Aerobic and anaerobic plaque bacteria. cariogenic bacteria

AT oral cavity There are more than 700 different types of bacteria in the human body. But only some of them are the cause of caries, these are the so-called cariogenic microorganisms: Streptococcus, Lactobacillus, Actinomyces and others.

Bacteria accumulate on the surface of the teeth in the form of a dense film. They easily convert nutrients into organic acid. It is acids that destroy our enamel, wash out calcium and fluoride. Due to the loss of "building materials", a carious hole is formed.

How do cariogenic bacteria work?

Cariogenic bacteria feed on carbohydrates, namely carbohydrate microparticles of food that remain in the oral cavity after each meal. As a result, the fermentation process starts.

In the process of fermentation, metabolic products are released in the form of organic acids: lactic, formic, butyric, etc.

With prolonged contact of the acid with the enamel, the structure of the dental tissue is disturbed, microspaces appear on the surface, and a cavity forms over time.

The main causative agents of caries

streptococci

These include Streptococcus mutans, Streptococcus sanguis, Streptococcus mitis, etc. These are acid-forming bacteria that are characterized by anaerobic fermentation. The main causative agent of caries is Str. Mutans. Its content in plaque is about 90% of the total number of microorganisms.

A direct relationship between Streptococcus mutans and enamel destruction has been proven. The more of these bacteria, the more intensively the carious process develops. In addition, scientists found that Str. mutans does not belong to the normal (natural) microflora of the oral cavity, the pathogen is transmitted from person to person through saliva.

specially processed coconut oil inhibits the growth of most strains of Streptococcus bacteria. They are what cause caries.

— Dentist (@A_B_Larina) September 14, 2012

lactobacilli

In the process of life, bacteria produce lactic acid, but they themselves are resistant to it. The number of lactobacilli in dental plaque is small. However, the concentration of these microbes increases significantly with the formation of a carious cavity.

actinomycetes

Most often, Actinomyces israelii and Actinomyces naeslundi live in the mouth, occupying an intermediate position between lower fungi and bacteria. They are considered less dangerous because they slightly increase the acidity on the tooth surface. However, a species such as Aktinomyces viscosus can provoke the development of dental root caries.

How to neutralize the bacteria that causes cavities

The main ways to combat the microflora of caries:

Mechanical removal of dental plaques.

This is a daily cleaning of the teeth at home, as well as the removal of tartar by the ultrasonic method in the dentist's office.

Rinsing the mouth with antiseptic solutions.

Chlorhexidine solution 0.2% has bactericidal properties. When exposed to it, the number of harmful bacteria in plaque is reduced by 80%, and in saliva - by 55%.

Use of toothpastes containing fluoride.

Fluorine and its salts (ZnF2, CuF2) inhibit the action of enzymes, that is, they slow down the process of fermentation and acid formation in the mouth.

Use of preparations containing xylitol: pastes, chewing gums.

Xylitol (Xylitol) is a naturally occurring sweet alcohol. It inhibits the growth of cariogenic bacteria, improving the microflora of the oral cavity.

Replacing sucrose with other carbohydrates.

It is for sucrose, or, more simply, sugar, that an active fermentation process is characteristic. Therefore, you should limit the use of sweets or replace them, for example, with fruits.

Prevention of caries with bacteria

It turns out that bacteria can be not only enemies, but also allies in the fight against caries. Researchers in Japan came to this unexpected conclusion.

Microorganisms Streptococcus salivarius live on the surface of the tongue and oral mucosa. Their main mission is to prevent their "bad relatives" - Str. mutans.

The bottom line is that "good" Streptococcus salivarius secrete special enzymes (protein molecules) that block the formation of elastic films of Streptococcus mutans. The name of this enzyme is FruA, it accelerates the breakdown of polysaccharides (carbohydrates), which are responsible for the stability of this very film.

Who knows, perhaps in the near future, FruA protein will be added to toothpastes to effectively prevent caries.

Cariogenic bacteria are the main pests of our teeth. But far from the only ones. Be sure to read other caries risk factors.

Plaque- this is an accumulation on the surface of the tooth of colonizing microorganisms, leukocytes and desquamated cells of the epithelium of the oral mucosa; other non-specific components of plaque can be: erythrocytes, crystal-like particles (fragments of cement, incipient calcification of food inclusions), food debris (for example, muscle fibers). WHO interprets the concept of "plaque" as a specific, but very different in structure, formation on the surface of the tooth, which is generated by the accumulation and growth of microbes.

Plaque classification:

• supragingival plaque - localized above the gum;
• subgingival plaque - localized (spread) in the gingival groove.

Plaque can be white, green or brown.

The quantitative and qualitative composition of the microbial flora of dental plaque is variable, since the species composition of microorganisms of the normal microflora of the oral cavity is also diverse. With poor oral hygiene, the number of rod-shaped organisms and gram-negative cocci increases. Most of the microorganisms in plaque are acid-forming. A typical reaction in response to the activity of plaque is damage to the connective epithelium of the gums and inflammation. Microbiological studies have identified several types of bacteria that are most common in dental plaque in periodontal diseases, including Actinomyces, Actinobacillus, Bacteroides, Eikinella corrodens, Fusobacterium, Vielonella recta, Treponema denticola, Capnocytophaga. Streptococci and staphylococci also play a significant role in the development of gingival inflammation.

The duration of plaque maturation ranges from 1 to 3 days. Ripe plaque causes irritation of periodontal tissues due to microorganisms and their exo- and endotoxins, which leads to inflammation of the gums:

• exotoxins - derivatives of gram-positive bacteria - are common in the oral cavity and do not cause inflammation;
• endotoxins - derivatives of gram-negative bacteria - are resistant to temperature effects, exhibit an aggressive effect at the location of plaque, stimulate the formation of antibodies, cause an increase in capillary permeability, disrupt cell metabolism, and lead to inflammation and hemorrhagic necrosis of the gums.

