Dental Caries

Index:

Part 1 = Introduction - Definition.
Part 2 = Classification Of Caries.
Part 3 = Factors Influencing Caries Etiology.
Part 4 = Histopathology Of Dental Caries.
Part 5 = Clinical Diagnosis Of Dental Caries.
Part 6 = Management of Deep Dental Caries.
Part 7 = Sequence of Dental Caries.

Introduction - Definition

What is Dental Caries:

It is a disease of microbial origin in which the dietary carbohydrates are fermented by the bacteria forming an acid which causes the demineralization of the inorganic part and disintegration of the organic part of the tooth.

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Classification Of Caries:

A. According to number of surfaces involved:

1) simple (1 surface involved)
2) compound (2 surfaces involved)
3) complex (2 surfaces involved)

B. According to anatomic site:
1) occlusal (pit-and-fissure) caries
2) smooth-surface caries (proximal and cervical caries)
3) root caries

C. According to histology:
1) enamel caries
2) dentinal caries
3) cemental caries

D) According to severity:
1) incipient caries
2) occult caries
3) cavitation caries

E) According to onset:
1) primary (virgin) caries
2) secondary (recurrent) caries
3) residual caries

F) According to duration:
1) acute (rampant)
2) chronic

G) According to chronology:
1) early childhood caries
2) adolescent caries
3) senile caries

H) According to progression:
1) arrested caries
2) recurrent caries
3) radiation caries

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Factors Influencing Caries Etiology.

A)Host factors:

1) tooth factors:
a. Composition surface enamel due to dense
mineralization and high F-
content more resistant to caries than
subsurface layers of enamel.

b. Morphology more chances of caries if deep ,
narrow occlusal fissures or buccal or lingual pits present

2) saliva factors:
a. composition
a1) inorganic less chances of caries if higher Ca2+
and PO43- concentration
a2) organic less chances of caries with higher
ammonia and urea content

b. pH decrease in pH of saliva below 5.5 (ka critical
pH) predispose to caries.
The remarkable buffering-capacity of saliva (due to HCO3-H2CO3 and phosphate buffer systems) controls the marked fall in pH, thus preventing caries formation.

c. Position more chances of caries if malaligned , rotated teeth.

d. quantity decreased amount or absence ( xerostomia)
increases the risk of caries.

e. viscosity

f. antibacterial properties: due to the presence of lysozyme (cleaves the N-acetyl glucosamine and N-acetyl muramic acid components of bacterial cell wall) and salivary peroxidase system ( salivary peroxidase and thiocyanateSCN- components of saliva interferes with glycolytic pathway of bacteria)

3) systemic factors:
a) heredity
even though no strong evidence has been found connecting caries-susceptibility with heredity, studies have shown
“high DMF” father and “high DMF” mother produced offspring with a “high DMF” rate
And “low DMF” parents produced offspring with “low DMF” rates.
b) Pregnancy and lactation
despite the popular belief, there is NO evidence suggesting increase in caries in pregnancy (unless the mother has neglected her general oral health care).

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B) Diet factors
a. physical nature of diet
person taking food with more fibre-content less
susceptible to caries than those taking soft, refined
(worse if sticky) food

b. local factors

b1) carbohydrate content
though all forms of fermentable sugar leads to caries , there is always a higher risk of caries with free sucrose than starches.
Because sucrose in addition to its acid- byproduct produced during fermentation also aids in plaque development and adherence of cariogenous microbes to the tooth surface.
However starches due to large molecular structure, shows limited diffusion and hence can not directly enter the plaque .

b2) vitamin content
vitamins like (vit.D, vit.K and vit.B6) have been found to decrease the incidence of caries,
vit. B-complex deficiency has shown decrease in the rate of caries
whereas even though it is well-established that vit C-deficiency causes severe periodonta land pulpal changes , no evidence of decrease in caries by Vit C-supplement has been reported.
however a more extensive study to confirm the link between vitamins and caries is still desireable.
b3) fluorine content
even though there is reduced incidence of caries with F-in drinking water, there is no significant caries reduction with dietary fluoride (because of its metabolic unavailabilty).

