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. 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
Role of bacteria:
 Germ-free animals.
 Gnatobiotic animals.
 Dental caries is infectious &
transmissible disease.
 Role of mother & relatives.
 Colonization of oral cavity of neonate
(vagina, skin of breast, saliva’s mother).
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.
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.
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.
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.
Fate of pulpitis
Pulpitis

Reversible Irreversible

Focal acute chronic

Pulp necrosis Pulp necrosis

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.
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