Abdul 8ahman lauzl

0918489
DENTAL CARIES

Definition of dental caries:
Dental caries is an inIectious disease oI the calciIied tissues oI the teeth, characterized by
demineralization oI the inorganic portion and destruction oI the organic portion oI the tooth. It is a
common chronic disease that leads to pain and disability across all age groups. The inIection results in
loss oI tooth minerals that begin on the outer surIace oI the tooth and can progress through the dentin
to the pulp, ultimately compromising the vitality oI the tooth. II leIt untreated, it may lead to pain,
inIection and even tooth loss. During the past Iew decades, changes have been observed not only in
the prevalence oI dental caries, but also in the distribution and pattern oI the disease in the population.
The first visible sign of dental caries on enamel surface
The earliest visible sign oI enamel caries is the white spot lesion`.The active lesion is matt and Ieels
rough iI a sharp probe is gently drawn across it.

A beautiIul series oI scanning electron microscope (SEM) studies, carried out in orthodontic patients
due to have a premolar extracted, showed what was happening at the tooth surIace. Bands allowing
plaque to accumulate beneath them were put onto teeth. AIter 4 weeks they were removed and the
classic matt, chalky white spots had Iormed. The SEM pictures showed that aIter 4 weeks oI plaque
accumulation there was marked dissolution oI surIace enamel. This partly explains why the surIace is
matt. Regular plaque control was now re-established and 3 weeks later the surIace was hard and shiny
and the white spot less obvious. Now the SEM pictures showed abrasion oI the surIace: the eroded
area had been partly removed.

Arrest of lesions
Inactive or arrested white spot lesions have a shiny surIace and may be brown in colour, having
picked up exogenous stains Irom the mouth. These lesions cannot be detected by gently drawing a
sharp probe across them because they Ieel the same as normal enamel. Histologically these lesions
show wide, well-developed dark zones at the Iront oI the lesion within the body oI the lesion and at
the surIace oI the lesion.

It is very important to realize that the carious process can be arrested by simple clinical measures such
as improved plaque control with a fuoride toothpaste and altered diet. It is thereIore the clinician`s
responsibility to detect enamel caries in its earliest Iorm by careIul visual inspection oI teeth aIter
cleaning and drying. The clinician can now help the patient tip the balance in Iavour oI arrest rather
than progression oI lesions. An arrested white spot is more resistant to acid attack than sound enamel.
It may be regarded as scar tissue and should not be attacked with a dental drill.

ACIDOGENIC THEORY
W.D Miller was the Iirst well known scientistand investigator oI dental caries andpublished his results
in 1882.According to him dental decay is achemoparasitic process. It is a two stage process there
isdecalciIication oI the enamel which alsoresults in the destruction oI the dentin. inthe second stage
there is dissolution oI thesoItened residue oI the enamel and dentin.
In the Iirst stage there is destruction isdone by the acid attack where as thedissolution oI the residue is
carried bythe proteolytic action oI the bacteria's This whole process is supported by thepresence oI
carbohydratesmicroorganisms and dental plaque


PROTEOLYTIC THEORY
There has been evidence that the organicportion oI the tooth plays an important rolein the
development oI dental caries. There are some enamel structure which aremade oI the organic material
such enamellamelle and enamel rods. These structure prove to be the path waysIor the advancing
microorganisms.

It has been established that enamel contains 0.56 oI organic matter oI which 0.18 is keratin
and0.17 is a soluble protein.Microorganisms invade the enamel lamelle and theacid produced by
the bacteria's causes damage tothe organic pathways in advance. The production oI the yellowish
pigment producedby the proteolytic bacteria`s the presence oI thispigment was only possible in the
presence oIdietary carbohydrates.

PROTEOLYSISCHELATION THEORY
Some oI the minor Ilaws oI theacidogenic and the proteolytic theorywere addressed in the
proteolysischelation theory.This theory was put Iorward by Schatzand his co-workers .

CHELATION
It is a process in which there iscomplexing oI the metal ions to Iormcomplex substance
throughcoordinate covalent bond whichresults in poorly dissociated /or weakly ionized compound
.Chelation is independent oI the PH oI the medium.The bacteria`s attack on the surIace oI the
enamelthis is initiated by keratinolytic microorganisms thisresult in the breakdown oI the protein
chieIlykeratin and results in the Iormation oI solublechelates which decalciIy enamel even at neutral
PH.Mucopolysaccarides may also act as secondarychelators.

As early as 1954, Orland et al demonstrated that, although germ-Iree animals do not develop caries,
even with Irequent sugar intake, all animals in the group rapidly develop carious lesions when human
cariogenic bacteria (mutans streptococci) are introduced in the mouth oI one animal. SpeciIic bacteria
(acidogenic and aciduric) that colonize the tooth surIaces are recognized as etiologic Iactors in dental
caries. Frequent intake oI Iermentable carbohydrates, such as sugar, is regarded only as an external
(environmental) modiIying risk Iactor or prognostic risk Iactor. In the presence oI these and
other external risk Iactors, the outcome may be modiIied by internal host Iactors, such as the quality
oI the teeth and the amount and quality oI saliva:
1. MicroIlora: acidogenic bacteria that colonize the tooth surIace.
2. Host: quantity and quality oI saliva, the quality oI the tooth, etc.
3. Diet: intake oI Iermentable carbohydrates, especially sucrose, but also starch.
4. Time: total exposure time to inorganic acids produced by the bacteria oI the dental plaque.