C) Cariogenic potential of the microorganism

Available data strongly suggest an active involvement of Streptococcus mutans in caries initiation (especially in pit and fissure caries, and smooth-surface caries; and to some extent the root surface caries)
On the other hand, oral actinomyces like
Actinomyces viscosus, and
Actinomyces neslundii, have a more important role in root surface caries.
Also A. neslundii, Lactobacillus spp. And other filamentous rods have been implicated in dep dentinal caries.

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Histopathology Of Dental Caries

Enamel is composed of tightly packed hydroxyapatite crystals, which are organized in long columnar rods (enamel rods), but during caries progression certain histological changes are seen in enamel .

The following 4 histological zones of an enamel lesion clearly explains the development of enamel caries

zone 1 translucent zone
zone 2 dark zone
zone 3 body zone
zone 4 surface zone

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Zone 1 translucent zone
Deepest zone representing the advancing front of enamel caries.
In this zone , pores or voids form along the enamel prism(rod) boundaries (due to easy H+ ion penetration)
It appears structureless when perfused with quinolone solution (having refractive index comparable to that of enamel) and seen with polarized light (hence translucent)

Zone 2 dark zone
Next deepest zone
Presence of many tiny pores block light transmission. These smaller air or vapor-filled pores make the regiion opaque.
Loss fo crystalline structure suggesting the process of demineralization and remineralization in this zone.

Zone 3 body zone
In demineralization phase, it is the largest portion of the lesion.
(whereas in remineralization phase, zone2dark zone is the largest portion which increases in the expense of the “body zone”)
Largest pores seen (pore volume 5 to 25%)
Presence of bacteria if pores large enough to permit their entry
Striae of Retzius well marked
(striae of Retzius is the primary point of entry of carious lesion into rodprism cores of enamel)

Zone 4 surface zone
Relatively unaffected by caries (only partial demineralization)
Because surface of enamel is relatively immune to caries (due to hypermineralization- because of saliva contact , and
higher surface F-content)
Also pore volume is lower than the body of lesion.

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After the involving the enamel, the carious lesion progresses to the dentinal structure.
Caries advancement in dentin proceeds through 3 stages:

1) demineralization of dentin (by weak organic acids)
2) degeneration and
dissolution of organic material of dentin , mainly collagen
fibers (type I)
3) bacterial invasion after the loss of structural integrity caused
due to 1) and 2).

During the development of dentinal caries, clinically 5 different zones of progression can be seen (ac to Sturdevant )
zone 1 normal dentin
zone 2 subtransparent dentin
zone 3 transparent dentin
zone 4 turbid dentin
zone 5 infected dentin

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Histologically , 5 zones of early dentinal caries progression can be seen (listed pulpally to occlusally)
zone 1 zone of fatty degeneration of Tomes’ fibers
zone 2 zone of dentinal sclerosis
zone 3 zone of decalcification of dentin
zone 4 zone of microbial invasion
zone 5 zone of decomposed dentin

Zone 1 zone of fatty degeneration of Tomes’ fibers
the most advancing front of dentinal caries characterized by the presence of a layer of fat globules ; hence stains red with the stain, sudan red.
significance

1) fat layer leads to impermiability of the dentinal tubules (DT) – trying to prevent further invasion of  carious lesion
2) favors sclerosis of dentin in zone 2.

Zone 2 zone of dentinal sclerosis
layer of sclerotic dentin which appears white in transmitted light
calcification of DT as a rxn of vital pulp and vital dentin to carious invasion , so as to prevent further penetration of microorganisms.
formation of this zone is minimal in rapidly progressing caries, and prominent in slow caries.

