PULP AND PERIAPICAL DISEASES
Submitted by Hina bhatia (521)
Contents Introduction
Pathobiology of periapex
Acute and chronic
Inflammation Vs Immunology
Classifications of pulpoperipaical pathoses
Clinical signs and symptoms
Healing mechanisms
Differential diagnosis
Ludwig’s angina , Cellulitis
Osteomyelitis , Periapical actinomycosis
Foreign body reactions
Conclusion
Contents
Introduction
Apical Pulp tissue less cellular more fibrous whitish in colour large conc of glycogen →anaerobic environment higher conc of sulfated glycosaminoglycans fibrous tissue ~ PDL
Apical dentin
Less tubular , more amorphous , irregular Sclerotic dentin increases with age Odontoblasts of the pulp are absent/flattened/cuboidal Optically transparent Less permeable
Pathways of infection
Opening in dental hard tissue wall
caries
clinical procedures
trauma induced fractures
microcracks
Bacteria from the gingival sulcus/ P.pocket
Endodontic reinfection
Anachoresis
HOST ALLERGEN
HOST ALLERGEN
Inflammation
Phagocyte system
Lymphatic system / T & B cells
Immune/complement system
Neural mechanism
chemotaxis
Endotoxins
Exotoxins
Enzymes
PUS / tissue damage
Stimulation of clast cells
Exudate (inflam edema)- pain
Acute (exudative)
Chronic (proliferative)
Classification by Franklin.s.weinePerapical pathosis of pulpal origin:
1.Painful pulpoperiapical pathoses
a. Incipient acute apical periodontitis
b. Advanced ’’ ’’ ’’
(i) acute periapical abscess
(ii) recrudescent / phoenix abscess
(iii) subacute peiapical abscess
2. Non painful periapical pathoses
a. Pulpopariapical osteosclerosis(condensing osteitis)
b. Incipient chronic apical periodontitis
c. Advanced ’’ ’’ ’’
(i) periapical granuloma
(ii) chronic periapical abscess
(iii) periapical cyst
Hirsch et al (1979) – surgically excised pulpoperiaical lesions
I. Periapical granuloma
II. Epithelial granuloma III. Radicular cyst with modern (chronic inflammation) IV. Radicular cyst with strong ( acute or subacute )
inflammation and epithelial necrosis V. Radicular cyst without inflammation (chronic or acute)
WHO(1995) CLASSIFICATION
Code number
CATEGORY
K04.4K04.5K04.6K04.60K04.61K04.62K04.63
K04.7
K04.8K04.80K04.81K04.82
Acute apical periodontitisChronic ’’ ’’ (periapicalgranuloma)Periapical abscess with sinusPeriapical abscess wth sinus to maxillary antrum ’’ ’’ ’’ to nasal cavity ’’ ’’ ’’ to oral cavity ’’ ’’ ’’ to skin
Periapical abscess without sinus
Radicular cyst(apical periodontal cyst, periapical cyst)Apical and lateral cystResidual cystInflammatory paradental cyst
Classification by Franklin.s.weinePerapical pathosis of pulpal origin:
1.Painful pulpoperiapical pathoses
a. Incipient acute apical periodontitis
b. Advanced ’’ ’’ ’’
(i) acute periapical abscess
(ii) recrudescent / phoenix abscess
(iii) subacute peiapical abscess
Painful pulpoperiapical pathoses
Early apical changeHealthy tooth
a. Incipient acute apical periodontitis
b. Advanced ’’ ’’ ’’
(i) acute periapical abscess
(ii) recrudescent / phoenix abscess
(iii) subacute periapical abscess
Abscess
Healthy tooth Early apical change
Abscess
Tooth becomes extremely tender
Vascular congestion
Regional anoxia
Cell breakdown(autolysis)
Neutrophils increase in number
Release osteolytic fragments
Pus core
Gumboil (parulis)
Breach the cortical bone (sinus opening)
“STOMA”
ACUTE
CHRONIC
parulis / gum boil
(acute/chronic)
stoma
(chronic)
Apical periodontitis
A draining sinus is evident on the labial aspect of the upper left lateral incisor. (A) A gutta percha (GP) point has been placed into the draining sinus in order
to trace its origin. (B) The radiograph taken with the GP point in the sinus shows that it tracks
from the periapical region of the upper left central incisor, which has a chronic apical abscess. The lateral incisor has chronic apical periodontitis but this tooth is not associated with the draining sinus.
