chemical injuries to orofacial structures

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CHEMICAL INJURIES TO OROFACIAL STRUCTURES

SHRUTHI RAJ

CONTENTS• Drug allergy• Contact stomatitis• Perioral dermatitis• Angioedema• Non allergic reactions to drugs taken

locally• Non allergic reactions to drugs taken

systemically

• Oral cavity frequently manifests a serious reaction to a wide range of drugs and chemicals.

• The tissue reaction can be a local response to a severe irritant.

• Drug or chemical that is administered systemically may manifests oral reaction.

ALLERGIC PHENOMENON

CONTACT STOMATITIS / STOMATITIS VENENATA

ANGIOEDEMA

DRUG ALLERGY / STOMATITIS MEDICAMENTOSA

DRUG ALLERGY • Drug idiosyncrasy, Drug

sensitivity,Stomatitis / Dermatitis medicamentosa

• Sensitivity reactions following exposure to drugs or chemicals but not related to pharmacological activity or toxicity of the material.

Pathogenesis of drug allergy• IgE mediated reactions may occur when drug reacts with

IgE antibody bound to mast cells with release of chemical mediators.

• An antibody binds to the drug that is already attached to a cell surface . The pathological changes that ensue depend on the target cell involved.

• Antigen circulates for extended periods allowing sensitization and production of new antibodies . The antigen antibody complex gets deposited at various sites and leads to dermatitis.

Clinical features

ALLERGIC REACTION OF SKIN IS DERMATITIS MEDICAMENTOSA.

•skin lesions are erythematous in type as in erythema multiforme.•Urtical in nature•Manifest as exfoliative dermatitis or fixed drug eruptions

Oral manifestations STOMATITIS MEDICAMENTOSA

• Stomatitis• Ulceration and necrosis• Hemmorhage• Gingival hyperplasia• Pigmentation• Altered salivary function• Altered taste sensation

• Common type – erythema multiforme characterized by multiple ulcerations of the tongue , palate, buccal mucosa and gingiva with pain and discomfort.

• Other patterns: anaphylatic stomatitis intraoral fixed drug eruptions lichenoid drug reactions pemphigus like eruptions nonspecific vesiculoulcerative

lesions

Anaphylatic stomatitis:• Arises after drug enters circulatory system

and binds to Ig E – mast cell complex.• Penicillin and sulfa drugs• Oral lesions may be alone or along with

urtical skin lesions or other signs and symptoms of anaphylaxis.

• Affected mucosa exhibit diffuse lesions varying from multiple areas of erythema to extensive areas of erosion or ulceration.

Intraoral fixed drug eruptions:• Occur in patients who are repeatedly

administered to drugs which they are sensitive.

• Barbiturates, salicylates, sulfonamides and tetracycline.

• Appears as localized areas of erythema and edema that can later develop to vesiculoulcerative lesions.

Lichenoid drug reactions, lupus erythematosus like eruptions and pemphigus like eruptions

• Bilateral and symmetric oral lesions in posterior buccal mucosa and lateral borders of tongue.

• Oral lesions of gingiva resemble necrotizing gingivitis or Vincent’s infection.

• Hairy tongue seen in penicillin therapy.

Histologic features• Nonspecific pattern of subacute mucositis with an

admixture of lymphocytes , eosinophils and neutrophils – anaphylatic stomatitis.

• Similar features along with spongiosis and exocytosis of the epithelium , vaculor changes of basal layer and individual necrotic cells – fixed drug eruptions.

• Distinctive annular fluorescence pattern string of pearl’s – lichenoid reactions.

• Detected circulating antibody – basal cell cytoplasmic antibody.

Treatment and prognosis• Signs and synptoms regresses with

discontinuing the drug.• Localized acute signs relieved by

administration of antihistamines .• Systemic signs relieved by administration

of antihistamines.

CONTACT STOMATITIS AND DERMATITIS

• STOMATITIS AND DERMATITIS VENENATA• Lesion of the skin or mucous membrane occurs at

a localized site after repeated contact with the causative agent.

• Causative agents are chemical in nature( hapten) that require conjugation with protein to be effective.

• With the aid of intraepithelial langerhan cells hapten is converted to a complement antigen and is presented to T lymphocytes for sensitization and production of Ig E with specific receptors.

