Dental caries

Definition

• Dental caries is a bacterial disease of the

calcified tissues of the teeth, characterized
by demineralization of the inorganic and
destruction of the organic substance of the
tooth.
 Etiology of dental caries:
• A) Risk factors:
1. Bacterial dental plaque.
2. Carbohydrates.
3. Susceptible tooth surface.
4. Time.
• B) Contributing factors:
1. Extrinsic factors.
2. Intrinsic factors.
 Contributing factors:
Intrinsic factors:
1. Tooth composition.
2. Tooth structure.
3. Tooth morphology.
4. Tooth position.
Extrinsic factors:
1. Saliva.
2. Diet.
3. Oral hygiene.
4. Immunity.
 Theories of dental caries

• Worm theory.
• Chemical theory.
• Enzymatic theory.
• Acidogenic (chemico-parasitic) theory.
• Proteolysis theory.
• Proteolysis-chelation theory.
Role of bacteria &
dental plaque
 Dental plaque

• It is a thin translucent biofilm consists of

complex microbial community, amorphous
matrix derived from bacterial products &
salivary mucins, desquamated epithelia,
leucocytes, & minerals.
Classification of dental plaque

• Supra-gingival & sub-gingival.

• Health-associated & disease-associated.

 Dental plaque formation:

• Acquired pellicle.
• Primary colonizers (first 24 hours), S.mutans.
• Secondary colonizers (7th day), cocci &
bacilli.
• Tertiary colonizers (14th day), anaerobic
filamentous bacteria.
 Role of dental plaque:

1. It produces acid, mainly lactic acid, by

fermentation of dietary sugars,.
2. Acid leads to drop in plaque pH by 2 units
within 10 minutes.
3. Critical pH (5.5) demineralization of enamel.
4. After 30-60 minutes the plaque pH slowly rises
to original value (by outward diffusion of acids
and sugars, inward diffusion of saliva buffer.
5. At neutral pH re-deposition of minerals on
enamel (F).
 The dental plaque lead to dental
caries when :
• Repeated demineralization of enamel with
out enough time for remineralization.

• Bulky dental plaque.

 Hypothesis of dental plaque

• Specific hypothesis.
• Non-specific hypothesis.
• Ecological hypothesis.
Microbiology of dental plaque
 Role of S.mutans:

1. Acidogenic (ferment sugar produce acid).

2. Aciduric ( survive & multiply in acidic
medium).
3. Produce extra-cellular polysaccharides
(mutan or dextran).
4. Production of intracellular polysaccharides.
5. Initiate dental caries.
6. Smooth surface caries.
Stript. mutans test
 Role of lactobacilli:

• acidogenic.
• Aciduric.
• Progression of caries .
• Fissure caries.
Lactobacilli count
 Role of actinomyces

• Acidogenic.
• Root caries.
 Role of veillonella:

• Supra-gingival plaque.
• Convert lactic acid into less cariogenic acids.
• Protective effect on dental caries.
 Role of carbohydrates:

• Epidemiological studies:
1. Westernization.
2. During World War 2.
3. Hopewood house.
• Experimental studies:
• Animal experiments (route, type).
• Human experiments.
 Factors affecting the
cariogenicity of carbohydrates
• Chemical composition.
• Physical form.
• Frequency of intake.
• Route of administration.
• Presence of other food constituents.
 Diet analysis & counseling

• Questionnaire, log book.

• Analysis of the diet.
• Give reasonable and attainable advice.
• Diet modification.
• Sugar substitutes.
 Clinical aspects of dental caries:
Classification of dental caries:

• According to the rate of progression:

1. Chronic caries.
2. Acute ( rampant caries).
3. Arrested caries.
• According to the site of attack:
1. Pits & fissures caries.
2. Smooth surface caries.
Clinical aspect of dental caries:
Histology of dental
caries
 Enamel caries:

• Early enamel caries shows four histological

zones:
1. Translucent zone (1%).
2. Dark zone (2-4%).
3. Body of the lesion (5-25%).
4. Surface zone.
• Late enamel caries:
• Lead to cavitation and loss of surface zone.
 Dentine caries:

• Early dentine caries: only acids and toxins pass

through the highly porous enamel to reach
dentine, it shows three zones:
1. Zone of demineralization.
2. Zone of sclerosis.
3. Zone of reparative dentine.
 Late dentine caries:

Bacteria mange to invade dentine due to the loss of

enamel (cavitation), it shows five zones:
• Zone of destruction.
• Zone of bacterial invasion.
• Zone of demineralization.
• Zone of sclerosis.
• Zone of reparative dentine.
Prevention of
dental caries
1. Reduce carbohydrates by dietary change &
utilizing sugar substitutes: lycasin, xylitol.
2. Increase tooth resistance: Fluoride
application & Fissure sealants.
3. Control dental plaque: Mechanical cleansing
& antimicrobial agents: chlorohexidine.
4. Vaccination.
Pulp diseases
 Causes of pulpitis

