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Sequelae of dental caries

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Sequelae of dental caries
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Sequelae of dental caries

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CONTENTS:-
1. Enamel caries
2. Dentinal caries
3. Pulpitis
4. Apical Periodontitis
5. Periapical abscess
6. Periapical Granuloma
7. Osteomyelitis
8. Periosteitis
9. Cellulitis
10. Abscess

CONTENTS:-
1. Enamel caries
2. Dentinal caries
3. Pulpitis
4. Apical Periodontitis
5. Periapical abscess
6. Periapical Granuloma
7. Osteomyelitis
8. Periosteitis
9. Cellulitis
10. Abscess

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Sequelae of dental caries

  1. 1. Sequelae of Dental Caries
  2. 2. DentalCaries • Dental Caries is defined as a multifactorial, transmissible, infectious oral disease caused primarily by the complex interaction of cariogenic oral flora (biofilm) with fermentable dietary carbohydrates on the tooth surface over time.
  3. 3. Enamel caries • Initiation- by formation of dental plaque. • Stages of enamel caries:- 1. Early( Sub-microscopic lesion) 2. Phase of non-bacterial crystal destruction 3. Cavity formation 4. Bacterial invasion of enamel 5. Undermining of enamel from below after spread into dentine Early Enamel Caries
  4. 4. Types of Enamel caries:- 1. Smooth surface caries 2. Pit & Fissure caries Early cavity formation
  5. 5. Zones of enamel caries Zones Key features 1. Translucent zone Present at advancing front of lesion. 1% mineral loss 2. Dark zone Superficial to Translucent zone Formed as a result of demineralization 2-4% mineral loss 3. Body of the lesion Superficial to Dark zone Area of greatest demineralization (5-25% mineral loss) 4. Surface zone Relatively unaffected Greater resistance of surface layer maybe due to greater degree of mineralization or greater concentration of fluoride on the surface of enamel 1% mineral loss
  6. 6. Dentinal caries Begins from DEJ and rapid involvement of great no. of dentinal tubules each of which acts as a tract leading to dentinal pulp along with micro-organisms. Events in Dentinal caries:- 1. Non-bacterial, Pre-cavitation, Acid softening of the matrix 2. Widening of tubules by demineralization 3. Migration of pioneer bacteria along the tubules 4. Distortion of tubules by expanding masses of bacteria 5. Breakdown of intervening matrix forming liquefaction foci 6. Progressive disintegration of remaining matrix tissue Early Dentinal Caries
  7. 7. Zones of dentinal caries Zones Key features 1. Zone of Fatty degeneration of Tomes’ fibres Deposition of fat globules Significance-Fat contributes to impermeability. Predisposing factor for dentinal sclerosis 2. Zone of Dentinal sclerosis Deposition of Calcium salts in dentinal tubules Above the fatty degeneration Appears white in transmitted light 3. Zone of Decalcified Dentin Above the dentinal sclerosis Occurs in advance of bacterial invasion of Dentinal tubule 4. Zone of Bacterial invasion Acidogenic organisms-more in early caries Proteolytic organism-predominant in deeper layers 5. Zone of decomposed dentin Necrotic mass of dentin of leathery consistency Bacteria in Dentinal tubules
  8. 8. Reactionary changes in dentin Response Key facts 1. Tubular Sclerosis Peritubular dentin reduces the size of dentinal tubules, preventing bacterial penetration and generating a more heavily mineralized dentin 2. Regular reactionary dentin Forms at pulp dentin and interface and retains tubular structure of dentin 3. Irregular reactionary dentin Forms in response to moderate or severe insult by caries and ranges from dentin with irregular tubules to a disorganized bone like mineralized tissue (eburnoid) 4. Dead tracts If peritubular dentin formation was extensive before odontoblast death, the dead tracts may be sclerotic and inhibit advance of caries. If not , it may allow more rapid progress. Dead tracts
  9. 9. Pulpitis • Inflammation of pulp, most common cause of dental pain and loss of teeth in younger persons. • Caused by infection or irritation of pulp, most commonly by dental caries. • Pulpal pain is poorly localized. Inflammatory reactions of pulp
  10. 10. Focal Reversible Pulpitis Acute Pulpitis Chronic Pulpitis Early mild transient pulpitis Extensive acute inflammation of the dental pulp Arises on occasion through quiescence of a previous acute pulpitis, but more frequently as the chronic type of disease from the onset. Localized chiefly to the pulpal ends of irritated dentinal tubules Immediate sequela of focal reversible pulpitis The signs and symptoms are considerably milder than those in the acute form of the disease. Application of ice or cold fluids to the tooth results in pain, but this disappears upon removal of the thermal stimuli or restoration of the normal temperature Severe pain is elicited by thermal changes, particularly when taking ice or cold drinks Mild, dull aching pain, which is more often intermittent than continuous
  11. 11. Periapical Periodontitis • Periapical Inflammation is usually due to spread of infection following death of pulp. • Spread of process can be only in one direction through the tract of root canal and into periapical region. Acute Apical Periodontitis Chronic Apical Periodontitis Acute inflammatory reaction Chronic inflammatory reaction Packing of tissue with neutrophils Characterized by lymphocytes, macrophages and plasma cells The immediately adjacent lamina dura becomes resorbed and abscess cavity may form Results in periapical granuloma(localized mass of chronic granulation tissue formed in response to infection, one of the most common sequalae o pulpitis) Acute periodontitis
  12. 12. Periapical abscess Periapical Cyst (Radicular cyst, periapical cyst, root end cyst) • An acute or chronic suppurative process of the dental periapical region. • It may develop either from acute periapical periodontitis or more commonly from a periapical granuloma • Most common odontogenic cyst encountered in a dental clinic • Sequela of the periapical granuloma originating as a result of bacterial infection and necrosis of the dental pulp, nearly always following carious involvement of the tooth • Consists of a pathologic cavity that is lined by epithelium and is often fluid- filled, the epithelial lining is derived from the epithelial rests of Malassez. Periapical abscess Periapical Cyst
  13. 13. Osteomyelitis • Inflammation of bone and bone marrow. • Secondary to the inflammation of the soft tissue components of the bone. Acute Osteomyelitis
  14. 14. Periosteitis • Focal gross thickening of periosteum of bone with peripheral reactive bone formation. • Results from mild irritation or infection Periapical abscess Periapical Granuloma
  15. 15. Cellulitis • Diffuse inflammation of soft tissue. • Tends to spread through tissue spaces and facial planes. • Caused by organisms producing hyaluronidase and fibrinolysins like Streptococci. • Cellulitis of face and neck most commonly results from dental infection either as sequaele an apical abscess or osteomyelitis or following periodontal infection. • Infection frequently tends to become localized and results in facial abscess formation.
  16. 16. References 1. Rajendran, R et. al. 2012 Shafer’s Textbook of Oral Pathology 7th ed. New Delhi: Reed Elsevier India Ltd. 2. Cawson, RA et. al. 2008 Cawson’s Essential of Oral Pathology and Oral Medicine 8th ed. Edinburgh: Churchill Livingstone, Elsevier

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