Clinical forms pathologies caused by dental plaque: tartar, caries, gingivitis, periodontitis(including periodontitis).

Diagnostics. To detect plaque, it is enough to examine the patient's mouth using a dental kit. However, plaque is more clearly detected when using solutions of erythrosin, basic fuchsin, Bismarck brown fluorescent Na and other harmless dyes, as well as special tablets (tablets stain invisible plaque on the teeth and gums, and help to correct the brushing technique; depending on the color of the tablet dental plaque turns blue or red). To quantify plaque, various hygiene indices are also used, of which the Greens-Vermillion “simplified oral hygiene index” and its various modifications, the PHP oral hygiene efficiency index (Podshadley, Haley, 1968), the PLJ index (Silness, Loe , 1967), etc.

Prevention. A lot of work is being done to study the means of preventing and removing deposits on the teeth. Under natural conditions in the oral cavity, there are certain mechanisms of self-cleaning, which are traced with the help of isotopes. Self-cleaning depends on the nature of the food, but in general, self-cleaning (according to the Nordic Dietary Service) is questionable and, if it exists, is at least ineffective in removing bacterial plaque. Looking for effective means, counteracting the deposition of plaque. There are attempts to use antibiotics, bactericidal substances, urea, drugs that reduce surface tension, enzymes, especially proteolytic, exchange resins.

Much depends on the correctness of brushing your teeth with a toothbrush: it must be used for its intended purpose twice a day: after breakfast or immediately after sleep, if you do not have breakfast, and before bedtime; you can brush your teeth more often if there are any problems in the oral cavity (for example, a tendency to bad breath or caries is very active); brush their teeth for less than three minutes; when brushing your teeth, you need to conditionally divide each jaw into several zones and clean each zone separately, systematically - do not spread plaque throughout your mouth in a fit of zeal; sweeping movements when cleaning the front and inner surfaces of the teeth: from the gums up on the lower jaw and from the gums down on the upper jaw, the chewing surface of the teeth is cleaned in a circular motion, after brushing, the toothbrush should be washed with soap and dried; it is necessary to change the toothbrush once every two to three months, it is necessary to buy brushes made of artificial bristles of medium hardness (unless the dentist has prescribed something else); electric and ultrasonic brushes are very common - the opinions of doctors about them differ. At least once a day before going to bed, you should brush your teeth with floss (dental floss). For even better cleaning of the interdental spaces and the gingival ridge surrounding the tooth, small food particles are also used. irrigators, which impulsively deliver a thin stream of water with which you can wash everything. Well prevents the formation of dental plaque cleaning the tongue with a toothbrush or a special spoon movements from distant areas to the tip; clean the back of the tongue and side surfaces.

Goals: consider the role of microflora in the occurrence and development of caries; to study the methods of sampling material for caries

Know: factors contributing to the development of caries, the main representatives of cariogenic microflora, microbiological methods for studying the microflora in caries.

Be able to: take material to follow the microflora in caries.

Topic justification: microorganisms - residents of the oral cavity play a leading role in the development of caries.

Questions for self-preparation:

1. dental plaque, mechanism of its formation, localization. The role of glucan biosynthesis. Adhesion and coaggregation of bacteria.

2. Factors contributing to the development of caries. The role of resident microflora in the development of caries.

3. Microflora in caries. Cariogenic types of microbes: microaerophilic streptococci, actinomycetes, lactobacilli.

4. Pathogenesis of caries. Significance of glycolysis and phosphorylation processes in enamel demineralization. Prevention of caries.

5. Microbiological methods for studying the microflora in caries and its complications.

PLAN

Program:

1. Mechanism of formation and localization of dental plaque.

2. Factors contributing to the development of caries. The pathogenesis of caries.

3. Study of the properties of cariogenic types of microorganisms and their antagonists.

4. Prevention of caries.

5. Study of microflora in caries.

Demonstration:

1. Smears of cariogenic species of microorganisms and their antagonists.

Assignment to students:

1. Disassemble the mechanisms of formation of dental plaque and draw in the form of a diagram.

2. Microscopically and sketch smears of cariogenic types of microorganisms and their antagonists.

Information material

Dental plaque, mechanism of its formation, localization. The role of glycan biosynthesis. Adhesion and coaggregation of bacteria.

The key mechanism for the onset and development of dental caries and periodontal disease is the formation of dental plaque. Dental plaque is an accumulation of bacteria in a matrix of organic substances, mainly proteins and polysaccharides, brought there by saliva and produced by the microorganisms themselves. Plaques are firmly attached to the surface of the teeth. Dental plaque is usually the result of structural changes in plaque, consisting of microorganisms with a slight inclusion of structureless organic matter and having a porous structure. Accumulation in the plaque of the end products of vital activity of microorganisms and mineral salts slows down the diffusion of saliva and liquid food components inside, as the porosity of plaque disappears. As a result, a new formation appears - a dental plaque, which can only be removed by force and then not completely.

In the formation of plaque, several mechanisms can be distinguished:

1. Precipitation of salivary glycoproteins forming a pellicle followed by specific adhesion of bacteria to it.

2. Adhesion to the enamel of epithelial cells invaded by bacteria, followed by the growth of microcolonies.

3. Precipitation of extracellular glycans produced by S. mutans and S. sanguis.

4. Agglutination of bacteria with antibodies followed by fixation on the enamel surface. Bacteria in plaque are known to be coated with immunoglobulins A and G.

