurrence2 0 .

Juvenile Ossifying Fibroma Juvenile (aggressive) ossifying fibroma was used in 2n d edition of WHO classification of odontogenic tumor of children to describe a lesion affecting the jaws under the age of 15 years. Definition The second edition of the WHO classification of odontogenic tumors defines juvenile (aggressive) ossifying fibroma as an actively growing lesion consisting of cell rich fibrous tissue containing bands of cellular osteoid without osteoblastic rimming together with trabeculae of more typical bone. Giant cells may also be present.

Classification It is the term used to describe two distinct histopathologic variants of ossifying fibroma of the craniofacial skeleton –

psammomatoid juvenile ossifying fibroma

trabecular juvenile ossifying fibroma1 6.

Juvenile active ossifying fibroma affects predominantly patients in the first two decades of l ife, the mean age of occurrence being 3 to 23 yrs1 6 . No signif icant sexual predilection is seen in any of the two forms1 2. Psammomatoid juvenile ossifying fibroma occurs overwhelmingly in the sinonasal and orbital bones of the skull , whereas trabecular juvenile ossifying fibroma is predominantly a gnathic lesion affecting the jaws, with a predilection for maxilla. In the mandible, the tumor occurs more commonly in the ramus than in the

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body of mandible 1 2 . The JOF is often characterized by a progressive and sometimes rapid expansion of the affected area. The clinical diagnostic characteristics suggestive of JOF are the patients age, rapid increase in lesion size and absence of pain, paresthesia and bruit. When the orbital bones and paranasal sinuses are involved, the patients may develop proptosis, exophthalmos, and bulbar displacement1 2 , 1 6 Rarely,

intracranial extension has resulted in meningitis1 2 , 1 6 . The lesion exhibits a primary radiolucent quality with varying amounts of internal radiopacity ,reflecting degree of mineralization. Some lesions contain numerous uniform, round, often laminated structures described as ossicles or psammoma like bodies. Foci of multinucleated giant cells may also be present.

References 1) M Mupparapu et al : Focal cemento -osseous dysplasia. Dentomaxillofacial Radiology 2005:34:39-43

2) Sakuma T, Kawasaki T: Concurrent cementifying and ossifying fibromas of the mandible: Report of a case. J Oral maxillofac Surg; 1998; 56: 778-82

3) Araki M, Hashimoto K, Matsumoto K, Ejima K, Kawashima S,Matsumoto N, et al . Radiographic patterns of f ibro-osseous lesions in the jaws -comparison with histopathological image. Dent Radiol 2005; 45: 97–104. (In Japanese).

4) M Araki et al . Fibro osseous lesions using binary images.J Dentomaxillofacial radiology 2010;39:246-251

5) Chong VFH,. Khoo JBK . Fibrous Dysplasia Involving the Base of the Skull . American Journal of Roentgenology 2002; 178:717-720

6) Di caprio MR , Enneking WF .Fibrous dysplasia : pathophysiology , Evaluation and Treatment. Journal of Bone and Joint Surgery. 2005; 87:1848-1864 7) Ricalde P, Horswell BB: Craniofacial Fibrous Dysplasia of the Fronto-Orbital Region: A case series and l iterature review. J Oral Maxillofac Surg 2001; 59, 157-168. 8) Singer SR, Muppurapu M: Clinical and Radiographic features of Chronic Monostotic Finrous Dysplasia of the Mandible. J Can Dent Assoc 2004,70(8) :548-552 9) Khadilkar VV, Khadilkar AV: Oral Bisphosphonates in Polyostotic Fibrous Dysplasia . Indian Pediatrics 2003; 40: 894-896 10) Gonclaves M, Pispico R: Clinical , Radiographic, Biochemical and histological findings of Florid

Cemento-osseous Dysplasia and Report of a Case. Braz Dent J 2005; 16(3) :247-250

11) Popoff SN, Marks SC: The regulation of skeletal modeling and remodeling in the jaws. Oral and Maxillofacial Clinics of North America 1997; 9 (4) : 563-580.

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12) Smith S., Patel K: Periapical cemental Dysplasia: a case of misdiagnosis. Br. Dent. Journal 1998;185(3) : 122-123

13) Frodel JL, Funk G. Mangement of Aggressive Midface and Orbital Fibrous Dysplasia. Arch Facial Plast surg .2000; 2:187-195 14) N A Alsufyani and EWN Lam: Cemento-osseous duslpasia of jaw bones. J Dentomaxillofacial Radiology 2011; 40:141-146 15) DS Mc Donald-Jankonaski. Focal cement osseous dysplasia:a systematic review. Dentomaxillofacial Radiology 2008;37:350-360

16) Y Liu et al : Ossifying Fibromas of jaw bones. J Dentomaxillofacial Radiology;2010;39:57-63