• Dental caries.
• Trauma.
• Chemicals.
• Physical: heat generated during crown preparation.
• Atmospheric pressure: aerodontalgia.
• Hematogenous.
 Classification of pulpitis

• Reversible pulpitis:
1. Focal reversible pulpitis.
• Irreversible pulpitis:
1. Acute pulpitis.
2. Chronic pulpitis.
 Focal reversible pulpitis

• Only acids & toxins reach the pulp causing mild

irritation.
• Sharp intermittent pain induced by thermal changes
& sweets.
 Investigations:

• Vitality test: vital.

• Electric pulp tester: low threshold.
• Percussion: not tender.
• X-ray: caries close to the pulp.
Electric pulp tester
 Histology

• Focal accumulation of PMNs.

• Dilated blood vessels.
• Pulp edema.
 Treatment

• Pulp capping.
 Acute pulpitis

• Bacteria manage to enter the pulp.

• Continuous, throbbing or sharp un-localized pain,
awake him at night.
• Aggravating factors: thermal changes, sweets,
lying down.
• Patient is irritated & febrile.
 Investigations:

• Vitality test: vital.

• Electric pulp tester: low threshold.
• Percussion: not tender.
• X-ray: caries reach the pulp.
Histology
 Treatment

• RCT.
• Extraction.
 Chronic pulpitis:

• Chronic pulpitis occur when:

1. Entering bacteria are of low virulence.
2. Good patient’s immunity (tissue resistance).
• Asymptomatic or dull pain.
 Chronic hyperplastic pulpitis
pulp polyp
• Children.
• Fleshy mass projects through carious cavity.
• Asymptomatic, only pain on chewing hard food.
Consequences of pulp inflammation

Pulpitis

Reversible Irreversible

Acute Chronic

Pulp necrosis

Periapical
inflammation
 Periapical
inflammation
 Definition

• Inflammation of the periapical part of the

periodontal ligament.
 Causes

1. Dental caries that lead to pulp necrosis.

2. Trauma to the tooth.
3. Endodontic treatment.
 Classification

• Acute periapical periodontitis.

• Acute suppurative periodontitis (dento-alveolar
abscess).
• Chronic periapical periodontitis (periapical
granuloma).
 Acute periapical periodontitis

• Causes: usually trauma or caries.

• A mild type of inflammation which may undergo
resolution on removal the cause.
• Severe pain on chewing hard food.
 Investigations:

• Vitality test: vital if trauma , non-vital if caries.

• V. Percussion: tender.
• X-ray: widening of periodontal ligament at the
apex.
 Acute suppurative periodontitis
(dento-alveolar abscess).
• Causes: high virulent bacteria.
• Pathogenesis: squelae of untreated acute periapical
periodontitis. Or acute exacerbation of periapical
granuloma.
 Clinical features

• Severe localized pain, increase on chewing.

• Swelling of adjacent soft tissues.
• Constitutional symptoms: fever, malaise, increase
WBC, regional lymphadenitis.
 Investigations:

• Vitality test: non-vital.

• V. Percussion: tender.
• X-ray: widening of periodontal ligament at the
apex. Or diffuse ill-defined periapical radiolucency.
 Sequelae of an untreated dento-
alveolar abscess:
• Sinus formation.
• Spread through soft tissue: cellulitis & Ludwig’s
angina.
• Hematogenous: cavernous sinus thrombosis,
bacteremia septicemia.
• Bone: osteomyelitis, periostitis.
• Chronic abscess.
Mucosal & skin sinuses
 Cellulitis

• Diffuse soft tissue inflammation associated with

streptococcal infection due to production of
destructive enzymes (streptokinase &
hyaluronidase).
 Ludwig’s angina
• A type of cellulitis in which there is involvement of
bilateral sub-mandibular, sub-lingual, sub-mental,& retro-
pharyngeal spaces.
Cavernous sinus thrombosis
 Periapical granuloma

• A localized granulation tissue at the apex, due to

continuous irritation by low virulent
microorganism.
• Non-vital tooth.
• Asymptomatic or dull pain on chewing hard food.
Periapical granuloma
 Investigations:

• Vitality test: non-vital.

• V. Percussion: slight tender.
• X-ray: widening of periodontal ligament at the
apex. Or well-defined periapical radiolucency.
Periapical granuloma
Histology
Sequelae of untreated periapical
granuloma
Hypercementosis