The process of plaque formation begins after brushing the teeth with the formation of a film on the surface of the tooth - pellicles. The main components of this film are components of saliva and gingival fluid, such as proteins (albumin, lysozyme), glycoproteins (lactoferrin, IgA, IgG, amylase), phosphoproteins and lipids. Bacteria colonize the pellicle during the first 2-4 hours after brushing. During this period, bacteria are weakly bound to the film and can be quickly removed by saliva flow. After primary colonization, the most active species begin to grow rapidly, forming microcolonies that invade the extracellular matrix. Then the process of aggregation of bacteria begins and at this stage the constituent components of saliva are connected. The first microbial cells settle in the recesses on the tooth surface, where they multiply, after which they first fill all the recesses, and then move on to the smooth surface of the tooth. Many microbial cells themselves are unable to attach directly to the enamel, but can settle on the surface of other bacteria that have already adhered, i.e. the process of coaggregation is underway. Another example of coaggregation is the synthesis of extracellular polysaccharides (glycans) by S. mutans from sucrose. These polysaccharides promote the attachment of bacteria to the tooth enamel and stabilize the plaque matrix.

The adhesion process is very fast: after 5 minutes the number of bacterial cells per 1 cm 2 increases from 10 3 to 10 5 -10 6 . Subsequently, the adhesion rate decreases and remains stable for about 8 hours. After 1-2 days, the number of attached bacteria increases again, reaching a concentration of 10 7 -10 8 . Thus, dental plaque is formed. Further, its structural changes and the formation of dental plaque occur.

If we talk about changing the microbial population, then the primary bacteria that attach to the tooth enamel are streptococci (S. mutans and S. sanguis). In addition, Neisseria, Veillonella, and diphtheroids take part in the formation of the "early" dental plaque (the first 1-4 hours). Further, the so-called dynamic plaque is formed (up to 4-5 days). At this stage, there is a decrease in the number of gram-positive cocci and an increase in gram-negative rods (leptotrichia, fusobacteria) and cocci (veillonella). On the 6-7th day, a mature dental plaque is formed. It is dominated by anaerobic rods. Such a plaque can remain balanced for a long time.

Thus, during the formation of plaques, aerobic and facultative anaerobic microflora predominates, which sharply reduces the redox potential in this area, thereby creating conditions for the development of strict anaerobes.

There are supra- and subgingival plaques. The former are pathogenetic in the development of dental caries, the latter in the development of pathological processes in the periodontium. The microflora of plaques on the teeth of the upper and mandible differs in composition: streptococci and lactobacilli more often live on the plaques of the teeth of the upper jaw, veillonella and filamentous bacteria live on the plaques of the lower jaw. Actinomycetes are isolated from plaques on both jaws in the same amount. It is possible that such a distribution of microflora is explained by different pH values ​​of the medium.

The concept of biofilms

Currently, scientists treat dental plaque as a biofilm. Biofilms (biological films) are organized communities of microbes that form under fluid conditions.

The main properties of a biofilm are: 1) an interacting community different types microorganisms (microbiocenosis) with symbiotic relationships; 2) microorganisms form microcolonies; 3) microcolonies are surrounded by a protective matrix permeated with channels through which nutrients, waste products, enzymes, metabolites and oxygen circulate; 4) microorganisms have a certain communication system; 5) microorganisms in the biofilm are resistant to antibiotics, antimicrobial agents, and the reaction of the host organism.

Studies conducted on biofilms in their natural state have shown that there are large differences in the behavior of bacteria in laboratory culture and in their natural ecosystems. For example, a bacterium in a biofilm produces substances that it does not produce when in culture. In addition, the matrix surrounding the microcolonies serves as a protective barrier. This helps to understand why antimicrobials are general action, and applied topically, do not always give successful results, even when they are aimed at a specific type of microorganism.

Dental caries (caries - decay) is one of the most urgent problems of dentistry. According to the definition of the scientific group of the World Health Organization, dental caries is "a localized pathological process of external origin, which entails softening of the hard tissues of the tooth and the formation of a cavity." This is an ancient disease, however, in prehistoric times, caries was rare and began to spread rapidly during the industrial development of society. Currently, it affects a large part of the population in Europe, America and other regions.

In most developing countries, tooth decay is less common, and often even in people old age All teeth are in good health. But in these countries, in the last 10-20 years, the problem of caries has sharply worsened, especially where more carbohydrates and refined foods have been consumed in food. Thus, caries has assumed a pandemic spread.

Currently, 414 theories of the origin of caries are known, but not a single researcher has yet been able to answer all the questions of the etiology and pathogenesis of this complex pathology. There are two directions in explaining the origin of caries.

Proponents of the first direction attach paramount importance in the occurrence of the carious process to exogenous influences, in particular to the microbial factor. They consider caries as an infectious process in which enamel and dentin are destroyed by the waste products of microorganisms that are part of the resident microflora of the oral cavity. For the first time such a point of view was expressed in 1884 by Miller and was called the "acid theory of caries". Miller believed that the root cause of caries is enamel decalcification with the help of acids synthesized by lactobacilli and streptococci as a result of lactic acid fermentation. After that, the proteolytic enzymes of bacteria are able to dissolve the organic matter of the tissues of the teeth. Teeth placed in broth cultures of bacteria producing lactic and other organic acids were subjected to gradual dissolution. This seemed to confirm the "acid theory of caries." However, later it was found that the histological changes in carious teeth in the oral cavity have nothing to do with the changes that were observed when acid-forming bacteria were exposed to the dead tissues of the extracted tooth. The main provisions of Miller's theory have been criticized.