Toxic components from pulp irritants / necrosis Occlusal disharmony – persistant periapical tissue
compression Related to root canal procedures
ETIOLOGY of Painful pulpoperiapical pathoses
Etiologic factors related to rot canal procedures
Note the space between the gutta-percha filling and the root canal walls clearly visible
JOSE´ F. SIQUEIRA
Common problems that may cause post-treatment disease
at least seven problems
1. Inadequate RCT without iatrogenically altered root canal morphology
2. Inadequate RCT with iatrogenically altered root canal morphology
3. Infection remaining in inaccessible areas in the apical portion of the
root
4. Extraradicular infection including extruded dentin debris with bacteria
present in
the dentinal tubules
5. True radicular cysts and tumors
6. Foreign body reaction to cholesterol crystals or extruded materials
such as talc-
contaminated guttapercha, particles of paper points, and particles of
sealer
7. Vertical root fractures
The quality of the root canal obturation as visualized on a buccal–lingual radiograph is in no way indicative that the root canal was well sealed, particularly when canals are oval or ribbon-shaped in transverse section. Note the discrepancy of the image taken in abuccal–lingual direction as compared to that taken in a mesio-distal direction.
Endodontic Topics 2005, 10, 123–147
Diagnosis
Slight tenderness to intense continuous throbbing pain
Sense of fullness Readily localised – tenderness on percussion Palpable fluctuant swelling Vitality test (if viable Cfibers ) Radiographs
2 . Non-Painful pulpoperiapical pathoses
a. Pulpopariapical osteosclerosis(condensing osteitis)
b. Incipient chronic apical periodontitis
c. Advanced ’’ ’’ ’’
(i) periapical granuloma
(ii) chronic periapical abscess
(iii) periapical cyst
2 . Non-Painful pulpoperiapical pathoses
a. Pulpopariapical osteosclerosis(condensing osteitis)
b. Incipient chronic apical periodontitis
c. Advanced ’’ ’’ ’’
(i) periapical granuloma
(ii) chronic periapical abscess
(iii) periapical cyst
Pulpoperiapical osteosclerosis (Condensing osteitis)
Occur most frequently in the mandible, around teeth with a periapical granuloma or radicular cyst, RCT,or restorations.
exudate from the pulp (low toxicity and long standing) the resulting mild irritation
circumscribed proliferation of the periapical bone.
“condensing osteitis or focal sclerosing osteomyelitis”
Incipient Chronic apical periodontitis Initially chronic periapical connective response to pulpal
irritants characterized by :
slightly widened apical periodontal space (containing dilated blood
vessels, a mild inflammatory exudate)
a dense accumulation of chronic inflammatory cells(plasma cells and
lymphocytes)
If the pulpal contaminants are not removed the response will intensify to one of the acute or chronic forms
a. Pulpopariapical osteosclerosis(condensing osteitis)
b. Incipient chronic apical periodontitis
c. Advanced ’’ ’’ ’’
(i) periapical granuloma
(ii) chronic periapical abscess
(iii) periapical cyst
Periapical granuloma
This is advanced form of chronic apical periodontitis; characterized by growth of granulation tissue and the presence of chronic inflammatory cells (granulomatous) in response to continued pulpal irritation.
Zones of periapical granuloma
Exudative
Granulomatous
Granulofibrotic
Fibrotic granulomas O3 OR,Endo 1996:81:93-102
Periapical cyst
“A periapical cyst is chronic inflammatory response of the periapex that develops from chronic lesions with preexisting granulomatous tissue.”
characterized by:
Central fluid filled epithelium lined cavity surrounded by
granulomatous tissue and peripheral fibrous encapsulation.
Periapical / Radicular cyst Direct sequel to chronic AP Incidence: 6-55% Two types : true and pocket Typical radiographic appearance-round/pear shaped radiolucent unilocular lesion less than 1cm in diameter Process of formation
Dormant cell rests of malassez proliferate
Epithelium lined cavity comes into existence
Cyst grows in size
Do periapical cysts heal ?