17) PubMed. http:/ /www.ncbi.nlm.nih.gov/sites/entrez/

18) Alsharif MJ, Sun ZJ, Chen XM, Wang SP, Zhao YF. Benign fibroosseous lesions of the jaws: a study of 127 Chinese patients and review of the l iterature. Int J Surg Pathol 2009; 17: 122–134. 19) I Ponniah et al : Ossifying Fibroma: J Dentomaxillofacial Radiology2011;000:1-4

20) Gondivkar SM et al : Ossifying fibroma of jaws. Oral oncol . 2011sep; 47 (9) : 804-809

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CASE REPORT

INTENSIVE CARE UNITS STAFF’S KNOWLEDGE AND ORAL HYGIENE PRACTICE IN CROATIAN HOSPITALS

Emina Kabil1, Maja Miladinović2, Matej Par3

1Undergraduate Student, Year 4, School Of Dental Medicine, University of Zagreb, Zagreb, Croatia 2Undergraduate Student, Year 4, School Of Dental Medicine, University of Zagreb, Zagreb, Croatia 3DMD, Private Dental Practice, Dankovečka 9/I Zagreb, Croatia


Emina Kabil Undergraduate Student, Year 4, School Of Dental Medicine, University of Zagreb, Zagreb, Croatia E-Mail: [email protected] Access this Article Online

AbstractAim: Intensive Care Unit (ICU) patients require thorough oral care. Inadequate oral care may predispose ICU patients to severe nosocomial infection, Ventilator Associated Pneumonia (VAP). On the other hand, appropriate oral hygiene in ICUs can potentially reduce morbidity from VAP and therefore shorten hospital stay and reduce ICU mortality. Aim of this study was to assess the awareness of this problem and oral hygiene practice of ICU medical staff. Material and Methods: The study was conducted among 249 members of ICU nursing staff from 14 Croatian hospitals. A written survey comprising questions divided into two groups: staff knowledge and oral hygiene practice was used. Results: 94.7% of respondents declared they were familiar with the VAP. Only 32.6% of respondents know the right cause of VAP. 44, 9% reported having an oral care protocol in their hospital. Tongue brushing was reported by 42.2% nurses, and the most frequently used oral hygiene agent is gauze soaked in paraffin oil (75.1%). Most of the nursing staff was aware of the importance of oral care practice in ICU and they allege lack of time (47.1%), lack of staff (39.6%) and the lack of resources (36.6%) as limiting factors in the implementation of adequate oral hygiene. Only 60.6 % wanted additional education and training. Conclusion: This study indicates a relatively low level of knowledge and great diversity of oral hygiene practices in Croatian ICUs. In order to improve oral hygiene in ICUs, a standardized written protocol should be introduced. Encouraging staff education and providing ICU nurses with sufficient resources is needed in order to improve oral hygiene enforcement in ICUs

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Introduction Intensive Care Unit (ICU) patients require 24-hour care and monitoring. Oral hygiene in critically ill patients is often neglected or inadequately performed by quickly swabbing patients' mouths [1]. Possible reasons for this practice are staff's attitude that other aspects of nursing care are more important than adequate oral care [1, 2, and 3], lacking awareness of thorough oral hygiene importance [4] and lack of standardized evidence-based protocol [1, 4, 5, 6, 7, and 8]. Oral flora of critically ill adults differs from that of healthy adults and contains bacteria that may cause pneumonia [1]. Inadequate oral care may predispose ICU patients to severe nosocomial infection, known as Ventilator Associated Pneumonia (VAP). VAP is defined as nosocomial pneumonia that develops in a patient who has been intubated for more than 48 hours [9]. Endotracheal intubation not only compromises the natural barrier between the oropharynx and trachea but also facilitates the entry of bacteria into the lower parts of respiratory tract [10]. Studies have shown that most cases of VAP were caused by bacteria that colonize the oral cavity and dental plaque [10, 11, and 12]. Furthermore, endotracheal tube may become colonized by bacteria. Intubation disables physiological cleaning of upper respiratory tract by coughing, compromises mucociliary transport and increases the secretion of mucilage. [13] All of these factors additionally facilitate development of VAP. VAP is associated with high morbidity, longer hospital stay, higher health care costs and increased mortality rate [8, 10, and 14]. Simple oral care interventions such as tooth-brushing and mouth rinsing with chlorhexidine may reduce the incidence of VAP and consequently morbidity as well as mortality in ICU patients [15, 16].