After that, a new, so-called bacterial theory was put forward. The search for a specific causative agent of caries began. This role was assigned to many microbes inhabiting the oral cavity. For a long time, the idea of ​​the predominant role in caries of the entire genus Lactobacillus, regardless of their species, was established. At the same time, facts were accumulating that testified to the predominant importance of streptococci. Most researchers argued that caries is an endogenous infection of mixed etiology and occurs as a result of the introduction of various microorganisms into the enamel. However, bacterial theories cannot answer why not all people develop caries, nor can they explain the pathogenesis of caries.

Supporters of the second direction deny the role of acids in the origin of caries. American scientists Schatz and Martin put forward the so-called chelation theory. Its essence lies in the fact that tooth decay is caused by the effects of bacterial proteolytic enzymes on the organic components of enamel. The inorganic substance is destroyed by complexons, which are formed in the oral cavity by combining the organic substance of the enamel with metal ions (primarily with calcium ions). The authors of this theory believe that oral acids even protect teeth from caries. However, the chelation theory also has significant shortcomings. One of the main ones is that the authors studied caries from purely biochemical positions and did not take into account clinical manifestations pathological process.

The current theories of dental caries cannot satisfy either theorists or practitioners, so scientists continue to create theories and concepts that shed some light on individual links in the development of the carious process.

There are a large number of factors that are important in the occurrence of caries. These factors can have both general and local action. These include social conditions, profession, constitutional features of the body, disorders of the trophic functions of oral tissues, etc.

For the occurrence of a carious process, the following conditions are necessary: ​​1) the presence of a sufficiently large amount of carbohydrates in food; 2) the presence of microorganisms in the oral cavity; 3) contact of carbohydrates and microorganisms with dental tissues.

Experimental data provide clear evidence of the role of carbohydrates in the occurrence of caries. All cariogenic diets contain more than 50% sucrose. When the diet of experimental animals contains smaller amounts of carbohydrates, the carious process either does not occur, or it develops slowly.

There is no disagreement about the role of carbohydrates in the occurrence of caries, however, there are various interpretations of the mechanism of action of carbohydrates. Some researchers (AE Sharpenak, 1964) believe that excessive intake of carbohydrates causes metabolic disorders in the body, and this in turn leads to the development of caries. However, it has now been proven that without contact of teeth with carbohydrates, the carious process does not occur. So, with the introduction of a cariogenic diet to experimental animals directly into the stomach through the fistula, the development of a carious process was not observed.

Indisputable evidence of the role of microorganisms in the occurrence of caries should be considered the studies of Orlandi (1955), carried out on microbial-free rats. The animals were divided into three groups: the first was on a cariogenic diet, the second received a normal diet, the third (control) group was kept under normal conditions on a cariogenic diet. Non-sterile (control) rats rapidly developed carious lesions, while they were absent in gnotobiotes. When all animals were transferred to the usual non-sterile conditions, the rats of the first group, which received an excess amount of carbohydrates, developed the same carious lesions as in the control group. In animals of the second group, which were on a normal diet, the teeth remained intact.

These experiments showed that microorganisms by themselves cannot cause caries. However, the high content of carbohydrates in food in the absence of microorganisms also cannot lead to caries. Caries develops under the simultaneous action of both factors.

Thus, the emergence and development of the carious process is influenced by a whole range of external and internal factors. Among the local factors importance attached to microbial plaque on the teeth.

Dental plaque (dental plaque) is an accumulation of colonies of oral microorganisms on the surface of the teeth. The substrate of plaque consists exclusively of microorganisms with minor inclusions of structureless organic matter.

Plaque begins to accumulate within two hours after brushing your teeth. During the first day, coccal flora prevails on the surface of the tooth, after 24 hours - rod-shaped bacteria. Two days later, numerous rods and filamentous bacteria are found in the plaque. The initially formed plaque contains aerobic microorganisms, in a more mature one, anaerobic ones appear along with aerobic ones.

In the formation of plaque, cells of the deflated epithelium play a certain role. They are attached to the surface of the tooth within an hour after it is cleaned. By the end of the day, the number of attached cells increases markedly. It has been established that epithelial cells adsorb microorganisms on their surface.

Dental plaque contains cariogenic microorganisms, of which the most important are Streptococcus mutans, Lactobacillus acidophilus, Actinomyces viscosus. It seems that there is a strong correlation between the presence of S. mutans and the development of caries in certain areas of the enamel. It is found in the places of the most frequent localization of caries (in the area of ​​fissures, on the proximal surfaces of the teeth). Before the development of carious lesions in these areas, S. mutans accounts for 30% of the total microflora.

In the mechanism of caries, the leading role belongs to organic acids produced by microorganisms. It has been proven that during caries on the surface of the enamel under plaque, the pH decreases to 6 - 5.0, which leads to

to enamel demineralization. The acid dissolves the interprismatic substance of the enamel, resulting in the formation of microcavities. They are filled with bacteria, as well as salivary and bacterial proteins. Local changes in pH explain the role of carbohydrates in the occurrence of caries, as well as the effectiveness of local treatment.

Evidence of the participation of microflora in the development of caries are also immunological studies. Thus, in monkeys immunized with S. mutans, within two years after immunization, caries did not develop or occurred to a lesser extent than in non-immunized animals.

There is a certain sequence of penetration of various types of microorganisms into the tissues of a carious tooth. Microbes begin to penetrate the enamel of the affected tooth after the destruction of the structure of all its layers. At the initial lesions of the dentin, microorganisms are found, which, according to their biochemical activity, can be divided into two groups: acid-forming and proteolytic.

Acid-forming bacteria include streptococci, lactic acid bacteria and actinomycetes. All of them are involved in the demineralization of hard tissues of the tooth, since they form a large amount of organic acids.