Differential diagnosis
Granuloma vs Cyst vs Abscess
Chronic
non painful
Definite outline
Smaller in size
Chronic
non painful
Sclerotic opaque border
Bigger in size
Contain more protein and albumins
Acute /Chronic
Pain/non painful
Swelling/parulis
Sinus opening(chronic)
Diffuse outline
Mobility of the tooth
historyConformative histology
Condensing osteitis
Hypercementosis …. Vital , lying within intact lamina dura
and PDL space
Periapical cemental dysplasia ….lesion is seperated from
the surrounding normal bone by a
radioluscent border , vital
Osteosclerosis …. idiopathic
Odontogenic pain
Dentinal hypersensitivity
Reversible pulpitis
Irreversible pulpitis
Acute apical periodontitis
Acute apical abscess
Non odontogenic pain –musculoskeletal Myofacial pain TMD bruxism
Non odontogenic pain– neuropathic Trigeminal neuralgia Atypical odontalgia Glossopharyng neuralgia
Non odontogenic pain– neurovascular migraine cluster headache
Non odontogenic pain – inflammatory allergic rhinitis bacterial sinusitis
Non odontogenic pain – systemic disorders Cardiac pain Herpes zoster Sickle cell anaemia Neoplastic disease
Ludwig’s angina
“potentially life-threatening, rapidly expanding, diffuse inflammation of the submandibular and sublingual spaces that occurs most often in young adults with dental infections.”
Symptoms: severe neck pain Swelling Fever Malaise Dysphagia
Stridor suggests an impending airway crisis. Causative bacteria include many gram-negative and anaerobic organisms, streptococci and staphylococci
Ludwig’s angina
The submandibular space is composed of two spaces separated anteriorly by the mylohyoid muscle: the sublingual space, which is superior, and the submaxillary space, which is inferior. The spread of infection is halted anteriorly by the mandible and inferiorly by the mylohyoid muscle. The infectious process expands superiorly and posteriorly, elevating the floor of the mouth and the tongue. The hyoid bone limits the process inferiorly, and swelling spreads to the anterior aspect of the neck, causing distortion and a "bull neck" appearance. This then evolves to an infectious compartment syndrome of the submandibular and sublingual spaces.
Cellulitis (Phlegmon)
Cellulitis is a diffuse inflammation of the soft tissues which is not circumscribed or confined to one area,but which,in contradistinction to the abscess,tends to spread through tissue spaces along facial planes.
Cellulitis –etiology (of face and neck)
Dental infection as a sequelae of an abscess or osteomyelitis,or following periodontal infection.
Pericoronitis (operculitis)
Infection following tooth extraction ( injection either thro an infected needle or infected area)
Cellulitis -pathogenesis
Microorganisms
Hyaluronidase / fibrinolysins
Breakdown or dissolve intercellular cement substance
(hyaluronic acid and fibrin)
Streptococci are particularly potent producers of hyaluronidase
Staphylococci – less potent – also pathogenic – freq give rise to cellulitis
Cellulitis – clinical features (of face and neck)
Painful swelling of the involved soft tissues Skin overlying is firm and brawny,inflamed,sometimes even
purplish (when spread is in deeper planes –normal) Moderatily ill-elevated temperature Leukocytosis Regional lymphadenitis
Infections arising in the maxilla – perforate the outer cortical layer of bone above buccinator attachment –swelling of upper half of face
In mandible –below buccinatorattachment – lower half of faceTreatment – analgesics + antibiotics + removal of cause
Osteomyelitis If the periapical infection and inflammation extend through the marrow spaces of the jaw, the result is osteomyelitis.
Odontogenic infection
Infection thro PDL space
Extraction wound
Trauma-fracture
Metastasis from remote area
of infection In this case, you can identify the offending tooth causing the diffuse and irregular bone
destruction
Osteomyelitis – predisposing conditions
Malnutrition Diabetes h/o Alchoholism Leukemia Various anaemias Conditions that are characterized by the formation of avascular
bone that precludes an effective defensive response • Osteopetrosis
• Paget’s disease
• Florid osseous dysplasia
• Post-irradiation states
• Flourosis
Classification - Osteomyelitis
Suppurative
> acute suppurative
> chronic suppurative
* primary
* secondary
> infantile
Non suppurative
> diffuse sclerosing
> focal sclerosing
> proliferative periosteitis
> osteoradionecrosis
Acute osteomyelitis
Develops in a matter of days Does not show any early radiographic changes Most commonly arises from a periapical abscess Ther is no swelling or redness until later-penetrated cortex and
involved periosteum WBC count and Temp Reflex spasm of muscles attached to the involved area of bone Local signs and symptoms:
severe pain,soreness of the involved teeth,which are also loose,regional lymphadenopathy,parasthesia/anaesthesia of lip.
