Dental caries is the most prevalent chronic disease
Classification
- Histopathologically-Enamal caries,Dentine caries,Cementum caries
- Clinically(according to location)-Pit and fissure,Smooth surface
- Clinial cause-Chronic,Acute
Smooth surface caries
- On approximal surface
- Early white spot lesion
- Then brown/black-due to pigmentation by dietary or bacterial products
- In SEM –cocci attached,small rounded dipressions and rough areas seen.
- Early lesions are conical in shape and 4 zones are seen.
- Translucent zone-due to demineralization
- Dark zone-due to remineralization
- Body of the lesion-due to greatest demineralization(subsurface decalcification)
- Surface zone-greater resistant to cariesactivity,30-40 micrometeres.relatively unaffected.
- Body-with water immersion with polarized microscope+bifringence-yellowcolour
- Surface zone-By a microradiograph
- Dark zone-with quinolne
Pit and fissure caries
- Cone shaped
- Base towards EDJ-because of this shape more dentinal tubules involved
- Occlusal surface caries(ground sec.-cz if demineralised 95% of inorganic part looses)
- Pit and fissure caries
- With steep walls and narrow bases easily cause caries
- In microradiograph lesion appear as radiolucent dark demineralised area
- In tooth-caries fissure is dark brown
- No loss of enamel surface continuity
- Morphology is intact
- Lesion can spread along DEJ
- Form cone shaped lesion in dentine
- With only small penetration of enamel is a common finding
Caries of dentine
- Caries of dentine(decalcified sec.-cz less inorganic part than enamel-so retain considerable amount after decalcification)
- After cavity forms in enamel carious process spreads along DEJ-rapid involvement of dentinal tubules-form- cone shaped lesion,apex towards pulp
- Dentine caries can occur as a result of exposure of dentine due to abrasion
- In ground section dentine show,
- pigmented zone
- Dark zone
- transparent zone-highly mineralized(radioopaque)deposition of ca2+salts in dentinal tubules to seal against bacteria.
- Decalcified section
- small amount on the surface of lesion
- involve deeper dentinal tubules-darkly stained
- initial decalcification of tubular walls-distention of tubules by placing microbes-focal areas of liquifraction necrosis form within dentinal tubules.those foci are filled with necrotic debris andd numerous microbes
- toward surface complete loss of dentine structure
- clefts parallel to contour lines of dentine(filled with necrotic debris + microbes)
Root caries
- After gingival recession
- Cementum is attached,readily decalcified
- Cementum softens beneth plaque over a wide area-cause soucer shaped cavity
- Underline dentine soon involved
- Cemnentum invade along sharpy’s fibers
- Infection spread belween lamelle along incremental lines-dentine split up and progressively destroy by demineralization and liquiofraction
Pulpitis
- Open –chronic hyperplastic pulpitis
- Closed –acute closed,chronic closed
Acute closed pulpitis
- Initial hyperemia limited to area underneath irritant.infiltration by inflammatory cells-destruction of odontoblasts & adjacent mesenchyme followed.
- Limited area of necrosis-form minute abscess localized by granulation tissue-inflammation spread until all pulp-entire pulp has been destroyed and replaced by inflammatory cells and dilated vessels
Chronic closed pulpitis
- Mononuclear cells infiltration
- More vigorus connective tissue reaction
- Small area of pulpal necrosis and pus formation is localized by well defined wall of granulation tissue-minute abscess form
- Reminder of pulp may appear normal
- Rarely inflammation is well localized beneth the exposure by-partial calcific barriersr benerth lesion(in X-ray dentine bridges) or reactionary dentine.
- Such changes likely to follow up pulp capping
- Calcific barriers usually poor-inflammation spread beneth but in successful reactionary entine-complete barrier-preserve rest of pulp.
- Open pulpitis
- Occationally pulp servives but chronically inflamed beneth wide exposure despite wide infection believed to be assiociate dwith open apices which allow adequate bld supply
Chronic Hyperplastic pulpitis(pulp polyp)
- Rarely despite of exposure and heavy infection.pulp not merely survive but proliferate through opening
- Clinically dusky red/pinkish soft nodule protruding in to cavity
- May tender/bleed on probing
- Histologically-odontoblasts survive,pulp replaced by granulation tissue,as mass grow out to cavity-it can become epithelialized and coverd by layer of well formed SSE
- Protects mass
- Subside
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