Objectives Data on oral hygiene practice of ICU staff in Croatian hospitals is lacking and up to date no research articles on this topic have been published. Aim of this study was to assess the awareness and knowledge concerning VAP as well as current oral hygiene practice of ICU medical staff in order to identify potential possibilities for improvement. Subjects and Methods The study was conducted from November 2010 to February 2011 among 249 members of ICU nursing staff from 14 Croatian hospitals. The research was approved by the Ethical Committee of the School of Dental Medicine, University of Zagreb. ICUs staff, who participated in this study, were informed about the research and signed informed consent. A written survey comprising questions divided into two groups: staff knowledge and oral hygiene practice was used. Ten true/false statements were used to assess knowledge and attitudes of respondents regarding VAP:

1. VAP is infection caused by specific pathogens.

2. VAP is infection caused by non-specific pathogens.

3. VAP may be caused by multi-resistant strains.

4. The most common cause of VAP is air or droplet transmitted pathogens.

5. The most common cause of VAP is oral cavity pathogens.

6. VAP has high mortality rate. 7. VAP is easy to cure and patients usually

recover well. 8. VAP is one of the most common nosocomial

infections. 9. Appropriate oral hygiene in intubated

patients may reduce the incidence of VAP. 10. Pneumonia may also occur in patients who

are not intubated. The following questions were used to assess staff’s education and interest for future education and training:

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1. Are you familiar with the VAP? 2. When were you first acquainted with

the VAP? (during education, while working in hospital, during professional training, in some other occasion)

3. Do you want additional training and education? (yes, no, do not care)

In terms of practice, respondents were asked about commonly performed oral hygiene procedures and limiting factors in the implementation of adequate oral hygiene. The following list was given and participant was asked to mark procedures which he/she routinely performs (multiple answers are possible):

1. cleaning teeth with toothbrush 2. cleaning teeth with toothbrush and

toothpaste 3. tongue brushing 4. rinsing with chlorhexidine 5. rinsing with hydrogen peroxide 6. rinsing with povidone iodine 7. rinsing with saline

8. rinsing with some other agent 9. cleaning with sponge and gauze 10. artificial saliva 11. gauze soaked with paraffin oil 12. something else

The following limiting factors were listed (multiple answers are possible):

1. lack of time 2. lack of education 3. lack of staff 4. lack of resources 5. something else

______________________________________________________________________________________

Results In terms of knowledge, ten true/false statements were given. Percentage of correctly marked statements is shown in Figure 1. Statement “VAP is infection caused by specific pathogens” showed the least percentage of correct answers (29.3%, n=73). Statement with most correct answers was “Appropriate oral hygiene in intubated patients can reduce the incidence of VAP” (90.8%, n=226). Overall percentage of correct answers was 65.8%.

29,340,1

87,9

42,5

84,3

70,2 70,6 69,8

90,7

71,8

0102030405060708090

100

1 2 3 4 5 6 7 8 9 10

Question No.

% c

orre

ct a

nsw

ers

Figure 1: Percentage of correctly marked true/false statements.

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1. VAP is infection caused by specific pathogens. 2. VAP is infection caused by non-specific pathogens. 3. VAP may be caused by multi-resistant strains. 4. The most common cause of VAP is air or droplet transmitted pathogens. 5. The most common cause of VAP is oral cavity pathogens. 6. VAP has high mortality rate. 7. VAP is easy to cure and patients usually recover well. 8. VAP is one of the most common nosocomial infections. 9. Appropriate oral hygiene in intubated patients may reduce the incidence of VAP. 10. Pneumonia may also occur in

patients who are not intubated.

Most of respondents (94.7 %, n=236) declared they were familiar with the VAP (Figure 2).

236

70

50

100

150

200

250

YES NO

Are you familiar with the VAP?

Num

ber

of r

espo

nden

ts

Missing data= 3

Figure 2: Answers to question “Are you familiar with the VAP? The most of nurses (86.3%, n=215) have received education concerning VAP during their work in the hospital, and significantly smaller number (28.9%, n=73) during formal school education.

0

50

100

150

200

250

during education while working inhospital

during professionaltraining

in some otheroccasion

When were you acquainted with the VAP?

Num

ber o

f res

pond

ents

Figure 3: Answers to question “When were you acquainted with the VAP?”

(Multiple answers are possible)

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When asked about possible additional education, 16% (n=38) of respondents declared they do not want any additional training and education, and 22% (n=54) of them do not care. Most of subjects (62%, n=151) noted they are interested in future education (Figure 4).

Do you want additional training and education?

YES62%

NO16%

DO NOT CARE22%

Missing data= 6

Figure 4: Answers to question: Do you want additional training and education? Oral care practice varied within each hospital. Gauze soaked with paraffin oil was the primary material used (75.1%, n=187), and the most common mouthwash was chlorhexidine (57%, n=142). Tongue brushing was reported by only 42.1% (n=105) nurses (Figure 5).

94114 105

142

48

13

77

128110

0

187

35

020406080

100120140160180200

1 2 3 4 5 6 7 8 9 10 11 12

Which oral hygiene procedures are commonly used?

Num

ber o

f res

pond

ents

Figure 5: Commonly performed oral hygiene procedures. (Multiple answers are possible)

1. cleaning teeth with toothbrush 2. cleaning teeth with toothbrush and toothpaste 3. tongue brushing 4. rinsing with chlorhexidine 5. rinsing with hydrogen peroxide 6. rinsing with povidone iodine 7. rinsing with saline 8. rinsing with some other agent

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9. cleaning with sponge and gauze 10. artificial saliva 11. gauze soaked with paraffin oil 12. something else

The most common factors limiting adequate oral hygiene are listed in Figure 6. Lack of time has been noted as the most common limiting factor (57.4%, n=143).