Radiograph – solitary/multiple small radioluscent areas
Trabeculae-decreased density,outlines become blurred or fuzzy.
Acute suppurative osteomyelitis
The clinical manifestations in this case are severe and debilitating.
Radiograph- Almost the entire body of the mandible is involved and shows diffuse mottled resorption. The decayed first molar is the guilty tooth.
Chronic osteomyelitis
is persistent abscess of bone charact by inflammatory processes , including necrosis of mineralised and marrow tissues,suppuration,resorption,sclerosis, and hyperplasia.
o Symptoms are milder,
o pain is less ,
o bone destruction is slower,
o sinus tracts develop intermittently and then cease draining and close.
Chronic sclerosing osteomyelitis
Here is an extensive chronic osteomyelitis characterized by bone formation only (chronic diffuse sclerosing osteomyelitis).
Garres osteomyelitis(COPP) Children/young adults Mandibular molars-inferior border of mandible Hard bony nontender swelling Size:1-2cm;cortex becomes 2-3cm thick R/f: onion skin appearance-alt radioluscent,opaque layers
Sequestrum In many cases of osteomyelitis there are bone sequestra. This necrotic piece of bone is being actively resorbed and is surrounded by intense inflammation and granulation tissue.
Treatment guideline for acute or chronic osteomyelitis
Disrupt the infectious foci. Debride any foreign bodies necrotic tissue, or sequestra. Culture and identify specific pathogens for eventual definitive antibiotic treatment. Drain and irrigate the region. Begin empiric antibiotics based on Gram stain. Stabilize calcified tissue regionally. Consider adjunctive treatments to enhance microvascular reperfusion (usually reserved for refractory forms only).
Trephination Decortication;sequestrectomy Vascular flaps Hyperbaric oxygen therapy
Reconstruction as necessary following resolution of the infection.
Extra radicular infections
Found in following situations:
1. Acute apical periodontitis lesions
2. Periapical actinomycosis
3. In ass with pieces of infected root dentin that may be displaced
into the periapex during RC instrumentation or have been cut
off from the rest of root by massive apical resorption
4. Infected periapical cysts, particularly in periapical pocket cysts
with cavities open to the root canal.
Actinomycosis is a chronic, granulomatous, infectious disease in humans and animals caused by the genera Actinomyces and Propionibacterium (McGhee et al.1982).
Etiological agent : Actinomyces bovis- first species to be identified(Harz 1879). in cattle - ‘lumpy jaw’ or ‘big head disease’ characterized by>extensive bone rarefaction, >swelling of the jaw, >suppuration > fistulation.
Actinomycosis
Causative agents nonacid fast, non-motile, Gram-positive ‘sulphur granules’ - yellow specks in exudates.a ‘starburst appearance’ ‘ray fungus’.
Actinomycosis
Human actinomycosis is clinically divided into Cervicofacial(60%) Thoracic(15%) Abdominal forms(20%) (Kapsimalis &Garrington 1968, Oppenheimer et al. 1978).
The most common species isolated from humans is A. israeliiwhich is followed by Propionibacterium propionicum (Buchanan & Pine 1962) (Wolff &
Israel 1891), Actinomyces naeslundii (Thompson & Lovestedt 1951),Actinomyces viscosus and Actinomyces odontolyticus in descending order (Batty 1958)
Foreign body reactions
Oral pulse granuloma Cellulose granuloma Gutta percha Other materials- amalgam,endo sealants, and calcium salts derived from periapically extruded
Ca(OH)2
CONCLUSION
It is essential that we understand the progressive nature of the periapical disease process as well as how and why the various stages occur so they can be diagnosed and managed appropriately.
Thank you
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