Dental Caries (I):The Etiology

Early Theories of Caries Etiology1.Worms: before B. C.2.Humors: four elemental fluids of the body3.Vital theory: analogous to bone gangrene 4.Chemical theory: inorganic acids corroded

enamel 5. Parasitic or septic theory: filamentous parasite6.Chemo-parasitic theory: blend of two theories7.Proteolytic theory: organic or protein elements

are the initial pathway of invasion by microorgasms

8.Proteolysis-chelation theory9.Other theories: bacteria take up phosphate

Current Concepts of Caries Etiology

Dental caries is a multi-factorial disease1) The Host : the saliva and teeth2) The microflora : S. mutans3) The substrate or diet : fermentable

carbohydrate4) Time: the duration of teeth attacked by

organic acid

Development of Dental Caries

food + dental plaque acid (carbohydrate) (bacteria)

production demineralization of

teeth cavities dental caries

Host factors: The Saliva and Dental Caries• Effect of desalivation on incidence and

extent of caries in animals• Decreased salivary flow and caries in

humans (Xerostomia)

Critical pH=5.5

The pH at which any particular saliva ceases to be saturated with calcium and phosphate is referred to as the critical pH; below this value the inorganic material of the tooth may dissolve.

PROTEIN AND NONPROTEIN CONSTITUENTS OF SALIVA

AlbuminAmmoniaAmylaesBicarbonateBeta-glucuronidaseCalcium ChlorideCreatinine CystatinsEsterasesFluorideGlucoseGustin

Nonspecific buffersPhosphatasesPhosphorusPotassiumProline–rich proteinsRibonucleasesSerum proteins (trace)Sialic acidSodiumStatherinSulfatesThiocyanateUric acid

HistatinsIgA (sIgA)IgGIgMIodineKallikreinLactoferrinLactoperoxidaseLDHLysozymeMagnesiumMucinsNitrogen

FUNCTIONS OF SALIVA

Function LubricationAntimicrobial

Remineralization

CleansingBufferingDigestive

Mucosal Integrity

Salivary Components Involved Mucins, Proline-rich proteins,H2OLactoferrin, Lysozyme, Lactoperoxidase, sIgA, Mucins, Histatins, Cystatins, Proline-rich proteinsCa, P, Pi, Statherin, Anionic proline-rich proteinsH2OHCO3, PO4Amylase, Lipase, Proteases, H2O, Nucleases, Mucins, Gustin

H2O, Electrolytes, Mucins

Salivary Composition and Caries

1. Salivary buffers– Bicarbonate (HCO3

- / H2CO3)– Phosphate (HPO4= / H2PO4

-)– Urea → Ammonia

2. Antibacterial factors– Lysozyme– Lactoferrin– Salivary peroxidase system– Immunoglobulins

Immunization :

The animal studies of immunization with killed cariogenic bacteria, can be divided into two groups:

1) Those involving stimulation of secretory IgA, either directly, locally, or indirectly via the gut.

2) Those involving stimulation of serum antibodies, which reach the plaque via the gingival sulcus.

Route of Immunization

1. Local immunity (direct stimulation of slgA)2. Oral immunization (indirect stimulation of

slgA)3. Stimulation of serum antibodies (IgG)4. Passive immunity

Host Factors : Tooth

Morphology : pit and fissure areas

Host factors : Tooth

Susceptibility to caries between different tooth types:

mandibular first molars (occlusal > buccal > mesial > distal > lingual) > mand. 1st molars > max. 1st molars >mand. & max. 2nd molars > 2nd premolars > max. incisors > first premolars > mand. incisors and canines

Arch form:

Irregularities in arch form, crowding and overlapping of teeth favor the development of caries lesions.

Tooth composition :

Enamel surface is more caries-resistant than the subsurface (more minerals).

Partially fluoridated hydroxyapatite: more resistant to demineralization

Bacterial Role in Caries EtiologyS. mutans has been suggested to play an

important role in the initiation of dental caries in human. Its cariogenicity is due to the bacterium’s capacity to produce various acid from dietary sugars with a resultant demineralization of tooth enamel.

Root Caries

Roots caries :1.Starts at or near the cementoenamel junction2. Appears only after cementum is exposed3. The frequency of involvement of a specific

surface being dependent upon the tooth type 4. Attack mand. molars most frequently, followed

by mand. premolars and max. canines, the mand. incisors being the least frequently involved teeth

5. Usually does not involve enamel

Bacterial interactions︰Veillonella alcalescens

Lactate → propionic and acetic acids

Bacteriocins are active against some strains of the same or closely related species, but not against unrelated species.

