Cariogenicity of lactobacilliAccording to the specific plaque hypothesis, some strains of lactobacilli are considered to be major caries pathogens along with S mutans and S sobrinus. Lactobacilli are acidogenic and even more aciduric than MS. Mutans streptococci are strongly correlated to the etiology of initial enamel and root surface lesions, because they can adhere to and colonize the tooth surfaces. Lactobacilli are more dependent on retentive sites for heavy colonization: Mutans streptococci are regarded as the pioneers, followed by lactobacilli in the succession toward more cariogenic plaque.

Methods of samplingAs mentioned earlier, the correlation between salivary MS counts and the number of MS-colonized tooth surfaces is relatively good (Lindquist et al, 1989), and simple salivary sampling methods are a more convenient and realistic means of assessing the severity of MS infection than sampling from individual tooth surfaces. Laboratory methods. Saliva is collected, mixed with a proper transport medium, and forwarded to a microbiologic laboratory. After incubation using a selective medium, mutans colonies are counted and the results are expressed as the number of colonyforming units per milliliter of saliva.

Cariogenicity of mutans streptococciMutans streptococci are acidogenic as well as aciduric and can adhere to tooth surfaces (Gibbons et al, 1986). Mutans streptococci can produce extracellular and intracellular polysaccharides from sucrose. Intracellular polysaccharides in particular can be degraded during periods of low nutrient supply, indicating that these polysaccharides increase the virulence of some MS species (S mutans and S sobrinus).  Because the microbial ecology of the mouth is highly complex, strains of the same species could vary considerably in virulence (Bowden and Edwardsson, 1994).

Role of Specific Cariogenic MicrofloraIntroductionMicroorganisms implicated in the etiology of dental caries must be acidogenic as well as aciduric. To initiate carious lesions in enamel, the microorganisms must also be able to colonize the tooth surface and survive in competition with less harmful species, forming biofilms¾the so-called dental plaque. As early as 1960, Fitzgerald and Keyes showed that certain microorganisms isolated from human dental plaque, when inoculated in germ-free rodents on a high-sucrose diet, resulted in the spread of rampant caries.

Strategies for prevention and control of caries based on plaque ecology hypothesis According to the plaque ecology hypothesis, low pH (less than 5) will promote overgrowth of aciduric microorganisms, such as the cariogenic mutans streptococci and lactobacilli, at the expense of less acid-tolerant plaque microorganisms, such as S oralis, which are associated with healthy tooth surfaces.  Therefore the treatment strategy would be to increase plaque pH and thereby promote reestablishment of the harmless normal microflora of the tooth surfaces.

Effect of plaque ecologyOwing to differences in local environmental conditions, the microflora of mucosal surfaces differs in composition from that of dental plaque. Similarly, the plaque microflora varies in composition at distinct anatomic sites on the tooth ¾ for example, in fissures, on approximal surfaces, and in the gingival crevice. The resident microflora of a site acts as part of the host defenses by preventing colonization by exogenous (and often pathogenic) microorganisms.

Colonization of microenvironmentsThe oral cavity consists of several major and minor compartments, each constituting a separate microenvironment not easily affected by major events in the oral cavity. Examples of major compartments are the tongue, the oral mucosa, and the tonsils. The different approximal tooth surfaces, occlusal fissures, and gingival sulci are regarded as minor compartments. A specific area that supports a bacterial flora is termed a habitat. The flora of a habitat develops through a series of stages, collectively called colonization.

Role of the Oral EnvironmentIntroductionIn certain aspects, the oral cavity may be regarded as a single microbial ecosystem. A major regulatory factor is the flow rate of saliva, which decreases to almost 0.0 mL/min during sleep, is approximately 0.4 mL/min at rest, and increases to 2.0 mL/min after stimulation. Although saliva is not a good medium for supporting the growth of many bacteria, 1.0 mL of whole saliva may contain more than 200 million microorganisms, representing more than 300 different species.

Rate of accumulation (Plaque Formation Rate Index)The quantity of plaque that forms on clean tooth surfaces during a given time represents the net result of interactions among etiologic factors, many internal and external risk indicators and risk factors, and protective factors:· The total oral bacterial population· The quality of the oral bacterial flora· The anatomy and surface morphology of the dentition· The wettability and surface tension of the tooth surfaces· The salivary secretion rate and other properties of saliva· The intake of fermentable carbohydrates· The mobility of the tongue and lips· The exposure to chewing forces and abrasion from foods· The eruption stage of the teeth· The degree of gingival inflammation and volume of gingival exudate· The individual oral hygiene habits· The use of fluorides and other preventive products, such as chemical plaque control agents This observation has been the rationale for the development of the Plaque Formation Rate Index (PFRI) by Axelsson (1989, 1991).

Measurement of plaqueAmount of accumulationSeveral indices for recording supragingival plaque have been developed. The two most frequently used are the Plaque Index (PI), developed by Silness and Loe (1964), and O'Leary's Plaque Index (O'Leary et al, 1972).The Silness and Loe Plaque Index has a four-point scale:· Score 0 = The tooth surface is clean.· Score 1 = The tooth surface appears clean, but dental plaque can be removed from the gingival third with a sharp explorer.

