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HISTOPATHOLOGY OF DENTAL CARIES
Table of contents
Introduction
Definition of dental caries
Classification
Epidemiology of caries
Theories of dental caries
Current Concepts
Saliva
Microflora
◦ Role of plaque
◦ Role of oral environment
◦ Role of cariogenic micro organism
Substrate/diet
Histopathology of dental caries
◦ Caries process in enamel
◦ Caries process in dentine
◦ Root caries
Conclusion
References
INTRODUCTION
Let us begin with the end:---- CARIES
Caries, a disease and its symptom--- lesion itself
The word caries is derived from Latin, meaning ‘rot’or decay. It is similar to the Greek word meaning death.
DEFINITIONS
Earnest Newbrun (1989): a pathological
process of localized destruction of tooth
tissues by microorganisms
Shafer(1993): Is an irreversible microbial
disease of the calcified tissues of the teeth,
characterized by demineralization of the
inorganic portion and destruction of the
organic substance of the tooth, which often
leads to cavitation.
Sturdevant’s defined it as an infectious
microbiologic disease of the teeth that
results in localized dissolution and
destruction of the calcified tissues.
Cavitations in teeth are signs of bacterial
infection.
CLASSIFICATIONS
Based on Anatomic site
◦ Occlusal (Pit snd Fissure)
◦ Smooth Surface (Proximal and cervical caries)
◦ Root Caries usually occurs in older age. The predisposing factor is the recession of gingival margin
Based on Severity
◦ Incipient Caries- the early carious lesion, best seen on the smooth surfaces of teeth, as a ‘WHITE SPOT’. ◦ Carious attack changes the optical behavior of
the affected enamel, resulting enamel becoming more opaque, because porous enamel scatters more light.
◦ Cannot be diagnosed radiographically and can be diagnosed with the help of Diagnodent.
◦ D/D- white developmental defects of enamel.
◦ Occult Caries: Hidden caries is used to describe a lesion which is not clinically diagnosed but detected only on radiographs. Prevalence of this caries from 0.8% in premolars (14-15 yr olds) to 50% in 20 year olds (Seow 2000)
◦ Bite wing, OPG, Fibre-optic transillumnation, lazer luminescence - for Diagnosis.
◦ Cavitation:
Based on Progression
◦ Arrested Caries: shift in oral conditions may lead to arrested caries appears as a marked brown pigmentation.
◦ Recurrent / Secondary Caries: Occuring next to a restoration. Due to poor adaptation of restoration leading to a marginal leakage.
◦ Radiation Caries: radiotherapy is frequently associated with xerostomia due to decreased salivary secretion. This may lead to a form of rampant caries.
Based on Chronology
◦ Early Childhood caries
◦ Nursing caries & rampant caries
◦ Linear enamel caries
◦ Adolescent caries: variant of rampant caries where the teeth generally considered immune to decay are involved.
◦ Adult caries: at the age of 55-60 yrs, the third peak of caries is observed which involves root & cervical caries. Due to gingivla recession.
HUME & G.MOUNT classification
Focused on carious lesion development &
progression rather than location of cavities.
Consisting of two sub classification:
- location of lesion
- size of lesion
The first parameters for the classification are
three sites:
Site 1: pits, fissures, and enamel defects on
occlusal surfaces of posterior teeth or other
smooth surfaces;
Site 2: a proximal enamel in relation to areas in
contact with adjacent teeth;
Site 3: the cervical one third of the crown or,
following gingival recession, the exposed root.
According to size of lesion
Size 0: The earliest lesion that can be identified
as the initial stage of demineralization.
Size 1: Minimal surface cavitation with
involvement of dentine just beyond treatment by
remineralization alone.
Size 2: Moderate involvement of dentin. After
limited cavity preparation, remaining enamel is
sound, well supported by dentine, and not likely
to fail under normal occlusal load.