Zone 3 zone of decalcification of dentin
this zone lies above the zone of sclerotic dentin
initial decalcification of only the walls of the DT
presence of PIONEER BACTERIA- first of the microorganisms penetrating DT before there is any clinical evidence of caries.
bacteria present in individual DT are in pure form (i.e. either completely cocci or completely bacilli; not in mixed form)

Zone 4 zone of microbial invasion
in a layer above zone 3.
characterized by the presence of microorganisms in early stage of caries- acidogenic microorganisms in deeper layer- proteolytic microorganisms replace acidogenic bacteria supports the hypothesis that initiation (by acidogenic bacteria) and progression ( by proteolytic microorganisms ) are 2 distinct processes in caries development.

During initiation phase- in the early stage when caries is not deep , acidogenic bacteria predominant which utilizes carbohydrate for their metabolism
Later in progression phase – as the caries goes deeper , less and less of carbohydrate substrate available , hence acidogenic bacteria are replaced by proteolytic microorganisms which uses dentinal protein for their metabolism.

Zone 5 zone of decomposed dentin
Most superficial zone of early dentinal caries.
no recognizable structure in decomposed dentin

collagen and minerals seem to be absent
great number bacteria dispersed in this decomposed granular matter.

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Clinical Diagnosis Of Dental Caries

By one or all of the following:
1) Visual changes in tooth surface texture or color
2) Tactile sensation with judicious use of explorer
3) Radiographs
4) Transillumination
Aided by the knowledge of the probability of overall caries risk and patterns of susceptibility.

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A) Diagnosis of Pit and Fissure Caries:

Any one or more of the following:
1) Softening at the base of pit and fissure
2) Opacity surrounding the pit or fissure, indicating demineralization of enamel
3) Brown-gray discoloration radiating peripherally from the pit or fissure
4) Softened enamel that may be flaked away by explorer radiolucency beneath the occlusal enamel surface

B) Diagnosis of Proximal Surface Caries:

1) Visual – white chalky appearance or shadow under the marginal ridge
2) Tactile- probing with explorer on proximal surface may detect cavitation, which is defined as the break in the surface contour of enamel
3) Radiographic diagnosis- made with bitewing radiographs which show radiolucency beneath the enamel surface in the proximal area (should not be confused with cervical burnout!)

Arrested Lesions on Proximal Surface:
1) Appears as brown spots
2) On probing, surface is intact and hard
3) Radiograph shows decreased radiographic density in the affected region
4) Usually seen in old patients

Proximal Surface in Anterior Teeth:
1) Transillumination- in which light source directed through the tooth from the lingual side. Proximal surface caries, other than incipient caries, appear as a dark area along the marginal ridge
2) Tactile- exploration to detect any cavitation
3) Radiographs – may detect any small incipient lesion as well.

C) Diagnosis of Smooth Surface caries on the Facial and Lingual surfaces (Usually Gingival)

Initial phase :
1) CHALKY-WHITE, OPAQUE AREAS (“WHITE SPOTS”) over the smooth surface of the tooth, that is visually different from adjacent translucent enamel , which is revealed only when the tooth surface is clean and dry and disappears partially or totally when the tooth is wet . This initial phase of caries in enamel is k/a “incipient caries”.
The tooth at this stage appears to have lost its translucency because of extensive subsurface porosity due to demineralization.
2) Undetectable tectilely since surface is hard , intact and smooth.

Advanced Phase:
1) White to dark brown discoloration
2) Demineralized and softness to penetration

Arrested Lesion:
1) Dark, discolored areas mostly due to extrinsic staining
2) Hardening of lesion (due to remineralization)
3) Sclerotic or eburnated dentin

D) Diagnosis of Root Surface Caries:

1) Look for the following features at CEJ or more apically on cementum
early stage-
a) Well-defined discoloration adjacent to gingival margin,
typically near the CEJ
b) Softened cemental tissue compared with adjacent structure
advanced stage- softening on exploration
and cavitation.

2) Usually in older individuals , or in patients who has undergone perio- surgery , with the following predisposing factors
a) Cemental exposure
b) Dietary changes
c) Systemic diseases
d) Medications that affect amount and character of saliva.