Materials that cause stomatitis venenata

Clinical features• Itching or burning sensation at the site of contact.• Followed by appearance of erythema and then

vesicle formation.• Vesicles then rupture forming erosions that is

extensive and if secondary infection occurs can be serious.

• In chronic contact skin becomes thickened and dry.

Oral manifestations• Oral cavity is less sensitive to allergic reactions

than skin because:

• Mucosa - inflammed and edematous leading to smooth, shiny appearance of surface.

• Gingiva - uniform bright red in all quadrants.

Shorter period of contact in oral cavitySaliva dilutes and removes antigensLimited keratinization of oral mucosa makes hapten binding more difficult and high vascularity tends to remove antigen more quickly

• Buccal mucosa is puffy and dark red revealing engorged and ejected superficial capillaries.

• Small vesicles are formed that may rupture and form small areas of erosion and ulceration.

• Secondary infection - burning sensation, itching, tingling and edema .

• In chronic cases the affected mucosa is erythematous or white and hyperkeratotic.

Allergic stomatitis caused by acrylic resin

Contact cheilitis in a patient who has developed an allergy to a component of her lipstick.

Lichenoid reaction of the oral mucosa, associated with a contact allergy to gold. The patient has a gold crown on tooth 36.

Erythema of the palate in the area in contact with a resin prosthesis, in association with a contact allergy to methyl methacrylate

Histologic features• Intra and intercellular edema of epithelium.• Vesicle formation within the epithelium or basement

membrane.• Connective tissue has edematous background and infiltrate

of lymphocytes and plasma cells.• Engorged and dilated blood vessels.

PERIORAL DERMATITIS• Unique skin disease that involves the

circumoral area .• Exogenous substance that initiate rash are

include bubble gum , moisturizers and night creams

Clinical features• Appears with persistent erythematous

papules and papulopustules that involve the skin surrounding the vermilion border.

• Classically a zone of spared skin is seen immediately adjacent to vermilion border.

Circumoral dermatitis – zone of erythema without papules or pustules

Histopathologic features• Variable pattern.• Chronic lymphohistiocytic dermatitis that

exhibits spongiosis of hair follicle.• Rosacea like pattern .

CONTACT STOMATITIS FROM ARTIFICIAL CINNAMON FLAVOURING

• Cinnamon oil is used as a flavouring agent in ice creams, soft drinks alcoholic beverages,toothpaste and mouthwashes.

• Concentration is 100 times more than in natural spices

Clinical features• Pattern depends on medium of delivery –diffuse

or localized.• Pain and burning sensation• Plasma cell gingivitis• Sloughing of superficial epithelium without any

erosion.• Lesions appears on buccal mucosa and lateral

borders of tongue.

• Buccal mucosal lesions are oblong patches along the occlusal pattern.

• Individual lesions have erythematous base but often white as a result of hyperkeratosis of surface epithelum

Histopathologic features• Acanthotic epithelium• Elongated rete pegs• Thinning of suprapapillary plates• Hyperkeratosis and extensive neutrophilic

exocytosis.• Superficial lamina propria heavy

inflammatory cell infilterate predominately lymphocytes intermixed with plasma cells, histiocytes or eosinophils.

• This infilterate obscures the epithelium and connective tissue interface.

• In localized cases there is presence of obvious perivascular inflammatory infilterate below interface zone

ANGIOEDEMA• ANGIONEUROTIC EDEMA , QUINCKE’S

EDEMA, GIANT CELL URTICARIA• Diffuse edematous swelling of the soft

tissues commonly involving the subcutaneous and submucosal connective tissue.

Pathogenesis• Allergic angioedema ( mast cell

degranulation)• Use of angiotensin converting enzyme

(ACE).• Activation of complement pathway.• Due to presence of high levels of antigen –

antibody complex• Grossly elevated peripheral blood

eosinophil counts.

Clinical features• Soft , non tender diffuse erythematous

swelling of relatively rapid onset .• Solitary or multiple.• Involving face around lips, chin , eyes ,

tongue, pharynx , larynx.• Arms, hands , legs , genitals and butocks

are involved.• Enlargements measures upto several cms .

• Eyes are swollen and shut and lips are puffy.

• A prickly or itching sensation precedes the urtical swelling.

• The skin appears to be normal colour or slightly pink .

• Enlargement resolves in 24- 72 hours .• Can appear daily or at intervals of months

or years.