Size 3: The lesion is enlarged beyond moderate
size. Remaining tooth structure is weakened to
the extent that cusps or incisal edges are split or
are likely to fail if left exposed to occlusal load.
Size 4: Extensive caries or bulk loss of tooth
structure (eg, loss of a complete cusp or incisal
edge) has already occurred
According to the World Health Organization (WHO) system, the shape and the depth of the carious lesion can be scored on a four-point scale (D1 to D4):
D1: clinically detectable enamel lesions with intact
(noncavitated) surfaces D2: clinically detectable "cavities" limited to the
enamel D3: clinically detectable lesions in dentin (with
and without cavitation of dentin) D4: lesions into pulp
•Intact tooth (43) •Primary enamel caries (42) •Primary dentin caries with cavitation (41) •Secondary caries with cavitation (31) •Advanced secondary caries (32) •Complete destruction of the crown (33)
EPIDEMIOLOGY OF CARIES
There was no evidence of caries found in the few teeth in skull fragments of our earliest known ancestors.
But extensive decay found in Neanderthal man and in prehistoric European race. (upto 7.2 DMF).
The prevalence and pattern of caries did not change significantly during 2000 years from Iron age to Medieval period (1066-1052 AD). The caries level was low found mostly on occlusal caries
Caries prevalence is generally lowest (0.5-1.7 DMF) For Asian and African countries and highest for Americans (12-18 DMF) and other Western countries.
THEORIES OF DENTAL CARIES
WORM THEORY- Sumerian text known as “legend of the Worm” –discovered in clay tablets (5000 BC).
Antony van Leeuwen hoek
(1700)- little worms taken
out of a corrupt tooth.
HUMORAL THEORY-
worm theory faded out in early centuries as Greek Physicians advanced to humoral theory
4 elemental humors were Blood, Phlegm, Black bile , yellow Bile. An imbalance in these humors resulted in the disease
Hippocrates accepted
Aristotle (384-322 BC)
According to Galen (Greek Physician and Philosopher) , caries was produced due to internal action of acid and corroding humors
VITAL THEORY- (given in end of 18th century) Greek physicians like Hippocrates, Celsius, Galen said that teeth are an integral part of body and they were vitally affected by and in turn affected the body.
So vital theory of tooth postulated that tooth decay originated, like bone gangrene from within the tooth itself
CHEMICAL THEORY-
Robertson (1835) proposed that caries was caused by fermentation of food particles around teeth. Since fermentation was considered to be a non-vital process not associated with microorganisms.
PARASITIC OR SEPTIC THEORY- Erdl and Ficinus (1843) described caries is caused by filamentous organism “Denticolae”. Early microscopic observations of scrapings from teeth by Antonie van Leeuwenhoek, indicated that microbes were associated with carious process.
MILLER’S CHEMO-PARASITIC THEORY (ACIDOGENIC THEORY) Caries caused by acids produced by micro-organisms of the mouth
Basis: Pasture had discovered that microbes mediate the process of conversion of sucrose to lactic acid. W.D.MILLER (1890)
University of Berlin
Facts of Miller experiments
Acid was present within the deeper
carious lesion.
Lactic acid was identifiable product
Different kinds of foods mixed with
saliva and incubated at 37°C could
decalcify the entire crown of a tooth.
Several types of mouth bacteria could
produce enough acid to cause dental
caries.
Different microorganisms invade
carious dentin.
Conclusion-
◦No single species of micro-organism caused caries.
◦ Dental decay is a chemo-parasitic process consisting of 2 stages:
Decalcification & softening of the tissues
Dissolution of the softened tissue
PROTEOLYTIC THEORY- it was espoused primarily by Gottlieb(1944), Frisbie(1947) and Pincus(1950) said that
the initial action was due to proteolytic enzymes attacking the lamellae, rod sheaths, tufts and walls of the dentinal tubules
And considered that the process involved depolymerization and liquefaction of the organic matrix of enamel.