Classification of Dental Caries

A.Black's classiIication:

Class I-Cavities on the occlusal surIace oI Premolars and Molars..

Class I-Cavities on Occlusal two-thirds oI the Facial and Lingual surIaces oI Molars..

Class I-Cavities on Lingual surIace oI Maxillary Incisors..

Class II-Cavities on the Proximal oI Posterior teeth..

Class III-Cavities on the Proximal surIaces on the Anterior teeth that do not involve the incisal angle..







Class IV-Cavities on the Proximal surIaces oI the Anterior teeth that do involve the incisal edge..

Class v-Cavities on the Gingival third oI the Facial or Lingual surIace oI all teeth..

Class VI-Cavities on the incisal edge oI the Anterior teeth or Occlusal cusp heights oI Posterior teeth..


B(1).According to location on individual teeth:

a)Pit and Fissure caries

b)Smmoth surIace caries


B(2).According to rapidity oI the process:

a)Acute dental caries

b)Chronic dental caries

B(3).A)Primary (Virgin)caries

B)Secondary (Recurrent)caries


Exams and Tests
Most cavities are discovered in the early stages during routine checkups. The surIace oI the tooth may
be soIt when probed with a sharp instrument. Pain may not be present until the advanced stages oI
tooth decay. Dental x-rays may show some cavities beIore they are visible to the eye.

Histopathology of caries
Enamel is composed oI 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 Iollowing 4 histological zones oI an enamel lesion clearly explains the development oI enamel
caries:
zone 1: translucent zone
zone 2: dark zone
zone 3: body zone
zone 4: surIace zone
zone 1: translucent zone
- deepest zone representing the advancing Iront oI enamel
caries.
- in this zone , pores or voids Iorm along the enamel prism(rod) boundaries (due to easy H ion
penetration)
- it appears structureless when perIused with quinolone solution (having reIractive index comparable
to that oI enamel) and seen with polarized light (hence translucent)


zone 2: dark zone
- next deepest zone
- presence oI many tiny pores block light transmission. These smaller air or vapor-Iilled pores make
the regiion opaque.
- loss Io crystalline structure suggesting the process oI demineralization and remineralization in this
zone.

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

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

AIter the involving the enamel, the carious lesion progresses to the dentinal structure.
Caries advancement in dentin proceeds through 3 stages-
1) demineralization oI dentin (by weak organic acids)
2) degeneration and
dissolution oI organic material oI dentin , mainly collagen
Iibers (type I)
3) bacterial invasion aIter the loss oI structural integrity caused
due to 1) and 2).



During the development oI dentinal caries, clinically 5 diIIerent zones oI 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: inIected dentin

Histologically , 5 zones oI early dentinal caries progression can be seen (listed pulpally to occlusally):
zone 1: zone oI Iatty degeneration oI Tomes` Iibers
zone 2: zone oI dentinal sclerosis
zone 3: zone oI decalciIication oI dentin
zone 4: zone oI microbial invasion
zone 5: zone oI decomposed dentin

Prevention
Oral hygiene is necessary to prevent cavities. This consists oI regular proIessional cleaning (every 6
months), brushing at least twice a day, and Ilossing at least daily. X-rays may be taken yearly to detect
possible cavity development in high risk areas oI the mouth.
Chewy, sticky Ioods (such as dried Iruit or candy) are best iI eaten as part oI a meal rather than as a
snack. II possible, brush the teeth or rinse the mouth with water aIter eating these Ioods. Minimize
snacking, which creates a constant supply oI acid in the mouth. Avoid constant sipping oI sugary
drinks or Irequent sucking on candy and mints.
Dental sealants can prevent cavities. Sealants are thin plastic-like coating applied to the chewing
surIaces oI the molars. This coating prevents the accumulation oI plaque in the deep grooves on these
vulnerable surIaces. Sealants are usually applied on the teeth oI children, shortly aIter the molars
erupt. Older people may also beneIit Irom the use oI tooth sealants.
Fluoride is oIten recommended to protect against dental caries. It has been demonstrated that people
who ingest Iluoride in their drinking water or by Iluoride supplements have Iewer dental caries.
Fluoride ingested when the teeth are developing is incorporated into the structure oI the enamel and
protects it against the action oI acids.
Topical Iluoride is also recommended to protect the surIace oI the teeth. This may include a Iluoride
toothpaste or mouthwash. Many dentists include application oI topical Iluoride solutions (applied to a
localized area oI the teeth) as part oI routine visits.