Treatment and prognosis• Causative agent to be discontinued.• Edema treated with antihistamines.• If not controlled – use of intramuscular epinephrine.

NON ALLERGIC REACTION TO DRUGS AND CHEMICALS USED

LOCALLY Aspirin

• Available as powder and tablet form• Effective systemically• Local obtundent especially for relief of

toothache chemical injury .• Tablet is placed aganist the offending

tooth allowing the lips and cheek to hold in position as it dissolves.

• Within few minutes burning sensation and the surface becomes whitened or blanched .

• Separation and sloughing of epithelium with bleeding if area is traumatized.

• Healing of Aspirin Burn Aspirin Burn usually a week or more

Endodontic materials• Use of certain endodontic materials can cause soft tissue

damage.• Paraformaladehyde used to devitalize pulp can leak from

pulp chamber to surrounding tissues necrosis of gingiva and bone

Sodium hypochlorite• Root canal irrigant• Cause severe tissue damage if comes in

contact with tissues or extrudes beyond apex.

• On contact with vital tissues it causes hemolysis ,ulceration, facial nerve weakness and necrosis , inhibits neutrophil migration and damages endothelial cells and fiberoblasts

• Inadvertent injection of NaOCl solution into periapical tissues leads to emphysema , permanent facial and trigeminal nerve weakness and allergic reactions

NaOCl was inadvertently expressed into the periapical tissues through the apical foramen of the right maxillary cuspid during cleaning andshaping.

Review: the use of sodium hypochlorite in endodontics — potential complications and their managementH. R. Spencer, V. Ike , P. A. Brennan

Bruising and oedema of patient who presented with hypochloriteextrusion into the soft tissues

BRITISH DENTAL JOURNAL VOLUME 202 NO. 9 MAY 12 2007

Gutta percha

• Biologicaly inert latex material• Used to fill the empty space inside the root of

tooth • when it is extruded out of the apex it causes

infective apical periodontitis caused by transport of bacteria beyond apex and an incomplete cleansing and foreign body reactions.

Hydrogen peroxide

• On contact it burns tissues and releases toxin free radicals , perhydroxyl anion or both.

• 30-35% hydrogen peroxide (superoxyl)is used along with heat for bleaching.

• It can damage tooth by causing irritation to cementum and periodontal ligament cervical resorption.

Sodium perborate• Used as a mouthwash , bleaching agent and in dentrifices .• Can cause erythema of mucosa sloughing of tissues.• When inflammation is aggravated edema and ulceration

occurs.• Lesions healed spontaneously with treatment.

Carbamide peroxide• Used as a component in bleaching agent.• Causes varying degree of damage to teeth and surrounding

tissues if not used cautiously.

Phenol • Used as cavity sterilizing agent and

cauterizing agent .• Extremely caustic.• Can cause severe painful burns of oral

mucosa and skin that heals slowly.

Silver nitrate• Used as cavity sterilizing agent , topically as caries

preventive agent and as chemical cautery .• Injudicious or overzealous use causes painful burns of oral

mucous membrane.

Trichloroacetic acid• Used as a cauterizing agent.• Extremely caustic• Can cause serious injury to mucosa and skin

Volatile oils• Oil of cloves, oil of wintergreen and eucalyptus oil.• Cause mild burns of mucous membrane.

Case reportIrrational use of Eucalyptus oil in dentistry: a case

reportRS Shishir, C Renita, AR Kumuda, BG Subhas

Bangladesh Journal of Medical Science Vol.10 No.2 Apr’11

The floor of the ulcer was covered with necrotic slough and the surrounding area appeared to be oedematous

deep cavitation was observed in distal aspect of the crown of 17

NON ALLERGIC REACTION TO DRUGS AND CHEMICALS USED SYSTEMICALLY

• The systemic administration of various drugs and chemicals frequently evokes an oral reaction which is not on the basis of an allergy or sensitivity.

• Part of general epidermal reaction .

Arsenic • Used both in organic and inorganic forms.• Can cause acute or chronic poisoning• Occupational hazard

Dermatological alterations :• Diffuse macular pigmentation• Palmar and plantar hyperkeratosis• Premalignant lesion - arsenical keratosis that can transform

to basal cell carcinoma and cutaneous squamous cell carcinoma

Arsenic keratosis on the palms of a patient who ingested arsenic from

contaminated well over a prolonged period

ORAL MANIFESTATIONS

• Intense inflammation of oral mucosa• Severe gingivitis• Tissue becomes painful• Local contact with arsenic trioxide

produces ulceration• Systemic poisoning can cause excessive

salivation

Bisphosphonate • Potent antiresorptive agent.• Management of benign and malignant diseases involving

bone resorption.