As the carious process develops, the microflora of the affected tooth becomes more abundant and diverse. All representatives of the resident microflora of the oral cavity, mainly obligate anaerobes, are present in the carious cavity.

With caries, the composition of the entire microflora of the oral cavity changes: the number of strictly anaerobic microorganisms, enterococci, and especially lactic acid bacteria increases.

3.2. Microflora at inflammatory processes in the oral cavity

Depending on the localization, inflammatory processes in the oral cavity can be divided into the following groups:

1) odontogenic inflammation;

2) inflammation of the gum tissue in periodontitis;

3) inflammation of the oral mucosa (gingivitis, stomatitis).

Odontogenic is an inflammatory process associated with the tissues inside and around the tooth.

Etiological factor of inflammatory diseases maxillofacial area in 96-98% of cases, it is an odontogenic infection, i.e., the spread of microorganisms from the tooth cavity with complications of caries into the pulp and periodontium, and then into the alveolar process through multiple holes in the cortical plate of the tooth socket. Much less often, festering periodontal cysts, alveolitis serve as a source of bone tissue infection, and only in 2-4% of cases there is a non-odontogenic infection, i.e., the penetration of microorganisms into the maxillofacial region by hematogenous, lymphogenous or contact routes.

Microflora in pulpitis. Inflammation of the pulp (pulpitis) in the vast majority of cases occurs as a complication of caries. It develops as a result of the combined effect of microbes, their metabolic products and the decay of the organic matter of the dentin.

A healthy pulp is a biological barrier that prevents the penetration of various biologically harmful factors, including microorganisms, into the periodontium. The destruction of the hard tissues of the tooth as a result of the carious process creates conditions for the penetration of microbes into the pulp.

Microbial entry routes may vary. The most common route is from the carious cavity along the dentinal tubules. In this case, the localization of the carious cavity is of no small importance. Carious damage to the cervical and proximal surfaces contributes to the involvement of both the coronal and root pulp in the inflammatory process, while in case of caries of the masticatory surface, the root pulp is not always and immediately affected.

In some cases, microbes can enter the dental pulp from saliva through the dentinal tubules under pressure during impression taking.

Relatively rarely, the infection retrogradely penetrates into the pulp through one of the apical foramina. In this case, a pathological periodontal pocket, osteomyelitic foci, sinusitis or other inflammatory lesions of the maxillofacial region serve as a source of microbial invasion. Hematogenous infection of the pulp can occur only with significant bacteremia. When a small number of microorganisms circulate in the blood, histohematic barriers are insurmountable for bacteria.

Acute pulpitis initially has a focal character and proceeds according to the type of serous inflammation. Most often it is caused by virulent and non-hemolytic streptococci of group D and streptococci that do not have a group C antigen, as well as lactic acid bacteria. Later, in most cases, abscesses form, and there is a rapid purulent fusion of the coronal part of the pulp. During this period, predominantly staphylococci with virulence factors, p-hemolytic streptococci of groups F and G are found.

The rapid death of the pulp is apparently due to the fact that acute inflammation in it proceeds according to the hyperergic type, i.e., the pulp is sensitized by microorganisms and their metabolic products. The experiment showed that in sensitized animals, a small dose of microbes is sufficient to cause a rapidly occurring severe inflammation of the pulp, although the tooth cavity was not opened and the pulp tissue was not traumatically damaged. Reduced phagocytic activity, edema, and other factors in the focus of hyperergic inflammation lead to the rapid spread of the pathological process and the death of the pulp within a few days. In non-sensitized animals, resorption of inflammatory foci is observed.

Acute pulpitis can turn into chronic, and with tissue breakdown, into gangrenous. In the necrotic pulp, anaerobic microorganisms with pronounced proteolytic properties are found in large quantities. These include peptostreptococci, bacteroids, spirochetes, actinomycetes, vibrios. Along with obligate anaerobes, there are facultative anaerobes and microaerophiles - streptococci of group D, p-hemolytic streptococci of groups F and G, pathogenic staphylococci. Putrefactive bacteria can also join - representatives of the unstable microflora of the oral cavity - bacteria from the genus Proteus, closgridia, bacilli. .

Microflora in periodontitis. Periodontium is a complex anatomical formation located between the root of the tooth and the wall of its hole. Depending on the route of infection, apical (from the root canal) and marginal (from the gum pocket) periodontitis are distinguished. Acute serous periodontitis is caused by the action of toxic products coming from the focus of inflammation in the pulp or gums. Purulent inflammation occurs as a result of the penetration of microorganisms into the periodontium.

A characteristic feature of purulent periodontitis is a sharp predominance of streptococcal flora over staphylococcal. In the initial stages of inflammation, green and non-hemolytic streptococci, devoid of the group C antigen, are usually found. If the infection penetrates through the opening of the root canal, then the composition of the microflora is determined by the flora of purulent or gangrenous pulpitis. During the transition of acute periodontitis to chronic periodontitis, anaerobic streptococci (Peptostreptococci) and representatives of other groups of these microorganisms play the main role.

Characteristic of periodontitis is the detection of not individual types of microbes, but their associations. Usually streptococci are isolated along with veillonella, lactobacilli, corynebacteria, yeast-like fungi. In apical granulomas, actinomycetes, bacteroids, fusobacteria, vibrios, spirochetes are found.

In people suffering chronic inflammation periodontium, with the help of skin-allergic tests, a state of hypersensitivity to antigens of streptococci isolated from the focus of inflammation was revealed.

It should be noted that, despite the good vascularization and innervation of periodontal tissues, inflammatory processes in the periodontium tend to have a protracted, chronic course. This, apparently, is due to the auto-allergic mechanism of the development of this disease.

