Dent 430 (Week 2) Dr.

Seghi 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 and middle classes -80% of caries resides in 20% of the population (rural areas and lower socioeconomic status) -Worldwide similar trends Cost to society -In 1986 Loesche described caries and periodontal disease as perhaps the most expensive infections that most individuals have to contend with during a lifetime (with perhaps 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)) DMF is most common measure of caries DMF=decayed, missing and filled (This is a cumulative number) MF component are historic markers as indicators of past disease D component is measure of active disease Changing patterns affect the nature of dental practice Examples: In USA decline of caries in children-more sealants aging population in US- expect more root caries, more non carious lesions from wear and attrition increase in caries in lower socioeconomic areas-processed food is cheap/calorie Third world countries- 3-5 fold increase in caries paradox its the wealthier populations affected DEFINITIONS OF CARIES AND PLAQUE Dental Caries - an infectious microbiological disease of the teeth that results in a localized dissolution and destruction of the calcified tissues.

Dent 430 (Week 2) Dr. Seghi Caries activity as evidenced by demineralization and loss of tooth structure is highly variable from one patient to another, and therefore the course of individual lesions are not always predictable. (can be rapid in some individuals and 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 of bacteria and extracellular matrix adhering to the tooth surface Caries Pathogenesis (cellular events and reactions which occur to cause the disease) Bacteria metabolize carbohydrates Organic acids are the metabolic byproduct produced by the bacteria Acids dissolve crystallites make up the tooth. Process is cyclicperiods of high activity which result in dissolution periods 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 in humans) 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 natural caries. 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 caries when there are some 200-300 species of bacteria, yeast, and even protozoa that are indigenous to the oral cavity -It has been established that a relatively small group of bacteria are associated with caries. Mutans Streptococcus MS (a group that consists of eight serotypes, labeled a through h) and lactobacilli appear to be the primary organisms associated with caries in man. -Streptococcus mutans and lactobacilli can produce great amounts of acid (acidogenic), are tolerant of an acid environment (aciduric), are vigorously stimulated by sucrose, and appear to be the primary organisms which cause caries (cariogenic). -Streptococcus mutans are most strongly associated with the onset of caries and lactobacilli are associated with active progression of cavitated lesions.

HYPOTHESIS CONCERNING THE ETIOLOGY OF CARIES -Non-specific Plaque Hypothesis -Specific Plaque Hypothesis

Dent 430 (Week 2) Dr. Seghi 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 has radically 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 pathogenfree plaque. Subsequent plaque will be dominated by noncariogenic bacteria, and will have little to no cariogenic potential. ECOLOGICAL BASIS OF CARIES Ecology-the science of interactions between organisms and their environment (how organisms are affected by their environment) The development and growth of plaque on teeth is a normal phenomenon. Certain environmental (ecologic) conditions can dictate the overall pathogenicity of the plaque community. 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. These proteins are both basic and acidic and adsorb to phosphate and calcium ions, respectively. Some of these proteins include: lysozyme, albumin, and immunoglobulins A (IgA) and G (IgG). Some are biologically active and serve to protect the tooth through various means (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 of events. Free-floating organisms are cleared from the mouth by salivary flow and

Dent 430 (Week 2) Dr. Seghi swallowing. Only very specialized organisms (primarily streptococci) are able to adhere to mucosa and teeth due to special receptors for adhesion to the tooth and the ability to produce a sticky matrix. Pioneering bacteria colonize the pellicle and spread laterally. Early stages are generally lacking in pathogenic potential, and are primarily aerobic communities. 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 spiral bacteria) now attach to pre-existing matlike covering of bacteria and grow vertically. Mature plaque is primarily anaerobic. Bacteria get nutrients from saliva whose composition is influenced by the patients diet. The bacteria reduces (as opposed to oxidizes) the nutrients to weak organic acids (lactic acid), amines, and alcohols through the glycolic pathway. In cariogenic plaque with high numbers of strep mutans or lactobacilli almost all sucrose is metabolized to acid and pH can drop to 5.0-5.5 for up to 1 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 sanguis are not Dietary sucrose (particularly frequency) provides a selective advantage to the establishment of Mutans Strep (MS) Plaque from carious lesions of patients with rampant caries have 22-40% MS of the cultivable flora. Oral (non-tooth) Habitats other places bacteria and plaque hang out Oral mucosa- does not have a chance to build-up very thick layers Dorsum 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 capacity Remineralization Host Diet: High frequency of sucrose exposure may be the single most important factor that leads to the development of cariogenic plaque.