According to Dawes et al (1963), dental plaque is "the soft tenacious material found on tooth surfaces which is not readily removed by rinsing with water." It is estimated that 1 mm3 of dental plaque, weighing about 1 mg, will contain more than 200 million bacteria. Other microorganisms, such as mycoplasma, "yeasts," and protozoa, also occur in mature plaque; sticky polysaccharides and other products form the so-called plaque matrix, which constitutes 10% to 40% by volume of the supragingival plaque.

Dental caries is an infectious, transmissible disease. As early as 1954, Orland et al demonstrated that, although germ-free animals do not develop caries, even with frequent sugar intake, all animals in the group rapidly develop carious lesions when human cariogenic bacteria (mutans streptococci) are introduced in the mouth of one animal. Specific bacteria (acidogenic and aciduric) that colonize the tooth surfaces are recognized as etiologic factors in dental caries. Frequent intake of fermentable carbohydrates, such as sugar, is regarded only as an external (environmental) modifying risk factor or prognostic risk factor.

INTRODUCTIONMOSTinjuries to the deciduous dentition take place between the ages of 1 and 5years when children are first learning to walk, and then, later, to run. climb,and play adventurously. The thinner and more elastic alveolar bone found inthese young children means that teeth are more likely to be displaced, withassociated fracture of the alveolar plate, than suffer crown or root fracture.In older children (4-6 years}, physiological resorption, which reduces the rootlength, also predisposes to displacement or avulsion.

Extra-oral examinationA general appraisal of the patient should he made andany cuts, abrasions, swelling, or bruises noted. A simple line drawing can bemade in the notes to indicate the extent of the injuries. The bony borders ofthe maxilla and mandible should be palpated, unless the extent of any oedemamakes this too uncomfortable. In addition, the tcmporo-mandibular joint shouldbe palpated during opening and closing of the mouth. Deviation on opening andclosing may indicate a fracture of the neck of the condyle on one side.

Introduction: In this study, we compared the pretreatment conditions, treatment characteristics, and orthodontic outcomes of 3 groups of subjects selected for the American Board of Orthodontics (ABO) phase III clinical examination. One group was selected retrospectively by graduating residents just before their graduation. The 2 prospective groups were treated at separate institutions. The students at 1 institution were not aware that these patients would be potential ABO cases (prospective, blinded), but the students at the second institution were aware that these subjects would serve as their pool of potential patients for the ABO examination (prospective, unblinded).

Excrete following groups of dental cements: zinc phosphate (phosphate cement, visfat-cement, unifas), bactericidal (phosphate cement with silver, dioksivisfat), zinc-ksidevgenolovye cements (kariosan), silicate (silitsin, silitsin-2, alyumodent) , silikofosfatnye (silidont, laktodont, infantid) polikarboksilatnye cements, cements GLASS. Zinc phosphate cements. Produced powder and liquid in the kit. Components powder: 75-90% zinc oxide (ensuring adhesion), with the addition of silicon oxide (giving, hyaline, transparent, light), magnesium oxide (an increase of ductility and mechanical strength), calcium oxide (acceleration setting, viscosity), aluminum oxide (an increase of strength and hardness).

Dental caries Dental caries - a pathological process, which appears after the dentition, at which the demineralization and softening of dental hard tissues with the subsequent formation of a defect in the form of cavities. Caries classified: 1. Dental caries in the stage of the spot. 2. Surface caries. 3. The average caries. 4. Deep caries. Physical methods of diagnosis, treatment and prevention are applied at different stages of the caries process. When caries in the stage of applying patches reminera-ization of dental tissues using electrophoresis of calcium fluoride.

Applied in cases where the treatment of caries and its complications is not complete in one visit. Some of these materials are also used as a bandage to cover medicines and as insulating pads under permanent seal. Requirements for the materials: to be malleable, easily introduced into the cavity and the implications, do not inactivate the drug substance does not dissolve in the oral fluid, to ensure hermeticism for the requisite period (not less than 2 weeks). Zinc sulfate cements. Artificial dentin.

The final stage of treatment of dental caries and its complications is filling. Sealing - a replacement of the defect of dental hard tissues special material for the restoration of anatomic form and function of the tooth. The ideal filling material must have the following physicochemical requirements: - Do not shrink; - Provide the ideal marginal adaptation; - Have a high adhesion in a wet environment; - Have a coefficient of thermal expansion close to the coefficient of thermal expansion of the tooth; - Have a hardness close to the hardness of enamel; - Must be chemically resistant, that is not dissolve in the oral fluid;  - To resist abrasion; - Do not have the abrasive properties, that is itself does not cause abrasion of antagonist;  - Curing time should be the maximum in time to form, seal.

Localized juvenile periodontitis (LJP) - an inflammatory disease that occurs in adolescents aged 10-13 years. For this form of periodontitis is characterized by intensive periodontal lesion with rapidly progressive destruction of bone tissue. High intensity of destruction at the beginning of the disease may continue to slow down or disappear. The clinical picture of localized Youth periodontitis periodontal lesions characterized mainly in the central incisors or first molars, usually located symmetrically.