Microflora in odontogenic purulent inflammation (periostitis, osteomyelitis, soft tissue abscesses, phlegmon). With purulent periodontitis, the exudate may not get out through the root canal into the tooth cavity or along the periodontal ligaments into the oral cavity. In this case, the next stage in the development of the inflammatory process will be the resorption of the bone tissue of the socket wall and the release of purulent exudate into the bone marrow spaces, which coincides with the transition of acute periodontitis to acute osteitis. The periosteum of the alveolar process may also be involved in the process. Under adverse conditions, acute purulent osteitis turns into a purulent-necrotic process, i.e., into osteomyelitis. Any disease from the group of acute odontogenic infection can be complicated by abscesses and phlegmon.

The causative agent of acute odontogenic infection in the vast majority of cases is Staphylococcus aureus, or epidermal, staphylococcus aureus. Staphylococci can be found in inflammatory lesions in pure culture or in combination with other coccal flora, such as p-hemolytic streptococcus. The course of phlegmon can be complicated by the penetration of clostridia, the causative agents of anaerobic gas infection, into the tissues. This greatly aggravates the course of the disease and worsens the prognosis.

Osteomyelitis of the jaw bones of a specific origin may occur, caused by actinomycetes, pale treponema, or Mycobacterium tuberculosis.

Syphilitic osteomyelitis is a gummous lesion characteristic of the tertiary period of syphilis.

Tuberculous lesions of the oral cavity, as a rule, are secondary. They can be observed with dissemination of the pathogen by the hematogenous route.

It should be noted that with odontogenic purulent inflammatory processes, generalization of the infectious process may occur (development of septicemia, septicopyemia).

In recent years, the course of acute odontogenic infection has changed: the number of diseases with severe clinical course, the number of life-threatening complications.

The causative agent of actinomycosis. Actinomycosis is a chronic granulomatous purulent lesion of various tissues and organs with tissue infiltration, abscesses and fistulas, usually caused by A. Israelii. The occurrence of diseases is promoted by injuries of the skin and mucous membranes (contusion or fracture of the jaw, surgical interventions, extraction wounds, etc.). Endogenous infection with actinomycetes is most often observed, since these microorganisms are permanent inhabitants of the oral cavity. Exogenous infection may also occur. In this case, actinomycetes vegetating on grasses, cereals, in the soil enter the body. Possible aerogenic infection.

In the oral cavity there are favorite places for the penetration of actinomycetes into the depths of tissues: inflamed gum near the wisdom tooth or near the destroyed roots of the teeth, pathological periodontal pockets, root canals teeth with necrotic pulp, ducts salivary glands, almonds.

For the occurrence of the disease, only the penetration of actinomycetes into the tissues is not enough. An important role is played by the reactivity of the macroorganism, as well as the previous sensitization by the waste products of actinomycetes.

The incubation period of actinomycosis is two to three weeks, but a longer duration is also possible. incubation period- 12 months and more. The disease can proceed acutely, more often chronically and largely depends on the accompanying microflora. There are primary actinomycosis and secondary, associated with the spread of the pathogen from the primary focus. The spread of actinomycetes from the primary focus can be carried out by subcutaneous tissue and through the connective tissue, as well as by the hematogenous route.

The clinical picture of actinomycosis is diverse and is associated with its localization. The appearance of bluish-red, and then purple infiltrates of a dense consistency is characteristic. Small multiple foci of fluctuations are found in the infiltrates, fistulas (fistulas) are formed, from which pus is released. The pus may contain a tissue form of actinomycetes - drusen, which are white or yellowish grains. The druse has a characteristic structure and consists of intertwining threads, along the periphery of the drusen, the threads thicken, forming pear-shaped "flasks". Druses go through several stages in their development. Initially, they look like tender lumps, later they are calcified dense bodies, often not containing a viable pathogen.

Drusen in the body are not formed at all stages of the disease, they are not characteristic of every variety of actinomycetes, and therefore are not always found.

With actinomycosis, as a rule, there is a secondary purulent infection caused by staphylococci, streptococci, anaerobic microorganisms. In the presence of a secondary infection, abscesses form, and without it, granulomas form, with a slight reaction in the surrounding tissues. Associated microorganisms, releasing hyaluronidase, contribute to the spread of the process. The addition of pyogenic flora worsens the course of actinomycosis, exacerbates the process, and changes its clinical picture.

There are several clinical forms actinomycosis. The most common is the maxillofacial form (up to 58% of all cases of actinomycosis). Approximately 20% of cases of actinomycosis of this localization affect the bone tissue, which leads to the occurrence of actinomycotic osteomyelitis.

In addition, actinomycetes can affect the lungs, intestines, liver, spleen, kidneys, and skin.

Actinomycosis is widespread everywhere, men are more often ill. In recent years, there has been a change in the clinic of actinomycosis, which is explained by the widespread use of antibiotics. Typical signs of the disease (density of the infiltrate, fistulas, characteristic coloration) may be absent.

3.3. Microflora in diseases of periodontal tissues

The periodontium is a complex of tissues that have a genetic and functional commonality: periodontium, alveolar bone with periosteum, gums and tooth tissues. Periodontal tissues are constantly exposed to bacterial, thermal and mechanical influences. The integrity of the periodontium is a reliable protection of the body from the action of adverse factors. When the internal environment is disturbed due to local (microbes, toxins, enzymes, trauma, overload, etc.) or general factors (hypovitaminosis, diseases, metabolic disorders, neurotrophic disorders), structural and functional changes in periodontal tissues develop, which leads to reduction of barrier functions and the development of diseases.