143

23

120111

6

0

20

40

60

80

100

120

140

160

lack of time lack of education lack of staff lack ofresources

something else

Limiting factors in the implementation of adequate oral hygiene

Num

ber o

f res

pond

ents

Figure 6: Limiting factors in the implementation of adequate oral hygiene. (Multiple answers are possible)

Discussion Most of respondents (94.7%, n=236) declared they are familiar with the VAP, but only 36.6% (n=91) provided correct answer to the question about etiology of VAP. This indicates great discrepancy between self- perceived and real level of knowledge. Generally low level of knowledge is the possible cause of staff's unawareness and false impression they are well informed about the VAP. This is indicated by relatively low overall score– average score for all 10 questions is only 65.7%. Also, significant variability between scores for individual questions was noted. Percentage of correct answers ranges from 29.3% up to 90.7% (Figure 1). This indicates great variability in knowledge of different aspects of VAP. For instance, the worst results were scored for two questions dealing with etiology of VAP (29.3 and 40.1% accordingly) and the best result (90.7%) was scored for the statement “Appropriate oral hygiene in

intubated patients may reduce the incidence of VAP”. High percentage of correct answers (84.3%) was also noted for statement “The most common cause of VAP are oral cavity pathogens”, which implies that nurses are relatively well informed about the role of oral bacteria in VAP etiology. Considering that the majority of nurses stated they got familiar with VAP only at work (Figure 2, 3), presumably by word of mouth from older colleagues, and not during formal school education, it is somewhat contradictory that many of them haven’t shown interest for additional training and education (38%, n=95) (Figure 4). This finding also suggests that current curriculum of Croatian nursing schools lacks some crucial lessons and therefore should be revised. We suggest that oral hygiene in critically ill patients should be integrated in nursing school’s curriculum as a nursing activity of very high priority. A high percentage of nurses (90.1% n=226) are aware that appropriate oral hygiene in ICUs

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could reduce the incidence of the VAP, but they reported some limiting factors (Figure 6). Lack of time has been noted as the most common limiting factor (57.4%, n=143). A possible cause of this problem is relatively small number of nurses employed in Croatian ICUs, which seems to be insufficient to fulfill all required nursing tasks. In such situation, nurses are more likely to dedicate their time to some other tasks they consider more crucial for patient well- being [1, 2, and 3] rather than performing oral hygiene measures. Increasing number of nurses would probably enable them to distribute their nursing activities more evenly and to avoid neglecting of oral care. Literature dealing with oral care of critically ill often emphasizes the correlation of poor oral hygiene in ICUs with the lack of awareness [19, 20]. According to these studies, low awareness of the problem is the main cause of neglecting oral hygiene in critically ill patients. Since recommended measures [18] are relatively simple and inexpensive, simple rising of awareness (without any other interventions) should motivate nurses to perform oral care more efficiently. Considering poor economic situation in Croatia, as well as insufficient nursing education, we assume that mentioned lack of awareness plays important role in oral hygiene inadequacy. It is important to note the long- term efficiency of improved oral care for critically ill patients. Evidence shows that correctly maintained oral hygiene could greatly reduce the incidence of VAP [15, 16]. Lower incidence of VAP is correlated with less complication during hospitalization, shorter hospital stay, lower mortality and better postoperative recovery [8, 10, and 14]. This is beneficial not only for patients, but also for hospitals and healthcare system as a whole, since it greatly reduces hospital expenses. It is therefore rational to encourage education and enforcement of oral care in critically ill patients. The first step in accomplishing this

goal should be raising awareness of the problem through formal school education, as well as during continuing lifelong education. The next step should be introducing a written evidence-based protocol (AACN) and providing staff with adequate materials and resources. 63.1% (n=157) of respondents perform oral hygiene measures as recommended by American Association of Critical- Care Nurses (AACN), i.e. brushing and rinsing with chlorhexidine [18]. There is some evidence available indicating that measures recommended by AACN are effective in prevention of VAP [22]. Even if AACN protocol isn’t generally accepted as an effective measure for prevention of VAP, we consider its practical implementation useful for dealing with the problem. Several studies demonstrated that enforcement of protocol recommended by AACN successfully reduced VAP morbidity and mortality in clinical environment [15, 16, and 18]. Since it is the only protocol which is as-to-date supported by evidence, it should be taught in nursing schools and introduced to nursing staff. Also, tongue brushing, combined with tooth brushing and rinsing with chlorhexidine has desirable effects [22, 23, 24], but this survey has shown that it is performed by only 42.2% (n=105) of nurses. The most common oral hygiene procedure is swabbing with gauze soaked in paraffin oil, what we found very unique to Croatian ICUs. Little information has been found in the available literature regarding this method. In one Croatian medical high school textbook [21] paraffin is listed as an agent for oral hygiene in ICUs, but as dental professionals we are dubious about the potential benefit of this agent, except lubrication, moistening and mechanical protection of mucosa. It certainly lacks required antibacterial properties and combined with gentle swabbing isn’t very effective in plaque removal. This practice should be replaced with brushing in order to mechanically remove the plaque. Using chlorhexidine after brushing inhibits