Bacterial interactions

Substrate: Diet and Dental Caries

Foods and beverages serve as substrates for fermentation by the plaque microflora, which form organic acids, thereby promoting demineralization of tooth structure and directly affecting caries activity. Patients with rampant caries frequently include sucrose–containing foods in their diet.

Influence of diet on the caries process：Epidemiology observation1.Sucrose consumption and prevalence of

caries2. Strict dietary control –> less caries3. Hereditary fructose intolerance (HFI) –>

less caries4. Bakeries and candy factories –> high

caries

Sucrose ←→ Caries

• Determining sucrose content• Cariogenicity of sucrose and other

carbohydrates

Adhesiveness of foods：

Sticky or adhesive forms sucrose –containing foods, which can maintain high sugar levels in the mouth, were more cariogenic than those forms that were rapidly cleared.

Ranking the foods：Cariogenic potential of foodstuffs

Using currently accepted methods (primarily plaque pH measurements and animal testing), foods can be categorized as having: 1. No cariogenic potential2. Low cariogenic potential3. High cariogenic potential

Conclusion ：

The physical form, consistency, and frequency of intake, as well as the sugar content, are major determinants of the cariogenicity of foods.

Other Dietary Components and Dental Caries：A) Phosphates：possible caries–preventive

agents1. Reduce the rate of dissolution of the

hydroxyapatite2. Redeposit calcium phosphate, particularly in

areas of enamel that have been partially demineralized

3. Buffer organic acids4. Desorb proteins from the enamel surface,

thereby modifying the acquired pellicle

B) Lipids：Medium chain fatty acids (C8 – C12) and their salts have antibacterial properties at low pH

C) Trace elements:

Dental Caries (II):Prevention

Caries prevention is based upon attempts to 1) Increase the resistance of the host：

fluoride therapy, occlusal sealants, immunization.

2) Lower the numbers of microorganisms in contact with the tooth：plaque control

3) Modify the substrate by selecting non-cariogenic foodstuffs

4) Reduce the frequency of intake sucrose

Approaches for controlling dental cariesFissure sealants– Occlusal pits and fissures︰ the most

caries-prone areas– For children

Fluoride– Water supply︰reduce the incidence of

caries by at least 50%

– Optimum concentration︰1 ppm

– Table salt, milk, toothpastes

– Mouthwash, gel, and vanish for topical

use

– Tablets︰ systemic effect

– Tea, fish bone

Fluoride– 90% absorbed by gut into blood– 50% rapidly excreted by kidneys – deposit in skeletal tissue, un-erupted

enamel, oral fluid– Fluoro-apatite resists acid– Inhibit bacteria acid production (enolase)

Dental Caries Vaccine

– Oral cavity has all the components for an immune response

– Formalin– or heat– killed S. mutans injected into the region of the salivary glands in primates

– Salive︰ sIgA, crevicular fluid︰IgG– Drawback︰ form Ab-Ag complex associates

with cardiac muscle– Damage to heart and kidney– Four protein in the cell well

Mechanisms︰unclear

– inhibiting the colonization– enhance phagocytosis by PMN– interfere bacterial metabolism

Question to anti – caries vaccine

– Non-life-threatening disease– Efficacy of vaccine in humans – Specificity: many species of bacteria can

cause caries– Cross reaction with heart tissue– Other approaches can control dental

caries

Antibiotics and antmicrobial agents

– Long-term antibiotic therapy → low caries experience

– May develop resistant-organisms– Overgrowth by opportunistic pathogens

Chlorhexidine

– inhibitory to fungi and wide range of Gram(+) and Gram(-) oral bacteria

– High concentration︰bactericidal, damaging the cell membrane

– low concentration︰bacteriostatic, reduce acid production by dental plaque

– S. mutans︰sensitive, S. snaguis︰resistance

Artificial sweetenersTwo typesI. Intense type︰– sweeter than sucrose– saccharin, cyclanates– carcinogenesis in rodents

II. Bulk agents

– not as sweet as sucrose– mannitol and sorbitol︰metabolized by S.

mutans slowly, six carbon cyclical structure

– xylitol︰not metabolize by plaque bacteria, five carbon cyclical structure

Reduce the frequency of Intake sucrose

Caries activity tests

Thank you for your attention