Diseases of the tissues surrounding the tooth are among the diseases known since ancient times. With the development of civilization, the prevalence of periodontal disease has increased dramatically. According to the World Health Organization (1978), in most countries, periodontal disease affects approximately 80% of the child population and almost all adults. In people older than 40, periodontal disease is more common than caries.

Periodontal disease is extremely diverse - from short-term reversible gingivitis, which can develop as a result of poor oral hygiene, stress or short-term malnutrition, to acute periodontal abscess and chronic irreversible periodontitis, leading ultimately to loss of tooth function.

Gingivitis. There are several forms of inflammation of the gum tissue, the most common is catarrhal gingivitis. It can be localized (in the region of one or two teeth) or generalized.

Gingivitis is manifested by redness, swelling of the gums, bleeding when brushing your teeth. The etiological factors of gingivitis are diverse. Local factors include tartar, defects in filling and prosthetics, insufficient oral care, etc. The appearance of catarrhal gingivitis can occur with a number of general somatic diseases and hormonal disorders (diseases of cardio-vascular system, gastrointestinal tract, dysfunction of the pituitary gland, thyroid gland).

The mechanism of development of inflammatory phenomena in the tissues of the marginal periodontium is closely related to the violation of tissue and vascular permeability. In essence, the increase in the permeability of connective tissue structures is the main link in the pathogenesis of all periodontal diseases that occur with an inflammatory component.

The leading role in the occurrence of gingivitis belongs to dental plaque. It surrounds the entire tooth, including the junction of enamel with gum tissue. It is customary to distinguish between a plaque above and below the gum.

The plaque contains a large number of microbes - in 1 mg of plaque there are 100-300 million bacterial cells, and the composition of different parts of the plaque within the same tooth and plaques on different teeth is different. In addition to cariogenic microorganisms, the plaque contains bacteria that cause periodontal disease: Actinomyces viscosus, Bacteroides melaninogenicus, Veillonella alcalescens, fusobacteria and spirochetes. The composition of the plaque also includes organic and inorganic substances, which are a good environment for the development and vital activity of microflora. Over time, the concentration of inorganic substances in the dental plaque increases, it is a matrix for the formation of tartar.

With the localization of dental plaque in the cervical region, the gum is subjected to prolonged irritation and chronic intoxication. It has been experimentally proven that with such localization, a plaque can cause not only inflammation of the gums, but also resorption of the alveolar bone.

A supragingival calculus has a significant impact on the state of periodontal tissues. Having a dense consistency, it injures the gum tissue. The resulting inflammation contributes to an even greater formation of dental deposits, which leads to the pressure of tartar on the gums and its subsequent atrophy.

Oral bacteria usually do not penetrate the gum tissue, but bacterial antigens do. The most active in this respect are lipopolysaccharides, dextrans and lipoteichoic acids. They cause local and generalized immune responses, along with this, they also have a destructive effect on tissues, causing damage to blood vessels, the development of inflammation and tissue necrosis. Lipopolysaccharides and other antigens of bacterial origin cause macrophages and leukocytes to secrete enzymes such as collagenase, which may also damage gum tissue. However, the true role of cellular enzymes in tissue damage remains unclear; it is likely that most of the enzymes outside the cells lose their activity.

Against the background of an altered reactivity of the body after illnesses, intoxications, with a deficiency of vitamins, ulcerative gingivitis may develop. In this case, the gingival margin ulcerates, which is accompanied by an increase in temperature, an increase in the submandibular lymph nodes, bad breath.

With ulcerative gingivitis, along with streptococci and staphylococci, fusobacteria and spirochetes are found in large numbers. The presence of fusospirochetosis indicates a violation of the resistance of periodontal tissues to microflora. oral cavity.

MICROFLORA OF PLAQUE

Lecture 4

1. Brief information about the structure of hard tissues of the tooth. 2. Organic membranes covering tooth enamel. 3. The composition of plaque. 4. Dynamics of plaque formation. 5. Factors affecting the formation of plaque. 6. Mechanisms of plaque formation. 7. Physical properties plaque. 8. Microorganisms of plaque. 9. Cariogenicity of dental plaque.

1 . Brief information about the structure of hard tissues of the tooth. The hard part of the tooth consists of enamel, dentin and cementum (Fig. 1).

Dentin makes up the bulk of the tooth. The crowns of the teeth are covered with enamel - the hardest and most durable tissue. human body. The root of a tooth is covered with a thin layer of bone-like tissue called cementum and surrounded by a periosteum through which the tooth is nourished. From the cementum to the periosteum are fibers that form the so-called ligament of the tooth (periodontium), which firmly strengthens the tooth in the jaw. Inside the crown of the tooth there is a cavity filled with loose connective tissue called pulp. This cavity continues in the form of channels into the root of the tooth.

The surface of the enamel is covered with organic shells, as a result of which, when examined in an electron microscope, it has a smooth relief; nevertheless, there are convex and concave areas that correspond to the ends of the prisms (the smallest structural units of enamel are crystals of an apatite-like substance that form enamel prisms). It is in these areas that microorganisms begin to accumulate for the first time or food residues may linger. Even mechanical cleaning of enamel with a toothbrush is not able to completely remove microorganisms from its surface.

Rice. one. Tooth structure:

1 - crown;

2 - root;

5 - dentin;

6 - pulp;

7 - mucous membrane of the gums;

8 - periodontal;

9 - bone tissue;

10 - opening of the root apex.

