Dental caries and diseases



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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