Dent 430 (Week 2) Dr. Seghi TOOTH HABITATS FOR PATHOGENIC PLAQUE AND CARIES INITIATION: Caries Locations: 1. Pits and Fissures- deep, tight, crevices/holes in enamel where developmental lobes failed to coalesce, partially or completely; have the highest prevalence of caries. The shape 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 after eruption may be the single most important event in providing resistance to caries. 2. Smooth Enamel Surfaces: second most susceptible areas to caries a. proximal enamel surfaces-immediately gingival to the proximal contact area is the second most susceptible areas of caries. Rough surfaces and poor soft tissue architecture can contribute to plaque accumulations b. gingival aspects of facial or lingual surfaces - plaque accumulates gingival to the 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 be decreased salivary flow, poor oral hygiene, and some root surface exposure. A. viscosus (Actinomyces viscosus) is the most likely organism responsible for initiation of root caries and is one of the early colonizers that is not associated with cariogenicity on enamel surfaces. Oral Hygiene: Recolonization of the tooth after tooth cleaning is called secondary succession. This process is more rapid than primary succession since all the resident bacteria are still in the mouth. Cleaning does not destroy bacteria it only loosens them. Brushing and flossing disrupts the plaque. MS and strep sanguis are competitive colonizers, better to have s sanguis than MS since sanguis are not cariogenic. Available Nutrients: Catabolic (breakdown) vs anabolic (buildup) processes Pioneering organisms have simple nutritional needs. MS and S Sanguis can produce all their amino acids from normal salivary proteins. Supragingival plaque- good oxygen supply, salivary supply, sucrose this area facilitates aerobes such as streptococci. Sucrose in the diet favors MS Subgingival plaque- low oxygen, low carbohydrate supply, few salivary proteins-strong selection for anaerobes Sulcular Fluids: Serous exudates that is produced from the sulcular epithelium Contains IgG immunoglobulins which can kill bacteria. The bacteria that are able to reside under the gums rarely cause caries. Saliva: the importance of saliva in maintaining normal oral flora is dramatically illustrated in patients with xerostomia (dry mouth) These patients can exhibit rapid destruction of the teeth.

Dent 430 (Week 2) Dr. Seghi bacterial clearance, Flushing effect removes all non adherent bacteria. Flushing most effective during mastication oral stimulation (Pavlovs dogs)-chewing gum- large volumes of saliva dilute and buffer acids. direct antibacterial activity, -saliva produces antimicrobial salivary proteins(lysozymes, agglutinins etc) not part of the immune system (no memory) but effective at attacking pathogens to some extent. buffer capacity-ability to raise pH is mostly due to bicarbonate ion but urea and sialins (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 called arrested 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

Dent 430 (Week 2) Dr. Seghi 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 DEJ wide area of surface involvement, narrow area of progression toward the DEJ V 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 section Progresses 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 is estimated 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 slow pit 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 a result of the successive apposition of enamel in discrete increments; can be considered growth rings) There are inherent spaces in the organic prism boundaries in enamel to provide sufficient porosity to allow movement of water and small ions through the enamel. The molecular sieve-like behavior of enamel explains why even incipient caries of enamel can produce an effect on the pulp even before bacteria have penetrated. It can also explain how dentin can be demineralized and greatly affected before the enamel has been cavitated. caries preferentially attack cores of enamel rods diffusion along prism boundaries

Dent 430 (Week 2) Dr. Seghi more permeable striae of Retzius* (organic rich) which promotes lateral spreading 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 lesions Zone 1- translucent zone: (Name of zone refers to appearance of structures when perfused with quinolin solution and examined with polarized light.) Deepest zone, and represents the advancing front of the lesion. In this zone, pores or voids form along the enamel prism (rod) boundaries, presumably due to the ease of hydrogen ion penetration during the carious process. Pore volume is 1% (10 times more porous than normal enamel). Zone 2- dark zone: does not transmit polarized light. Pores are too small for quinoline to fill therefore it is opaque to light. Is made up of 2-4% pore volume. Size of this 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 very large pores, and the highest porosity ranging from 5% at the periphery to 25% at the center. The striae of Retzius are areas of relatively high porosity and act as the initial location of demineralization. The interprismatic areas and striae of Retzius are organic rich 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 porosity size is great enough. Zone 4- surface zone: relatively unaffected by the caries attack. It has less than 5% pore volume but a radiopacity similar to unaffected enamel. This surface reforms if removed (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 as a barrier to bacterial penetration. As an enamel lesion progresses, conical-shaped defects in this zone can be seen by SEM, and may be the first sites where bacteria gain entry into a carious lesion. Caries can be arrested at this stage.