incipient caries notes2-1

8/6/2019 Incipient Caries Notes2-1

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Dent 430 (Week 2)Dr. Seghi

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Topics for Today

Caries Trends

Role of Plaque in caries process

Incipient Caries

Clinical detection and preventive treatments

INTRODUCTION AND DEFINITIONS

Dental Caries (tooth decay)

-One of the most chronic diseases in the world-Increased with refined sugar-Peaked in the 1970s and 1980s-Has declined with applications of fluoride

(toothpaste, fluoridated water)Trends

-The major decline in caries in developed countries has occurred more in the upper andmiddle classes

-80% of caries resides in 20% of the population (rural areas and lower socioeconomicstatus)-Worldwide similar trendsCost to society

-In 1986 Loesche described caries and periodontal disease as perhaps the mostexpensive infections that most individuals have to contend with during a lifetime (withperhaps the exception of HIV infection)-$56 billion cost for dental care in United States in 1999-Only 40-50% of population regularly seeks dental care services

EPIDEMIOLOGY OF CARIES- (prevalence of disease in a population))

DMFis most common measure of caries

DMF=decayed, missing and filled (This is a cumulative number)MF component are historic markers as indicators of past diseaseD component is measure of active disease

Changing patterns affect the nature of dental practiceExamples:

In USA decline of caries in children-more sealantsaging population in US- expect more root caries, more non carious lesions from

wear and attritionincrease in caries in lower socioeconomic areas-processed food is cheap/calorie

Third world countries- 3-5 fold increase in caries paradox its the wealthier populationsaffected

DEFINITIONS OF CARIES AND PLAQUE

Dental Caries - an infectious microbiological disease of the teeth that results in alocalized dissolution and destruction of the calcified tissues.


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Caries activity as evidenced by demineralization and loss of tooth structure ishighly variable from one patient to another, and therefore the course ofindividual lesions are not always predictable. (can be rapid in some individualsand slow in others)

Carious lesions only occur under a mass of bacteria (dental plaque) capable of

producing a sufficiently acidic environment to demineralize tooth structure.

Plaque-a gelatinous mass ofbacteria andextracellular matrix adhering to the toothsurfaceCaries Pathogenesis (cellular events and reactions which occur to cause the disease)

Bacteria metabolize carbohydratesOrganic acids are the metabolic byproduct produced by the bacteriaAcids dissolve crystallites make up the tooth.Process is cyclic-

periods of high activity which result in dissolutionperiods of low activity when salivary fluids can remineralize crystallites

Teeth, bacteria, and carbohydrate source are all required to produce decay

Evidence for the role of bacteria in the genesis (origin) of caries:1. Teeth free from infection with bacteria (germ free animals or unerupted teeth inhumans) do not develop caries.2. Antibiotics are effective in reducing caries in animals and humans.3. Oral bacteria can demineralize enamel in vitro and produce lesions similar to naturalcaries.4. Specific bacteria can be isolated from plaque over carious lesions.

Which bacteria?

-It is difficult to establish a direct cause and effect between a specific bacteria and carieswhen there are some 200-300 species of bacteria, yeast, and even protozoa that areindigenous to the oral cavity-It has been established that a relatively small group of bacteria are associated withcaries.Mutans Streptococcus MS (a group that consists of eight serotypes, labeled athrough h) and lactobacilliappear to be the primary organisms associated with caries inman.-Streptococcus mutans and lactobacillican produce great amounts of acid (acidogenic),are tolerant of an acid environment (aciduric), are vigorously stimulated by sucrose, andappear to be the primary organisms which cause caries (cariogenic).-Streptococcus mutans are most strongly associated with the onset of caries andlactobacilliare associated with active progression of cavitated lesions.

HYPOTHESIS CONCERNING THE ETIOLOGY OF CARIES

-Non-specific Plaque Hypothesis

-Specific Plaque Hypothesis


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Non-specific plaque hypothesis

-(Older more widely accepted theory) all plaque contains pathogens that can cause caries,therefore all plaque accumulations are considered pathogenic.-This theory requires a therapeutic goal of removing all plaque in a patients mouth.-Total plaque control is not a realistic goal.