PROTEOLYSIS – CHELATION THEORY
Implies a simultaneous microbial degradation of the organic components and dissolution of the minerals of the tooth by process of chelation.
Chelation is a process involving complexing of a metal ion to a complex substance through a covalent bond which results in a highly soluble , weekly ionizable compound.
SCHARTZ and MARTIN (1955)
Proteolytic enzymes act on the organic content and release chelates
Both organic & inorganic compounds are attacked.
O O O O
C c
HC ca CH
H3C OH OH CH3
CURRENT CONCEPT IN DENTAL CARIES In the epidemiological model a disease
state is due to interplay of three primary factors (Keyes and Jordan, 1960).
◦ Host
◦ Agent
◦ Environmental influences
Newbrun (1982) postulated that many secondary factors also influence the rate of progression of caries.
Primary factors:- ◦ Host tissue- tooth
◦ Microflora with a cariogenic potential
◦ A suitable local substrate
Orland (1954) bacteria are a prerequisite for the initiation and progression of dental caries.
Fizgerald (1968) concluded that:
◦ Microbes are a prerequisite for caries initiation
◦ A single type of organism is responsible for initiating caries.
◦ Not all acid producing organisms are cariogenic
◦ Organisms vary greatly in their capacity to induce caries
CARIES BALANCE
KEYES TRIOLOGY 1960
Newer concept
NEWBRUN TETRALOGY 1982
Overview Of Factors Affecting The Development Of Dental Caries
Internal Modifying factors
HOST FACTOR SALIVA
COMPOSITION OF SALIVA
• Organic: 1. protien:
Amylase
Lysozyme
Glycoproteins
IgA
Traces of blood proteins
Albumin, IgM, IgG
Transferrin
Lipoproteins
2.Nitrogenous constituents:
Aminoacids
Urea
Uric acid
Ammonia
Creatin
Statherin
sialin
3. Glucose
4. Blood group
substances A, B, O.
5. vitamins- water
soluble
6. Intrinsic factor-
apoerythein
7. Lipids : Cholesterol,
fatty acids,
triglycerides,
phospholipids.
8. Enzymes
Acid phosphatase
Esterases, Lysozyme
kallikrein
9. Other organic
compounds
Citrates
Nitrates
10. Anti –bacterial
Proteins
Lysozyme
Sialoperoxidase
Lactoferrin
99 % water 1 % solids
• Inorganic:
Calcium
Phosphate
Sodium
Potassium
Chloride
Fluoride
Bicarbonates
Thiocynate
Iodine
Magnesium
Sp. Gravity – 1.002 – 1.008
pH range – 6.2 – 7.6
Avg. pH – 6.7
Cells in saliva
Epithelial
Leucocytes
Bacteria
Yeasts
Protozoa
Gases dissolved in saliva:
02, N2, CO2
Role of saliva in dental caries Secretion rate
{ml/min}
Stimulate Non-stimulated
Normal >1.0 0.25
Low 0.7- 1.0 0.1- 0.25
Very low <0.7 <0.1
Frank and Herdly 1965
Principle properties of saliva that protect the teeth against dental caries:
◦ Dilution & clearance of dietary sugars
◦ Neutralization & buffering of acids in plaque
◦ Supply of ions for remineralization
◦ Antiplaque and antimicrobial factors
Neutralization & buffering of acids in plaque:
◦ Mainly due to bicarbonate buffer
◦ Unstimulated saliva – low levels
◦ Stimulated saliva - greater levels
◦ Restore the pH of saliva
WHY TEETH ARE MORE PRONE TO DECAY DURING SLEEP???
Dangerous at bed……Canadian dental association
DEMINERALIZATION-REMINERALIZATION CONCEPT
Caries is not a result of a single acid attack by the acid formed, rather an outcome of the imbalance occurring in the demineralizaton-remineralization cycle continuously in oral cavity.
