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.
4. 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
5. Types of Enamel caries:-
1. Smooth surface caries
2. Pit & Fissure caries
Early cavity formation
6. 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
7. 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
8. 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
9. 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
10. 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
11. 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
12. 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
13. 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
14. Osteomyelitis
• Inflammation of bone and bone marrow.
• Secondary to the inflammation of the soft tissue components of the bone.
Acute Osteomyelitis
15. Periosteitis
• Focal gross thickening of periosteum of bone with peripheral reactive bone formation.
• Results from mild irritation or infection
Periapical abscess Periapical
Granuloma
16. 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.
17. 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