Specific plaque hypothesis

-(more recent theory) provides a new scientific basis for the treatment of caries that hasradically altered treatment-Plaque is assumed to be pathogenic only when signs of disease are clinically present.-Treatment is to eliminate or suppress cariogenic plaque and replace them with pathogen-free plaque. Subsequent plaque will be dominated by noncariogenic bacteria, and willhave little to no cariogenic potential.

ECOLOGICAL BASIS OF CARIESEcology-the science of interactions between organisms and their environment

(how organisms are affected by their environment)

The development and growth ofplaque on teeth is a normal phenomenon. Certainenvironmental (ecologic) conditions can dictate the overall pathogenicity of the plaquecommunity.

ETIOLOGIC AGENT OF CARIES: PATHOGENIC BACTERIAL PLAQUE

How does plaque form?

Stages of plaque succession:

Non-Pathogenic Bacterial Plaque

1. Acquired Pellicle

After professional tooth cleaning all organic material and bacteria are removed.Within two hours a relatively cell-free organic layer is formed on the surface of the tooth(pellicle). The pellicle is formed from selective precipitation of salivary proteins. Theseproteins are both basic and acidic and adsorb to phosphate and calcium ions, respectively.Some of these proteins include: lysozyme, albumin, and immunoglobulins A (IgA) andG (IgG). Some are biologically active and serve to protect the tooth through variousmeans (i.e. lethal to some organisms, slows bacterial growth, etc.)

Function of pellicle

1. protect enamel

2. reduce friction between the teeth

3. possible matrix for remineralization

2. Early stages of recolonization(12-24hrs)(S. sanguis, Actinomyces viscosus,Actinomyces naeslundii, and Peptostreptococcus)

The accumulation of plaque on teeth is a highly organized and ordered sequence ofevents. Free-floating organisms are cleared from the mouth by salivary flow and


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swallowing. Only very specialized organisms (primarily streptococci) are able to adhereto mucosa and teeth due to special receptors for adhesion to the tooth and the ability toproduce a sticky matrix. Pioneering bacteria colonize the pellicle and spread laterally.Early stages are generally lacking in pathogenic potential, and are primarily aerobiccommunities. It is easily removed with brushing.

Potential Pathogenic Bacterial Plaque

3. Late stage colonization(1-3 days)Bacteria that originally could not adhere to tooth surface (filamentous and spiralbacteria) now attach to pre-existing matlike covering of bacteria and grow vertically.Mature plaque is primarily anaerobic. Bacteria get nutrients from saliva whosecomposition is influenced by the patients diet. The bacteria reduces (as opposed tooxidizes) the nutrients to weak organic acids (lactic acid), amines, and alcohols throughthe glycolic pathway. In cariogenic plaque with high numbers ofstrep mutans orlactobacilli almost all sucrose is metabolized to acid and pH can drop to 5.0-5.5 for up to1 hr after exposure. This process can lead to demineralization of enamel and begin the

caries process.

Plaque Community Structure

Plaque dominated with S mutans are cariogenic while plaques dominated with S sanguisare notDietary sucrose (particularly frequency) provides a selective advantage to theestablishment of Mutans Strep (MS)Plaque from carious lesions of patients with rampant caries have 22-40% MS of thecultivable flora.

Oral (non-tooth) Habitats other places bacteria and plaque hang outOral mucosa- does not have a chance to build-up very thick layersDorsum of tongue-in some patients can be significant- can be related to halitosis

FACTORS THAT SERVE AS ECOLOGICAL DETERMINANTS

Host Diet

Tooth habitats for pathogenic plaque and caries initiation

Oral Hygiene

Available Nutrients

Sulcular Fluids

Saliva

bacterial clearance,direct antibacterial activity,buffer capacityRemineralization

Host Diet: High frequency of sucrose exposure may be the single most importantfactor that leads to the development of cariogenic plaque.