Governed by an number of factors which is either caries promoting (DEMIN.)or caries inhibiting (REMIN.)
Note- all the 3 factors are present in every individual’s oral cavity but in different proportions determining the direction of demin-remin cycle.
DEMINERALIZATION: the mineral content of tooth surface is hydroxyapatite [Ca(PO4)6(OH)2] which is in equilibrium and neutral environment saturated with Ca2+ & PO4-
At pH of 5.5 and below H+ ions react with the phosphate group in the aqueous environment immediately converting phosphate to hypophosphate which does not contribute to normal hydroxyapatite equilibrium. Thus its demineralization.
REMINERALIZATION: the demineralization can be reversed if the pH is neutral and there are sufficient Ca2+
& PO4- ions in the immediate environment.
The Ca2+ & PO4- ions in saliva can inhibit the process of dissolution through the common ion effect which enables the rebuilding of partly dissolved apatite crystals and hence remineralization.
Demineralization & Remineralization cycle:
◦ Factors governing the stability of enamel apatite :
pH
Free active conc. of calcium, phosphate & fluoride
Equilibrium at normal pH
Saliva is supersaturated with respect to enamel
Saliva
Enamel
Ca10(PO4)6OH2
[Ca] [PO4] [Ca] [PO4]
Ca+statherin Ca+aPRP
Demineralization
Saliva
Enamel
Ca10(PO4)6OH2
[Ca] [PO4] [Ca] [PO4]
Ca+statherin Ca+aPRP
Dietary CHO + biofilm = lactic acid; diffusion into enamel = local pH drop
Enamel solubility increases
[Ca] [PO4] exit to saliva
CHO CHO CHO
[H+]
[H+]
[H+]
[H+] [H+]
Remineralization
Saliva
Enamel
[Ca] [PO4] [Ca] [PO4]
statherin Ca+aPRP
Saliva flow clears CHO; salivary HCO3 returns pH to normal
Enamel becomes less soluble
[Ca] [PO4] move into enamel
CHO
CHO
[HCO3]
[HCO3] [HCO3]
pH < 5.5
pH >5.5 Caries Erosion pH > 6.7
STEPHAN’S CURVE
Dr. Robert Stephan and Miller 1944, which reflected the fall in salivary pH following glucose rinse.
Caries inactive subjects were taken and said not to brush 3-4 days. Before rinsing with 10ml of a 10% glucose for 10s, pH readings were obtained & after rinsing with glucose solution pH readings were obtained again. Graph- Resting pH, Rapid fall in pH, Critical pH, Recovery pH.
Stephan’s Curve Dr. Robert Stephan 1940s
A-- rapid pH drop indicates sugar instantaneously converted to acids--overwhelming salivary buffers
B-- persistence of low pH (plateau) due to catabolism of ICP--can be >60 minutes
C-- gradual return to resting pH due to diffusion, dilution & buffering effect
1. Resting plaque pH
1. Decrease in pH level-
◦ Microbial composition
◦ Speed with which plaque bacteria metabolize CHO
◦ Buffering capacity of unstimulated saliva
2. Critical pH- generally accepted at 5.5 (HA dissolve)
3. Increase in pH level- it remains for 30-40 minutes to return to N
HISTOPATHOLOGY OF DENTAL CARIES
60
(a)Surface zone. (b)Body of lesion. (c) Dark zone surrounds body of
lesion while. (d)Translucent zone is evident over
entire advancing front of lesion.
The deepest zone is the translucent zone, the advancing front of the enamel lesion. The name refers to its structureless appearance when perfused with quinoline solution and examined with polarized light.
The pores or voids form along the enamel prism (rod) boundaries
Zone 1 :Translucent zone
Zone 2: Dark zone
The next deepest zone is known as the dark zone because it does not transmit polarized light.
The total pore volume is 2% to 4%.
Average reduction of mineral per unit volume for enamel-6%
Zone 3: Body of the Lesion
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