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formation of new plaque and recolonization of bacteria to mechanically cleansed tooth surfaces [25, 26]. A great variety of performed procedures (Figure 5) is probably the result of lack of written oral hygiene protocol in Croatian hospitals. Having no precise guidelines, nurses perform oral hygiene procedures at their own discretion and in accordance with available materials. Many different materials for oral hygiene are used (Figure 5), presumably depending on their availability in individual hospitals. Conclusion The results of this survey indicate that present level of knowledge among nurses and oral practice currently performed in Croatian ICUs may be ineffective in prevention of VAP. Implementation of standardized written protocols, as well as additional nurse training should be done. References 1. Munro CL, Grap MJ. Oral health and care in the intensive care unit: State of the science. Am J Crit Care.2004; 13:25-34. 2. Binkley C, Furr La, Carrico R, McCurren C. Survey of oral care practices in US intensive care units. Am J Infect Cont. 2004; 32(3):161-9. 3. Jones H, Newton J, Bower EJ. A survey of the oral care practices of intensive care nurses. Intensive Crit Care Nurs. 2004; 20:69—76. 4. Cutler CJ, Davis N. Improving oral care in patients receiving mechanical ventilation. Am J Crit Care. 2005; 14:389-94. 5. O’Reilly M. Oral care of the critically ill: a review of the literature and guidelines for practice. Austral Crit Care. 2003;16(3):101-10. 6. Berry AM, Davidson PM, Masters J, Rolls K. Systematic literature review of oral hygiene practices for intensive

care patients receiving mechanical ventilation. Am J Crit Care. 2007;16:552-62. 7. Berry AM, Davidson PM. Beyond comfort: oral hygiene as a critical nursing activity in the intensive care unit. Intensive Crit Care Nurs. 2006;22:318-28. 8. Craven DE, Duncan RA. Preventing ventilator-associated pneumonia. Am J Crit Care Med. 2006; 173:1297-99. 9. http://www.ihi.org/knowledge/Pages/Changes/ImplementtheVentilatorBundle.aspx 10. Craven DE, Driks MR. Nosocomial pneumonia in the intubated patient. Semin Respir Infect. 1987; 2:20-33. 11. Torres A, el-Ebiary M, Gonzalez J, et al. Gastric and pharyngeal flora in nosocomial pneumonia acquired during mechanical ventilation. Am Rev Respir Dis. 1993; 148:352-7. 12. Valles J, Artigas A, Rello J, et al. Continuous aspiration of subglottic secretions in preventing ventilator-associated pneumonia. Ann Intern Med. 1995; 122:179-86. 13. Levine SA, Niederman MS. The impact of tracheal intubation on host defenses and risks for nosocomial pneumonia. Clin Chest Med. 1991;12:523-43. 14. Hutchins K, Karras G, Erwin J, Sullivan KL. A comprehensive oral care program reduces rates of ventilatorassociated pneumonia in intensive care unit patients. Am J Intensive Care. 2008;36(5):81-2. 15. Yao LY, Chang CK, Maa SH, Wang C, Chen CC Brushing teeth with purified water to reduce ventilator-associated pneumonia. J Nurs Res. 2011 Dec;19(4):289-97. 16. Garcia R, Jendresky L, Colbert L, Bailey A, Zaman M, Majumder M. Reducing ventilator-associated pneumonia through advanced oral-dental care: a 48-month study 17. Schwartz SN, Dowling JN, Benkovic C et al. Sources of gram-negative bacilli colonizing the tracheae of intubated patients. J Infect Dis 1978;138:227-31.

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18. AACN Web site: http://www.aacn.org/WD/Practice/Docs/PracticeAlerts/oral%20care%2004-2010%20final.pdf. Accessed March 31, 2012 19. Adams R 1996 Quali.ed nurses lack knowledge related to oral health, resulting in inadequate oral care of patients on medical wards. Journal of Advanced Nursing 24(3): 552–560 20. Price B 1990 Body Image-nursing Concepts and Care. Prentice Hall, London 21. Prlić N. Zdravstvena njega za ucenike I. II. razreda srednjih medicinskih škola, u zanimanju medicinska sestra. 12. izd. Školska knjiga. Zagreb. 2009. 22. Feider LL, Mitchell P, Bridges E. Oral care practices for orally intubated critically ill adults. Am J Crit Care. 2010 Mar;19(2):175-83. 23. Wilkins EM. Clinical Practice of the Dental Hygienist. Philadelphia: Lippincott Williams & Wilkins, 1999. 24. Christensen GJ. Why clean your tongue? Journal of the American Dental Association 1998; 129 (11):1605-1607.

