DENTAL CARIES

A) PERIAPICAL ABSCESS

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def:
it is defined as “ the localized, acute or chronic suppurative (associated with the discharge of purulent exudate- “the pus”) infection in the periapical region of the tooth.

It is also k/a dentoalveolar abscess

etiopathogenesis
Progression of pulpal infection into the periapical tissue.
Accidental perforation of the apical foremen during endo- rx , leading to the entry of pulpal microorganisms into the periapical area
Spread of periodontal infection into the periapical tissues
Fracture of tooth with pulp exposure
Secondary bacterial invasion into the pre-existing periapical granuloma or cyst or scar
Anachoretic infection of periapical tissues

Due to strict anaerobes like
prevotella,
porphyromonas etc.
Also , anaerobic streptococci,
staphylococci.

It is a common odontogenic infection (2% of all apical radiolucencies)

Clinical features
Severe pain
localized swelling and erythematous overlying mucosa
Extreme tenderness to persussion and to pressure on
chewing
Slight extrusion of the tooth
non- vital , mobile tooth
fever and localized lymphadenitis
Pain – aggravated by heat,
relieved by cold
In chronic periapical abscess –
dull, mild pain with
intraoral/extraoral pus discharging sinuses.

Sequelae of acute periapical abscess
If untreated, invades cortical plates of bone (mostly buccal) and invades adjacent soft tissues , leading to space infection and finally cellulitis
pus discharging sinus-
either intraorally (on alveolar mucosa over the apex of root)
or extraorally (on skin over the jaw)
Chronic periapical abscess
(if host defense is high, or
virulence of microorganisms is low)
Osteomyelitis
(I f the abscess invades the medullary spaces of the bone)
Infection of fascial spaces
(further complicated by ludwig’s angina, septicaemia, cavernous sinus thrombosis etc.)

Radiographic finding
Acute periapical abscess
as it develops rapidly, no time for bone resorption to occur; hence the only r/f that is seen is-
the thickening (slight) of PDL spaces in the apex region of the tooth involved.

Chronic periapical abscess
small radiolucent areas at the apex of the root with poorly defined margins.

Histological features
Lesion consists of “ZONE OF LIQUEFACTION NECROSIS” , which consists of
Protein exudates
necrotic tissues , and
a large no. of viable or dead neutrophils (pus).
Dilated blood vessels and
neutrophilic infiltration, adj. to the lesion
PDL and adj bone marrow also shows inflammatory changes
bony trabeculae in the periapical region may show empty lacunae (due to the death of osteocytes)
In chronic periapical abscess
- chronic inflammatory cells (like lymphocytes)
- area of bone destruction accompanied by
area of bone regeneration and fibrosis
- pus discharging sinus lined by
either granulation tissue
or squamous epithelium.

treatment
Drainage established
either through an opening in the tooth
or by incision over soft tissue swelling at apex

Antibiotic administration (START WITH PENICILLIN; IF ALLERGIC TO PENICILLIN, DO ERYTHROMYCIN OR CLINDAMYCIN)

Rct or
extraction of the tooth (after the acute phase of the disease is controlled)

References: (DENTAL CARIES)

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1)Rajendran r, sivapathasundaram b: shafer’s textbook of oral pathology, 6 e/d, elsevier, 2009.

2)Roberson,T.M. Heymann, H.O. Swift,E.J. Sturdevant’s art and science of operative dentistry, 4 e/d, mosby, 2002.

MANAGEMENT OF DENTAL CARIES

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A)CHEMICAL MEASURES FOR CARIES CONTROL
Use of:
1) substances which alter the tooth surface or tooth structure
a) fluoride exposure/application
üFluoridation of water supply ( with 1 ppm of F-)
üTopical application of fluoride
i) self-application
§Low dose/high frequency rinses
(0.05% NaF daily)
§High potency/low 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

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

3) SUBSTANCES WHICH INTERFERE WITH BACTERIAL 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) NUTRITIONAL MEASURES FOR CARIES CONTROL
1) diet counselling
2) restriction of soft, sticky refined carbohydrate
intake
3) limiting in between meals.

CLINICAL DIAGNOSIS OF CARIES

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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.

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 CARIES IN ANTERIOR TOOTH
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 OF TOOTH (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.

HISTOPATHOLOGY OF CARIES

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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

zone 1: translucent zone
ü deepest zone representing the advancing front of enamel
caries.
ü in this zone , pores or voids form along the enamel prism(rod)
boundaries (due to easy H+ ion penetration)
ü 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
ü next deepest zone
ü presence of many tiny pores block light transmission. These smaller air or vapor-filled pores make the regiion opaque.
ü loss fo crystalline structure suggesting the process of demineralization and remineralization in this zone.

zone 3: body zone
ü in demineralization phase, it is the largest portion of the lesion.
ü(whereas in remineralization phase, zone2/dark zone is the largest portion which increases in the expense of the “body zone”)
ü largest pores seen (pore volume 5 to 25%)
ü presence of bacteria if pores large enough to permit their entry
ü striae of Retzius well marked
(striae of Retzius is the primary point of entry of carious lesion into rod/prism cores of enamel)

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

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 (a/c to Sturdevant )
zone 1: normal dentin
zone 2: subtransparent dentin
zone 3: transparent dentin
zone 4: turbid dentin
zone 5: infected dentin