• Causes osteoradionecrosis • Eg : pamidronate and zolendronate• Osteoradionecrosis results from inability of

hypodynamic and hypovascular bone to meet an increased demand for repair and remodeling .

Other terms

biphosphonate osteochemonecrosis bi – phossy jaw

Treatment and prognosis :• No response to surgical intervention , antibiotic therapy,

hyperbaric oxygen.• Current approach is sequential removal of sequestrum with

minimal epithelial manipulation.• Topical and systemic antibiotics

Bismuth • Treatment of syphilis .• Used for certain dermatological conditions. ORAL MANIFESTATIONS• “BISMUTH LINE”: a thin blue black line in the

marginal gingiva sometimes confined to gingival papillae.

• Also seen in buccal mucosa and ventral surface of tongue

• Pigmentation shows precipitated granules of bismuth sulfide produced by action of hydrogen sulfide on bismuth.

• Hydrogen sulfide is produced by bacterial degradation of organic material or food debris.

• Burning sensation• Metallic taste

HISTOLOGIC FEATURES• Granules of sulfide seen as small irregular

black collections of pigment .• Perivascular in location or diffuse without

any apparent arrangement.• Material may be present in endothelial

cells or mononuclear phagocytes in tissues but usually in intermediate cells

TREATMENT AND PROGNOSIS• No specific treatment• Prevented by good oral hygiene during

therapy.• Good prognosis• Line will disappear if use of bismuth

compound is discontinued

Gold • Used selectively in rheumatoid arthritis.

Complications:• Dermatitis often preceded by pruritis.• Generalized exfoliative dermatitis leading to alopecia.• Loss of nails• Slate blue discolouration of sun exposed skin - chrysiasis

ORAL MANIFESTATIONS • Metallic taste• Severe oral mucositis affecting buccal mucosa ,lateral

border of tongue, palate and pharynx.

Dilantin Sodium

• Anticonvulsant drug

• Fiberous hyperplasia of the gingiva• Hyperplasia is seen only in less than half of the cases but if

good oral hygiene is maintained this can reduce to 10%.

ORAL MANIFESTATIONS• Gingival hyperplasia can occur early in 2 weeks• First change is painless increase in the size of

gingiva starting with one or two interdental papillae .

• Increased stippling• Finally a cauliflower , warty or pebbled surface

• As enlargement increases the gingival tissue becomes lobulated and clefts remains between each enlarged gingiva.

• On palpation tissue is dense , resilient and insensitive .• Little tendancy to bleeding.• Hyperplasia is usually confined to gingival tissues around

the teeth. • In dentulous cases with few edentulous areas the gingival

tissues around teeth shows extreme hyperplasia while edentulous area appears to be normal .

HISTOLOGIC FEATURES• Thick stratified squamous epithelium with a thin keratin

layer.• Extremely long and thin rete ridges – “test tube pegs”.• CT : bundles of collagen fibers intersepted with fiberoblast

and fiberocyte.• Vascularity not prominent.• Plasma cells and leukocytes seen if chronic inflammation

present.

TREATMENT AND PROGNOSIS• Hyperplasia when interfer with function,

surgical excision is done.• Hyperplasia can recur often.• Discontinuing the drug will relieve

hyperplasia.

Cyclosporin • Immunosuppressant drug used in organ transplant patients• Generalized hyperplasia and perioral hyperesthesia.

Nifedipine• Calcium channel blocker• Interfere with production of collagenase by

altering Ca influx into fiberoblast accumulation of collagen without degrading.

• Gingival enlargement starts 1 – 3 months of taking drugs.

• Gingiva is firm and nodular .

Lead • Lead poisoning – “plumbism” • Caused by accidental exposure of either acute or chronic

nature.

Clinical features

ORAL MANIFESTATIONS

• Gray or bluish black line of sulfide pigmentation in gingiva – “ lead line” or “burtons line”.

• Found in other areas of oral cavity.• Diffuse in nature.• Excessive salivation • Metallic taste

TREATMENT AND PROGNOSIS

• Treatment of oral lesions is secondary to systemic treament.