25. Scannapieco FA, Yu J, Raghavendran K, Vacanti A, Owens SI, Wood K, Mulotte JM: A randomized trial of chlorhexidine gluconate on oral bacterial pathogens in mechanically ventilated patients. Crit Care 2009, 13:R117. 26. Munro CL, Grap MJ, Jones DJ, McClish DK, Sessler CN: Chlorhexidine, toothbrushing and preventing ventilator-associated pneumonia in critically ill adults. Am J Crit Care 2009, 18:428-437. ______________End of article________________

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REVIEW STUDY

A RETROSPECTIVE STUDY ON OCCUPATION‐RELATED MAXILLOFACIAL FRACTURES IN CHONGQING, CHINA FROM 2008 (YEAR) TO 2011 (YEAR)

Piyush Sharma1a, Zhou Ningbo1b, Yang Kai2

1aPost Graduate Student, Department of Oral and Maxillofacial Surgery, Chongqing Medical University, Yuzhong district, Chongqing, China 1bPost Graduate Student, Department of Oral and Maxillofacial Surgery, Chongqing Medical University, Yuzhong district, Chongqing, China 2Professor, DDS PhD (Oral and Maxillofacial Surgery), Affiliated hospital of Stomatology, Chongqing Centre of Oral and Biomedical Research ,Chongqing medical university Chongqing, China

Note: Authors ‘1a’ and ‘1b’ are Co-First Authors


Prof. Wang Tao DDS PhD (Oral and Maxillofacial Surgery), Affiliated hospital of Stomatology, Chongqing Centre of Oral and Biomedical Research, Chongqing medical university Chongqing, China E-Mail: [email protected] Access this Article Online

AbstractBackground Maxillofacial trauma constitutes of hard and soft tissue injuries, in this study we have discusses the fractures in maxillofacial region related to occupations .Fractures constitute a substantial proportion of cases of maxillofacial trauma. This retrospective study was designed to analyze the sex, age, cause, site distribution and treatment of maxillofacial fractures and their relationship with patients’ occupations in Chongqing, China. Methods A retrospective study on maxillofacial fractures was carried out in the Department of Oral and Maxillofacial Surgery, the First Affiliated Hospital of Chongqing Medical University (Chongqing, China) between January 1, 2008 and December 31, 2011. The study included 173 patients with 248 maxillofacial fractures. Sex, age, cause, occupation�site distribution of patients and treatment modalities in hospital were recorded. Results The males consisted 67.6% of maxillofacial fractures and females (32.4%) Middle-aged had more fractures than young and old-aged, and the yearly distribution showed no significant variation. Road traffic accident was the most common causative factor (33.6%), followed by fall of an object�20.2%, and falls (18.5%). Taxi/truck drivers (24.3%) were most prone to have maxillofacial fractures, followed by construction workers (19.6%) and mine workers (16.2%). Regarding the site distribution of mandibular fractures, the majority (32.4%) occurred in the parasymphysis, 19.8% in the angle, and 12.6% in the condylar region. 71.3% of patients had rigid fixation with plates and 15.3% had inter maxillary fixation (IMF). Conclusion Occupation distribution and causes of maxillofacial fractures reflected trauma patterns within the community and can provide guidelines for the design of programs geared toward prevention and treatment. In our study the drivers and construction workers were more prone to maxillofacial fractures, proper safety measures while driving and working will significantly reduce the incidence of such injuries. Key Words: maxillofacial fractures, occupation-related, mandible fractures, rigid internal fixation (RIF), prevention .

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Introduction Many studies have reported the anatomic localization, causes, age and gender distributions, treatments, treatment results, and incidences of maxillofacial fractures.[1-3] As reported in previous studies the major cause of maxillofacial fractures was traffic accidents.[4] Other causes are assaults, falls, sports-related injuries, and civilian warfare.[5] Some studies shown assault was the most common cause of maxillofacial fractures in many developed countries, whereas traffic accidents was the most frequent causes in many developing areas.[6,7] The causes, types, and site distributions of these fractures seem to change with geographic locations. [1] Treatment of maxillofacial fractures includes fixation with miniplates, wire fixation, intermaxillary fixation, elevation and reduction. Moreover, graft and proplast applications for reconstruction of bone defects and elevation by Gillies method in the case of zygoma fracture are the most common treatments used worldwide and also in our department. Nevertheless, the treatment protocols of the patients with maxillofacial fracture may vary according to the types and locations of the fracture as well as the surgeon’s experience and preference. Because of cultural, social and environmental factors, both the incidence and etiology of maxillofacial fractures change from country to country.[8] China is the fastest growing economy in the world and is a developing country, this study was carried out in a major municipal province, Chongqing, which geographically locates in southwest China and is a fast-developing city. However, there have been few detailed reports about the occupation-related maxillofacial fractures in Chongqing. This article presents the sex, age, cause, site distribution, treatment and their relationship with patients’ occupations for 173 patients treated for maxillofacial fractures from January 2008 to December 2011 in the Department of Oral and Maxillofacial Surgery, the First Affiliated Hospital of Chongqing Medical University (Chongqing, China).