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
ü the most advancing front of dentinal caries
ü characterized by the presence of a layer of fat globules ; hence
stains red with the stain, sudan red.
ü 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
ü layer of sclerotic dentin which appears white in transmitted light
ü calcification of DT as a rxn of vital pulp and vital dentin to carious invasion , so as to prevent further penetration of microorganisms.
ü formation of this zone is minimal in rapidly progressing caries, and prominent in slow caries.

zone 3: zone of decalcification of dentin
ü this zone lies above the zone of sclerotic dentin
ü initial decalcification of only the walls of the DT
ü presence of PIONEER BACTERIA- first of the microorganisms penetrating DT before there is any clinical evidence of caries.
ü 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
ü in a layer above zone 3.
ü characterized by the presence of microorganisms
ü in early stage of caries- acidogenic microorganisms
üin deeper layer- proteolytic microorganisms replace acidogenic bacteria
ü 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
üMost superficial zone of early dentinal caries.
ü no recognizable structure in decomposed dentin
ü collagen and minerals seem to be absent
ü great number bacteria dispersed in this decomposed granular matter.

CLASSIFICATION OF CARIES

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A.a/c to no. of surfaces involved:
1) simple (1 surface involved)
2) compound (2 surfaces involved)
3) complex (>2 surfaces involved)
B. a/c to anatomic site
1) occlusal (pit-and-fissure) caries
2) smooth-surface caries (proximal and cervical caries)
3) root caries
C. a/c to histology
1) enamel caries
2) dentinal caries
3) cemental caries

D) a/c to severity
1) incipient caries
2) occult caries
3) cavitation caries
E) a/c to onset
1) primary (virgin) caries
2) secondary (recurrent) caries
3) residual caries
F) a/c to duration
1) acute (rampant)
2) chronic

G) a/c to chronology
1) early childhood caries
2) adolescent caries
3) senile caries
H) a/c to progression
1) arrested caries
2) recurrent caries
3) radiation caries

Factors influencing caries etiology

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ALSO SEE KEYES' CIRCLE.

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 (k/a 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.

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

d. viscosity

e. 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 thiocyanate/SCN- 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).

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.

DENTAL CARIES: INTRODUCTION AND THEORIES OF CARIES FORMATION

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DENTAL CARIES

def.

Dental caries is defined as the irreversible multi-factorial disease of microbial origin affecting the calcified tissues of the teeth, which is characterized by demineralization of the inorganic portion and destruction of the organic constituents of the tooth, often leading to cavitation.

etiology

Various theories have been proposed trying to explain the etio-pathogenesis of dental caries, which are-

a)Early theories
1) the legend of worms (5,ooo B.C.)
2) endogenous theory
3) chemical theory
4) parasitic theory

b)Miller’s chemicoparasitic theory
(acidogenic theory)

c)Proteolytic theory
d)Proteolysis-chelation
e)Sucrose-chelation theory
f)Current concept of caries etiology

The legend of worms
In the past, dental caries was thought to be caused by living worms inside the tooth structure.

Endogenous theories
Includes 1) humoral theory- according to which an imbalance
between the humors of body caused tooth decay.
2) vital theory- according to which tooth decay
originated from within the tooth itself, like a bone
gangrene.

Chemical (acid) theory
On the basis of findings of Robertson, this theory proposed that tooth decay was caused by the fermentation of food particles around the teeth.

Parasitic (septic) theory
This was the first theory that related microorganisms with caries on a causative basis (by ERDLE, 1843)Accordingly, it was proposed that even though caries starts purely as a chemical process BUT microorganisms continued the disintegration in both enamel and dentin.

Miller's chemico-parasitic theory(the acidogenic theory)

Proposed by Willoughby D Miller.
This theory is a blend of both chemical and parasitic theory proposed earlier.
a/c to this theory, dental caries is a chemico-parasitic process consisting of 2 stages:
first, decalcification of enamel and dentin (preliminary stage)
second, dissolution of the softened residue (later stage)
and the acid causing primary decalcification is produced by the fermentation of starches and sugar from the retained corners of teeth.

Hence Miller advocated an essential role of 3 factors in the caries process: the oral microorganisms,
the carbohydrate substrate, and
the acid.
Even though, at that time, this theory couldn’t explain
1) predilection of specific sites on a tooth
2) initiation of smooth surface caries
3) why some populations are caries free
4) the phenomenon of arrested caries.
This theory is still considered as the backbone of current knowledge and understanding of the etiology of dental caries.

The proteolytic theory
By Gottlieb and Gottlieb.
a/c to this theory,
the organic or protein elements of tooth (not the inorganic constituents of enamel ) are the initial pathways of invasion by microorganisms;
And, caries is essentially a proteolytic process , in which the microorganisms invade the organic pathways and destroy them while advancing through them by forming acids.
Hence certain structures of enamel having high organic material composition, like enamel lamellae and enamel rod sheaths, could serve as a pathway for microorganism invasion through the enamel .

Drawbacks of this theory
1)It couldn’t provide sufficient evidences to support the claim that the initial attack on enamel is proteolytic;
2)also experimental studies have shown the occurrence of caries even in the absence of proteolytic microorganisms
However , this theory is still helpful in explaining the progression of a more advanced carious lesion.

Current concept of caries etiology

a/c to the current concept , caries occurs as a result of interplay between 3 primary factors:
the host,
the microorganism,
the substrate.
In addition a fourth factor- the time , is also taken into consideration.

(TO BE CONTD/...)