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 Management of Deep Dental Caries

A) Chemical Measures For Caries Control:
Use of:

1) Substances which alter the tooth surface or tooth structure

a) Fluoride Exposure Application
Fluoridation of water supply ( with 1 ppm of F-)
Topical application of fluoride

i) Self-application
- Low dosehigh frequency rinses
(0.05% NaF daily)
- High potencylow frequency rinses
(0.2% NaF weekly)
- Fluoridated Dentifrices Toothpastes
(twice daily)
ii) Professional Application
- acidulated phosphate fluoride gel (APF gel)
(1.23% annually or semi-annually)
- NaF solution (2%)
- stannous fluoride (8%)

b) Bis-biguanides ( like chlorhexidine , alexidine)

c) Silver Nitrate

d) Zinc Chloride and Pottasium Ferrocyanide Solution

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2) Substances Which Interfere With Carbohydrate Degradation Through Enzymatic Alteration:

a) Vitamin K – Use of Synthetic Vit K (2-methyl-1,4-naphtoquinone)
b) Sarcoside - Na Lauroyl Sarcosinate,
Na Palmitoyl Sarcosinate,
Na Dehydro Acetate

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3) Substabces Which Interfere With Bacteria Growth And Metabolism:

a) Urea and Ammonium Compounds
b) Chlorophyll
c) Penicillin
d) Other antibiotics ( erythromycin, kanamycin, spiromycin, tetracycline, tyrothricin, vancomycin)
e) Caries vaccine
f) Nitrofurans – furacin, furadroxyl

B) Mechanical Measures For Caries Control:

1) Dental Prophylaxis (routine scaling and polishing)
2) Toothbrushing
3) Mouth Rinsing
4) Dental Floss
5) Oral Irrigators
6) Chewing Xylitol Gums (for 5 to 30 mints after meal)
7) Detergent Foods in Diet (hard, fibrous foods)
8) Pit and Fisure Sealants

C) Nutrietional Measures For Caries Control:

1) Diet Counselling
2) Restriction of Soft, Sticky Refined Carbohydrate Intake
3) Limiting in Between Meals.

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Sequence of Dental Caries

The Dental Caries can cause DEATH !!!

- First of all, We should know that the caries is the most common infectious disease for the humans.
- The Caries is a bacterial infection, which occurs briefly due to bacteria that ferment the carbohydrates to produce the Lactic acid which causes the demineralization of the enamel surfaces, causing the decay and cavities.
- The Caries may extend deeply into the tooth layers, to reach the dentin layer, which is sensitive, causing the tooth pain.
- Then the bacteria will penetrate the dentinal layers soon if neglected to reach the pulp chamber (or horns), causing the pulpitis, which will start as reversible OR irreversible.
- The Bacteria may drown deeply inside the pulp chamber to reach the orifices of the pulp causing pulp inflammation that would, if neglected, cause partial pulp necrosis that requires partial pulpectomy to manage.
- Then, the bacteria drown inside more deeply that will necrose the rest of the pulp canals causing complete pulp necrosis, then the patient will feel no pain.
- In this stage, the tooth is most commonly ( Badly Decayed ) and black in color, the patient may no seek dental help because he/she suffers of no pain, this neglection will cause the next serious step, which is the periapical abscess.
- The Periapical Abscess may be acute, because of the sudden increase of the pathogens strength or sudden decrease of the host immunity, causing pain specially during biting and percussion.
- And the periapical abscess may become chronic soon or after, if the immunity increased or the pathogens strength decreased, to wall of the infection.
- The chronic abscess may exacerbate to transform the chronic abscess into acute painful one again that leads the patient to seek dental help.
- The infection may then spread to the facial spaces, lower molars may spread infection to the submandibular and sublingual spaces, while the anterior teeth may spread this infection to the submental space.
- The neglected infection may spread to the spaces causing facial cellulitis and subsequent Ludwig's angina that may be fatal.

So, Caries may Lead to DEATH !!!

This Article Has Been Authored By :: World Of Dentistry :: TEAM