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TOOTH HABITATS FOR PATHOGENIC PLAQUE AND CARIES INITIATION:

Caries Locations:

1. Pits and Fissures- deep, tight, crevices/holes in enamel where developmental lobesfailed to coalesce, partially or completely; have the highest prevalence of caries. Theshape of the pits and fissures of a tooth contribute to their caries susceptibility (provide

excellent mechanical shelter for organisms). Sealing the pits and fissures shortly aftereruption may be the single most important event in providing resistance to caries.

2. Smooth Enamel Surfaces: second most susceptible areas to cariesa. proximal enamel surfaces-immediately gingival to the proximal contact area

is the second most susceptible areas of caries. Rough surfaces and poor soft tissuearchitecture can contribute to plaque accumulations

b. gingival aspects of facial or lingual surfaces - plaque accumulates gingival tothe height of contour of the tooth and can be cariogenic if left undisturbed.

3. Root surfaces- often more rapid progression, often asymptomatic, closer to the pulp,

and more difficult to treat, and is associated with aging population where there may bedecreased salivary flow, poor oral hygiene, and some root surface exposure. A. viscosus(Actinomyces viscosus) is the most likely organism responsible for initiation of rootcaries and is one of the early colonizers that is not associated with cariogenicity onenamel surfaces.

Oral Hygiene: Recolonization of the tooth after tooth cleaning is called secondarysuccession. This process is more rapid than primary succession since all the residentbacteria are still in the mouth. Cleaning does not destroy bacteria it only loosens them.Brushing and flossing disrupts the plaque. MSand strepsanguis are competitivecolonizers, better to have ssanguis than MSsincesanguis are not cariogenic.Available Nutrients:

Catabolic (breakdown) vs anabolic (buildup) processesPioneering organisms have simple nutritional needs. MSand S Sanguis can produce alltheir amino acids from normal salivary proteins.Supragingival plaque- good oxygen supply, salivary supply, sucrose this areafacilitates aerobes such as streptococci. Sucrose in the diet favors MSSubgingival plaque- low oxygen, low carbohydrate supply, few salivary proteins-strongselection for anaerobes

Sulcular Fluids:

Serous exudates that is produced from the sulcular epitheliumContains IgG immunoglobulins which can kill bacteria. The bacteria that are able toreside under the gums rarely cause caries.

Saliva: the importance of saliva in maintaining normal oral flora is dramaticallyillustrated in patients with xerostomia (dry mouth) These patients can exhibit rapiddestruction of the teeth.


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bacterial clearance, Flushing effect removes all non adherent bacteria. Flushingmost effective during mastication oral stimulation (Pavlovs dogs)-chewing gum- largevolumes of saliva dilute and buffer acids.

direct antibacterial activity, -saliva produces antimicrobial salivaryproteins(lysozymes, agglutinins etc) not part of the immune system (no memory) but

effective at attacking pathogens to some extent.buffer capacity-ability to raise pHismostly due to bicarbonate ion but urea andsialins (tetrapeptides) hydrolyse to ammonia causing pH rise also.

Remineralization- when local pH is above 5.5 remineralization can occur.Saliva saturated with calcium and phosphate ions. Remineralized caries is calledarrested caries. Arrested caries on the dentinal surface is eburnated dentin.

Clinical appearance Arrested (remineralized) lesion-usually brown or black spots-discolored from trapped impurities-usually more resistant to further attack

-do not restore unless esthetically objectionable

PATHOPHYSIOLOGY OF CARIES

-plaque accumulates-pH at plaque-tooth interface drops from plaque metabolism-only strep mutan and lactobacillus rich plaque can sufficiently lower pH-exposure to sucrose rapidly metabolized to lactic acid-acid results in pH drop (5.5 critical) which dissolves mineral-frequency of sucrose exposure critical

Incipient Caries: Caries limited to enamel

-intact surface-subsurface porosity due to demineralization (up to 25% pores in body of lesion)-demineralization of enamel occurs in pH range 5.0-5.5 (lower pH demineralizes surface)Cavitation: a break in the surface contour of enamel

CLINICAL CHARACTERISTICS OF CARIES

Clinical sites for caries initiation

Developmental pits and fissures

Smooth enamel surfaces

Root surfaces

Progression of pit and fissure caries

-initial demineralization on lateral walls of fissures: follows enamel rods,site appears smaller than actual lesion (lab today)-inverted V shape in enamel

affect lots of dentin due to shape


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V shaped from DEJ toward pulp