Materials and methods We retrospectively investigated 173 patients with maxillofacial fractures who were treated in our department between January 2008 and December 2011. Various parameters including sex, age, cause, occupation and site distribution, treatment modalities and duration in hospital were recorded. The site distribution of fractures was classified into frontal, nasal and nasoethmoidal, zygomatic, orbital, dento-alveolar, maxillary and mandible. Results This retrospective study included 173 patients (117male and 56 female) with maxillofacial fractures treated in the Department of Oral and Maxillofacial Surgery, the First Affiliated Hospital of Chongqing Medical University (Chongqing, China) from January 2008 to December 2011. In addition to the sex, age, yearly distribution, cause and occupation of maxillofacial fractures in Tables 1-4, site distribution of maxillofacial fractures are shown in Table 5 and the treatment protocols for each patient and the number of the patients treated with each protocol are presented in Table 6.

Table 1. Sex and age distribution of maxillofacial fractures

Age groups Total

number Male Female

Upto20 38 23 15

20-40 47 34 13

40-60 46 31 15

Above 60 42 29 13

Total 173 117 56

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Table 2. Yearly distribution of occupation related fracture cases

0

10

20

30

40

50

2008 2009 2010 2011

Table 3. Causes of fractures

Causes of fracture Number of patients Percentage

Traffic accidents 58 33.6

Fall of an object 35 20.2

Falls 32 18.5

Blows 24 13.8

Assaults 17 9.9

Work related injuries/sports injuries 7 4.0 Total 173 100

Table 4. Occupations of patients with maxillofacial fractures

Occupation Driver Construction workers

Mine workers

Factory workers

Forest workers

farmers Others Total

Number of patients

42 34 28 22 18 15 14 173

Percentage 24.3 19.6 16.2 12.7 10.4 8.7 8.1 100

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Table 5. Site distribution of maxillofacial fractures

Anatomic location of mandibular fractures

Site Number Percentage Symphysis 7 9.9 Parasymphysis 23 32.4 Condylar 9 12.6 Coronoid 3 4.3 Angle 14 19.8 Body 4 5.6 Ramus 11 15.4

Table 6. Treatment protocols of patients with maxillofacial fractures

Treatment Number of patients Percentage Intermaxillary fixation(imf) 38 15.3 Rigid fixation with plates 177 71.3 Fixation with wire 12 4.8 Elevation reduction 17 6.9 Iliac bone graft 4 1.7 Total 248 100

Discussion In general, our results were concordant with earlier studies. [9] The male is likely to have more maxillofacial fractures (67.6%) than female, which is possibly because more males engaged in more physical and dangerous works than females. The sex ratio was about 2:1, which was lower than previous reports from Nigeria, [10] Austria, [11] and Japan, [12] and higher that report from Libyan children. [13]

The number of patients was found mostly in the 20-40-year-old group. This was similar to results reported in previous studies. And the yearly distribution almost had no change. The most common cause of maxillofacial fractures in our study is traffic accidents (33.6%). A higher incidence of traffic accidents had been reported from Saudi Arabia, [10] Austria, [11] and Japan, [12]. More recent studies have shown assault as the most common cause of maxillofacial fractures in many developed countries, whereas traffic accidents remain the most frequent cause in

Sites of fracture Driver Construction workers

Mine workers

Factory workers

Forest workers

Farmers Others

Frontal 3 6 7 4 4 - - Nasal and nasoethmoid

12 7 8 4 3 2 3

Zygomatic 8 6 5 5 1 3 2 Orbit 6 4 2 1 1 - - Dentoalveolar 11 6 5 8 3 4 6 Maxilla 9 5 1 6 2 2 2 Mandible 18 10 8 8 7 11 9 Total 248 67 44 36 36 21 22 22

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many developing areas. [14] ,the results of our study are in accordance with other developing countries having higher incidence of traffic accidents .We found fall of an object was the second most frequent cause (20.2%) of maxillofacial fractures. This incidence was higher than in the United Arab Emirates (4.1%) [15] But similar with the results from Brazil (22.5%) [16]. Occupations like forestry construction and mining are more prone to suffer injuries due to fall of an object due to lack of appropriate safety measures and equipments. The results reflect the socioeconomic conditions had great relationship with the causes of maxillofacial fractures. Our study

showed traffic accidents was the first highest cause and fall of an object the second highest, like in other developing countries like Brazil. [16] Our study found that taxi/truck drivers (24.3%) were the most to have maxillofacial fractures, followed by construction workers. Workers in these occupations carried a (24.3+19.6)/ (10.4+8.7) =2.3-fold while compared to workers in forestry and farm. The road conditions in the Mountain city Chongqing is not so good, heavy traffic in the city and lack of safety measures while driving may be the possible reasons leading to higher incidence of maxillofacial fractures.