• Prognosis depends on systemic condition of patient.

Mercury

• Acute or chronic• Chronic mercuialism occurs after prolonged

contact with mercurial compounds.CLINICAL FEATURES:

• Gastric disturbances, diarrhea, excitability, insomnia, headache and mental depression.

• Tremors of fingers and limbs as well as of lips and tongue.

• Desquamative dermatitis• Nephritis

ORAL MANIFESTATIONS:

• Increased salivary flow – ptyalism• Metallic taste• Salivary glands become swollen • Tongue is painful and enlarged• Hyperemia and swelling of gingiva• Ulceration on gingiva , palate and tongue• Pigmentation of gingiva• Loosening of teeth leading to exfoliation.

TREATMENT AND PROGNOSIS:• Treatment of oral lesions is secondary to

the treatment of poisoning .• Prognosis is good although there is

periodontal destruction and loss of teeth.

Acrodynia (Pink disease / Swift’s disease)

• Uncommon disease of unknown etiology .• Striking cutaneous manifestations• Cause of disease is either mercury

poisoning or an idiosyncrasy to the metal.• Source of mercury is teething powder

ammoniated mercury ointment , calomel lotion or bichloride of mercury disinfectant.

CLINICAL FEATURES:

• Most frequently affects young infants before the age of two although affected upto age of five or six.

• Skin of feet, hand , nose, ears and cheeks becomes red or pink and has cold, clammy feeling.

• Raw beef appearance.• Skin over affected areas peels off.

• Maculopapular rashes which is pruritic.• Severe sweating• Extreme irritability• Photophobia with lacrimation• Muscular weakness , tachycardia ,

hypertension , insominia, GIT upset.• Children frequently tear their hair out in

patches.

ORAL MANIFESTATIONS

• Profuse salivation with dribbling• Gingiva becomes sensitive and or painful

and shows ulcerations• Bruxism • Loosening and premature shedding of

teeth.• Difficult mastication

TREATMENT:• Identify and remove the source of

mercury.• Immediate chelation therapy• Dimercaprol, D- pencillamine • Administer BAL (British anti lewisite)• Heavy or prolonged exposure can cause

irreversible damage.

Silver (Argyria ,Argyrosis)

• Accumulates as subepithelial deposits in skin.

• Deposits results as a diffuse grayish black pigmentation occuring in sun exposed areas.

• Sclera or nails are also pigmented.

Occupational hazardTherapeutic use of silver arsphenamine or silver nitrate.

• Earliest sign - appearance of slate – blue silver lines along the margins due to deposition of metallic silver and silver sulfide pigments.

• Diffuse bluish colour of mucosa

Amalgam tattoo • Accidental implantation of silver

containing compounds into the oral mucosa that results in permanent grayish – black pigmentation.

• Modes of entry:

CLINICAL FEATURES:• Appears as macules or slightly raised lesions.• Borders can be well defined, irregular or diffuse.• Common locations are gingiva, buccal mucosa, alveolar

mucosa

HISTOLOGIC FEATURES

• Chronic inflammatory response manifesting as foreign body granuloma with either foreign body giant cells or langhans giant cells.

• Amalgam fragments appear as black or olive brown granules .

• Granules arranged in linear fashion along with collagen fibers and around blood vessels.

Tetracycline• Discolouration of either deciduous or

permanent teeth occur during therapeutic regimens.

• Selective affinity for deposition in bone and tooth surface by formation of complex with Ca ions on surface of microcrystals of hydroxyapatite.

• Grossman and associates – use of oxytetracycline or doxycycline diminish tooth discolouration if tetracycline therapy is indicated in pregnant female or during first six to seven years of life

Tetracycline hydrochloride burn

• The portion of the tooth stained by tetracycline is determined by the stage of tooth development at the time of drug administration.

• It can cross placental barrier and affect teeth developing antepartum.

• Semisynthetic derivative of tetracycline , minocycline hydrochloride can cause significant discolouration in tooth that are fully developed .

• Drug bind to collagenous tissue like dentin, pulp, bone and dermis and gets oxidised discolouration .

• The stained pulp is seen through translucent dentin and enamel.