-spreading laterally at DEJ (DEJ extremely weak to caries resistance)-narrow entrance and wider area of progression and DEJ involvement

Progression of smooth surface caries

-V shaped progression with apex of V toward DEJwide area of surface involvement, narrow area of progression toward the DEJV shaped from DEJ toward pulp (same as above)

-spreading laterally at DEJ (DEJ extremely weak to caries resistance)

Progression of root caries

U shaped cross sectionProgresses more rapidly (less mineral, easier to attach to)Increase in prevalence with increase population aging

Progression of Carious Lesions-Variable: depends on location and conditions in mouth-Progression from incipient caries to clinical caries (cavitation) on smooth surfaces isestimated 18 mo. + or 6 mo. (1956 ref.). Current estimates: 4-6 years-Peak rates for new lesions are 3 years after the tooth erupts-Caries rates in healthy individuals usually slowpit and fissure caries more rapid than smooth surface

HISTOPATHOLOGY OF CARIES

Enamel Caries

Histology of Enamel

-structure of enamel allows it to act as molecular sieve-Prism boundaries and striae of Retzius are organic rich areas that allow ions to diffuse

(*striae of Retzius: variations in structure and mineralization of enamel as aresult of the successive apposition of enamel in discrete increments; can beconsidered growth rings)

There are inherent spaces in the organic prism boundaries in enamel to providesufficient porosity to allow movement of water and small ions through the enamel.The molecular sieve-like behavior of enamel explains why even incipient caries ofenamel can produce an effect on the pulp even before bacteria have penetrated. Itcan also explain how dentin can be demineralized and greatly affected before theenamel has been cavitated.

caries preferentially attackcores of enamel rodsdiffusion along prism boundaries


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more permeable striae of Retzius* (organic rich) which promotes lateralspreading and undermining of adjacent enamel

Clinical Characteristics of Incipient Caries-earliest evidence of caries is white spots

-chalky white, opaque areas revealed when desiccated (dried)-white spots disappear when wet (differentiated from hypocalcification)-can be seen radiographically on proximal surfaces

Remineraliztion of incipient caries (arrested caries)

-incipient caries can remineralize-non-cavitated enamel lesions retain most of the organic framework-etched crystallites are reactive and serve as nucleating agents for remineralization-saliva saturated with Ca and PO4 ions help remineralize-fluoride aids this process-appear as brown or black spots

Zones of incipient lesionsZone 1- translucent zone: (Name of zone refers to appearance of structures when

perfused with quinolin solution and examined with polarized light.) Deepest zone, andrepresents the advancing front of the lesion. In this zone, pores or voids form along theenamel prism (rod) boundaries, presumably due to the ease of hydrogen ion penetrationduring the carious process. Pore volume is 1% (10 times more porous than normalenamel).

Zone 2- dark zone: does not transmit polarized light. Pores are too small forquinoline to fill therefore it is opaque to light. Is made up of 2-4% pore volume. Size ofthis zone probably an indicator of amount of remineralization that has occurred recently.

Zone 3- body of lesion: the largest portion of the incipient lesion. It contains verylarge pores, and the highest porosity ranging from 5% at the periphery to 25% at thecenter. The striae of Retzius are areas of relatively high porosity and act as the initiallocation of demineralization. The interprismatic areas and striae of Retzius are organicrich and provide the path for acid penetration and the dissolution pattern that occurs. Rod(prism) cores are preferentially attacked. Bacteria may be present in this zone if porositysize is great enough.

Zone 4- surface zone: relatively unaffected by the caries attack. It has less than5% pore volume but a radiopacity similar to unaffected enamel. This surface reforms ifremoved (such as through polishing). Thus the intact surface over incipient caries(surface zone) seems to be a phenomenon related to the caries process, and also serves asa barrier to bacterial penetration. As an enamel lesion progresses, conical-shaped defectsin this zone can be seen by SEM, and may be the first sites where bacteria gain entry intoa carious lesion. Caries can be arrested at this stage.

incipient caries notes2-1

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