Fractures in drivers. It is acknowledged that the most common mandibular fracture location was the condyle (36%) followed by the corpus by previous studies [4,16] .Earlier studies showed the corpus region as the most common location.[1,2] However, our findings are similar to other studies in this regard, demonstrating the parasymphysis(32.4%) as the most common region followed by angle(19.8%) and condyle. Different site distributions of fractures appeared to relate to the nature of the work and the cause of the injury. Road traffic accidents appear to be the cause in most sites of facial fractures. There are many treatment regimens of maxillofacial fractures, and the selection may vary according to the types and size distributions of the fractures, patients’ characteristics, and the surgeon’s experiences and preference. Each fracture and patient has particular character; therefore, standardization is hard to meet. However, the common applications are rigid fixation using mini-plates or wire inter-maxillary fixation using arch bars, extraoral bandage, elevation and reduction procedures for zygoma fractures, [17] or a combination of these methods. We preferred rigid fixation with plates in most cases (71.3%). Other protocols we used were intermaxillary fixation, fixation with wires, and elevation reduction or a combination of these protocols. In conclusion, maxillofacial fractures are observed with different causes and site distributions of each patient. Age and sex variations may also contributed to incidences.

Also we found that maxillofacial fractures are occupation-related with the most happened in bus/taxi drivers. The best way of treating occupation-related maxillofacial fractures is through prevention. That should include recognition of possible occupational hazards, safety training of workers and implementation of safety measures in the road and work place. The treatments are not the same in each case and the surgeon should evaluate the patients and fractures individually. References 1. Güven O. A comparative study on maxillofacial fractures in central and eastern Anatolia. A retrospective study. J Craniomaxillofac Surg 1988;16:126-9. 2. Ellis E 3rd, Moos KF, el-Attar A. Ten years of mandibular fractures: an analysis of 2,137 cases. Oral Surg Oral Med Oral Pathol 1985;59:120-9. 3. Taher AA. Maxillofacial injuries due to road traffic accidents in Kuwait. Br J Oral Maxillofac Surg 1986;24:44-6. 4.Haug RH, Prather J, Indresano AT. An epidemiologic survey of facial fractures and concomitant injuries. J Oral Maxillofac Surg 1990;48:926-32. 5.Telfer MR, Jones GM, Shepherd JP. Trends in the aetiology of maxillofacial fractures in the United Kingdom (1977-1987). Br J Oral Maxillofac Surg 1991;29:250-5. 6.Brown RD, Cowpe JG. Patterns of maxillofacial trauma in two different cultures.

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A comparison between Riyadh and Tayside. J R Coll Surg Edinb 1985;30:299-302. 7.Adi M, Ogden GR, Chisholm DM. An analysis of mandibular fractures in Dundee, Scotland (1977 to 1985). Br J Oral Maxillofac Surg 1990;28:194-9. 8.Cheema SA, Amin F. Incidence and causes of maxillofacial skeletal injuries at the Mayo Hospital in Lahore, Pakistan. Br J Oral Maxillofac Surg 2006;44:232-4. 9.Ashar A, Samerr Khateery, Adam Kovacs. Etiology and patterns of facial fractures in Al Ain, United Arab Emirates. Saudi Dent J 1999;11:109-13 10.Lawoyin DO, Lawoyin JO, Lawoyin TO. Fractures of the facial skeleton in Tabuk North West Armed Forces Hospital: a five year review. Afr J Med Med Sci 1996;25:385-7. 11.Hackl W, Hausberger K, Sailer R, Ulmer H, Gassner R. Prevalence of cervical spine injuries in patients with facial trauma. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001;92:370-6. 12. Iida S, Kogo M, Sugiura T, Mima T, Matsuya T. Retrospective analysis of 1502

patients with facial fractures. Int J Oral Maxillofac Surg 2001;30:286-90. 13. Jaber MA, Porter SR. Maxillofacial injuries in 209 Libyan children under 13 years of age. Int J Paediatr Dent 1997;7:39-40. 14.Adi M, Ogden GR, Chisholm DM. An analysis of mandibular fractures in Dundee, Scotland (1977 to 1985). Br J Oral Maxillofac Surg 1990;28:194-9. 15.Muraoka M, Nakai Y, Nakagawa K, Yoshioka N, Nakaki Y, Yabe T, et al. Fifteen-year statistics and observation of facial bone fracture. Osaka City Med J 1995;41:49-61. 16.Brasileiro BF, Passeri LA. Epidemiological analysis of maxillofacial fractures in Brazil: a 5-year prospective study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006;102:28-34. 17.Khalil AF, Shaladi OA. Fractures of the facial bones in the eastern region of Libya. Br J Oral Surg 1981;19:300-4.

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