CLINICAL FEATURES:• Teeth exhibits yellowish or brownish gray diffuse bands of

discolouration .• More pronounced at the time of eruption.• On light exposure turns more brownish.• Chlorotetracycline brownish gray colour• Oxytetracycline and tetracyline yellowish colour.

a. Outer view showing grey discoloration of crown and yellow discoloration of upper part of the root.

b. Cut surface showing the band-like appearance of the discoloration indicating several administrations of the drug. 

 c. Ground section also illustrating the band-like discolorations in the enamel and a tiny yellow line in the dentin.

• Under ultraviolet light tetracycline fluoresece bright yellow but gradually diminishes.

• Teeth viewed under microscope in uv light shows narrow bands or rings seen coinciding with part of tooth development at the time of administration of drug .

Cancer chemotherapeutic drugs

• Treatment of certain malignant neoplastic disease.

• Non neoplastic cells can also be affected.• CANCER CHEMOTHERAPEUTIC AGENTS• Alkylating agents• Antimetabollites• Antitumor antibiotics• Plant alkaloids• Nitrosurease

CLINICAL FEATURES:• Alopecia due to arrest of mitosis of germinating

hair roots.• Stomatitis• Radiation sensitization – reactivation of radiation

reaction within the fields of radiation following administration of antineoplastic drugs.

ORAL MANIFESTATIONS• Mucosal irritation and ulceration which is diffuse and

multiple.• Seen in lips , tongue and buccal mucosa.• Hemorrhage • Presence of any one of the infection commonly herpes

simplex , candidal infections.• Hyperpigmentation

Oral manifestations of occupational diseases according to etiologic agent

Physical state Specific factor

Occupation Possible oral manifestations

Solid

Tar Fisherman, asphalt and coal tar workers, pavers, pitch roofers , wood preservers

StomatitisCarcinoma of lip and mucosa

Ray

Radium , x - ray

technicians, watch dial painters , research men

Gingivitis, periodontitis , osteomyelitis and necrosis,xerostomia, osteosclerosis

Actinic Sailors and fishermen

Carcinoma of lips

InorganicArsenic Chemical workers,

metal refinersNecrosis of bone

Bismuth Bismuth handlers, dusting powder markers

Blue pigmentation of gingiva and oral mucosa , gingivostomatitis

Chromium Aniline compound, photographic and steel workers

Necrosis of bone, ulceration of oral mucosa

Dust Fluorine Cryolite workers osteosclerosislead Electrotypers,

insecticide and storage battery makers

Blue – black pigmentation of gingiva, gingivostomatitis

Mercury Battery and paint makers, dentist, mercury salt workers

Gingivostomatitis osteomyelitis pytalism

Phosphorus Match factory workers,fertilizer makers

Gingivostomatitis ulceration of oral tissues osteomyelitis

Organicsugar Refiners , bakers ,

candy makerscaries

Hot food (coffee,tea, soup)

Tasters Stomatitis leukoplakia

Aniline Painters, aniline, coal tar and explosive workers

Blue colouration of lips and gingiva

Liquidbenzene Dry cleaners,

vulcanizers, smokeless powder makers

Hemorrhage from gingivaBlue colouration of lips

cresol Coal tar, rubber tar , distillery and surgical dressing

stomatitis

Wine and liquor tasters Anesthesia and paresthesia of tongue

AcidsH2SO4, HNO3, Acid and catridge

dripers, petroleum refiners, explosives and gun cotton workers

BleedingStomatitis decalcification of enamel and dentin

GasHCl , HFAmyl acetate Alcohol,

explosive, shoe factory workers

Stomatitis

Acrolein Bone grinders, lard, soap makers

Stomatitis

SO2, NH3 , BR , Cl2

Acetylene, dye, photographic film, laundry workers.

Stomatitis

CO ,CO2 Miners, smelters, gasoline motor workers

Coloration of lips ( cherry red, blue)

REFERENCES• Shafer’s Textbook of oral pathology- 7th edition.• Textbook of oral and maxillofacial pathology –

Neville ,Damm, Allen,Bouquot• Burkets Oral medicine. – 11th edition• Text book of oral medicine – Ghoms• Irrational use of Eucalyptus oil in dentistry: a case report RS

Shishir, C Renita, AR Kumuda, BG Subhas Bangladesh Journal of Medical Science Vol.10 No.2 Apr’11

• Review: the use of sodium hypochlorite in endodontics — potential complications and their management