On the surface of the teeth, one can often observe dental plaque (PL), which is a white soft substance localized in the neck of the tooth and on its entire surface. The pellicle, which lies under the layer of plaque and is a thin organic film, is a structural element of the surface layer of enamel. A pellicle forms on the surface of a tooth after it has erupted. It is believed that it is a derivative of the protein-carbohydrate complexes of saliva. Electron microscopy of the pellicle revealed three layers and feature- jagged edge and write, which are receptacles for bacterial cells. The thickness of the daily pellicle is 2-4 microns. Its amino acid composition is somewhere between that of dental plaque and salivary mucin precipitate. It contains a lot of glutamic acid, alanine and few sulfur-containing amino acids. The pellicle contains a large amount of amino sugars, which are derivatives of the bacterial cell wall. Bacteria are not observed in the pellicle itself, but it contains components of lysed bacteria. Perhaps the formation of pellicle is the initial stage of the appearance of plaque. Another organic shell of the tooth is the cuticle (reduced enamel epithelium), which is lost after the eruption of the tooth and does not play a significant role in the physiology of the tooth in the future. In addition, a thin film of mucin released from saliva covers the mucous membrane of the oral cavity and teeth.

Thus, the following formations are noted on the surface of the tooth enamel:

cuticle (reduced enamel epithelium);

pellicle;

plaque;

food leftovers;

mucin film.

The following scheme for the formation of acquired surface tooth structures has been proposed: after teething, the surface of the enamel is exposed to saliva and microorganisms. As a result of erosive demineralization, ultramicroscopic tubules are formed on the surface of the enamel, which penetrate the enamel to a depth of 1-3 microns. Subsequently, the tubules are filled with an insoluble protein substance. Due to the precipitation of salivary mucoproteins, as well as adhesion and growth, and then destruction of microorganisms, a thicker organic, in varying degrees mineralized pellicle layer.

Due to local conditions, microbes invade these structures and multiply, which leads to the formation of a soft MN. mineral salts are deposited on the colloidal basis of GN, greatly changing the ratio between mucopolysaccharides, microorganisms, salivary bodies, thickened epithelium and food residues, which ultimately leads to partial or complete mineralization of GN. When its intense mineralization begins, tartar can form, which occurs by impregnation of GN with calcium phosphate crystals. The time required for the hardening of the soft matrix is ​​about 12 days. The fact that mineralization has begun becomes apparent already 1-3 days after the formation of plaque.

3. The composition of plaque. With the help of biochemical and physiological research It has been established that GN is an accumulation of colonies of microorganisms incorporated into the matrix and living in the oral cavity and on the surface of the teeth.

In studies using a scanning electron microscope, it was shown that the GN consists exclusively of microorganisms with a slight inclusion of a structureless substance of an organic nature. Of the organic components in the ON, protein, carbohydrates, and enzymes were identified. Its amino acid composition differs from that of mucin and pellicle, as well as saliva. The carbohydrate components of the ON (glycogen, acid mucopolysaccharides, glycoproteins) have been most thoroughly studied.

There is a hypothesis that GN enzymes play an important role in the carious process. Chemical composition MN varies greatly in different parts of the mouth and in different people depending on age, sugar intake, etc. Calcium, phosphorus, potassium, sodium were found in plaque. About 40% of the dry mass of inorganic substances is in it in the form of hydroxyapatite. The content of trace elements in GN is extremely variable and insufficiently studied (iron, zinc, fluorine, molybdenum, selenium, etc.). Assumptions about the mechanisms of the caries-inhibiting action of microelements are based on their influence on the activity of bacterial enzymes, as well as on the ratio of various groups of microorganisms. Certain trace elements (fluorine, molybdenum, strontium) cause less susceptibility of teeth to caries, affecting the ecology, composition and metabolism of GN; selenium, on the contrary, increases the possibility of caries. Fluorine is one of the most important components influencing the biochemistry of the ON. There are three ways of incorporating fluorine into the GN: the first one is through the formation of inorganic crystals (fluorapatite), the second one is through the formation of a complex with organic substances (with the plaque matrix protein); the third is the penetration of bacteria. Interest in the metabolism of fluorine in the ON is associated with the anti-caries effect of this microelement. Fluorine, firstly, affects the composition of dental plaque, secondly, it affects the solubility of enamel, and thirdly, it inhibits the activity of bacterial enzymes that make up plaque.

Inorganic substances of GN are directly related to mineralization and formation of tartar.

4. Dynamics of plaque formation. GN begins to accumulate within 2 hours after brushing your teeth. Within 1 day, coccal flora prevails on the surface of the tooth, after 24 hours - rod-shaped bacteria. After 2 days, numerous rods and filamentous bacteria are found on the surface of the GN (Fig. 2).

As MN develops, its microflora changes according to the type of respiration. The initially formed plaque contains aerobic microorganisms, the more mature plaque contains aerobic and anaerobic bacteria.

Desquamated epithelial cells, which are attached to the tooth surface within an hour after its cleaning, play a certain role in the formation of GN. The number of cells increases significantly towards the end of the day. Further, epithelial cells adsorb microorganisms on their surface. It was also found that the formation of GN and its adhesion to the enamel is largely promoted by carbohydrates.

The most important role in the formation of GN is played by S. mutans, which actively form it on any surface. But there is a certain sequence in this process. Under experimental conditions, it has been shown that S.salivarius first adheres to a clean tooth surface, and then S.mutans adheres and begins to multiply. At the same time, S.salivarius disappears very quickly from plaque. The formation of the GN matrix is ​​influenced by enzymes of bacterial origin, for example, neuraminidase, which is involved in

cleavage of glycoproteins to carbohydrates, as well as in the polymerization of sucrose to dextran-levan.

Rice. 2. Microorganisms on the surface of plaque (electronogram).

Saliva contains IgA, IgM, IgG, amylase, lysozyme, albumin, and other protein substrates that may be involved in the formation of MNs. The pellicle, as a rule, contains all classes of immunoglobulins (A, M, G), while in the ON, IgA and IgG are most often detected (however, the share of participation)