Dental plaque and the mechanisms of its formation microbiology. Plaque

TOOTH CALCULUS

Tartar plays a significant role in the development of periodontal disease. Many authors consider it one of the etiological factors in the development of this disease. It is believed that tartar, especially located at the neck of the tooth, causes mechanical irritation of the gums, closes the exit from the periodontal pocket and thereby prevents the exit of microbes, migrating leukocytes and their decay products.

Tartar is formed from soft plaque on teeth. A few weeks after the formation of the latter, the first signs of mineralization appear in it. One-day dental plaque contains about 19 mg/g dry weight of calcium and 27 mg/g of phosphorus. Such a high content of ions is apparently due to their precipitation from saliva in the composition of mucopolysaccharide complexes. The precipitation of these complexes is facilitated by the loss of carbon dioxide and the associated rise in salivary pH. Already on the 2nd day, the concentration of calcium and phosphorus in dental plaque decreases by almost 1.5 times.

The formation of oxyapatite crystals is greatly facilitated by an increase in pH in the dental plaque. In this case, its alkaline reaction is created due to ammonia formed from urea in saliva under the action of bacterial urease. There is a direct proportional relationship between the degree of increase in pH of the supragingival dental plaque and the depth of the periodontal pocket. It is possible that such an alkaline environment has a very beneficial effect on the proteolytic enzymes of microorganisms.

A detailed study of the structure of tartar using methods of chemical, X-ray analysis and infrared spectroscopy showed that 80% of tartar consists of inorganic substances, the main of which are calcium phosphates. In particular, octacalcium phosphate (brushite) makes up almost 50% of dental calculus.

The mechanism of tartar formation has not yet been fully elucidated, but not only Ca ions play an important role in its formation, but also the activity of a number of salivary enzymes. Thus, Nowalska-Kwapisz, studying the activity of acid phosphatase and the rate of tartar deposition, showed a direct relationship between the activity of acid phosphatase and the deposition of tartar.

Kobylanska found that regardless of the location of plaque collection (lower incisors, upper incisors, lingual or labial surface), they always contain foci of calcification, determined by the histochemical method based on the reaction to calcium.

Broukal and Svejda, using a scanning microscope, studied the structure of the surface, internal and adhesive layers of human tartar depending on the age and topographical features of this deposit. The first signs of mineralization are observed 3-6 weeks after the formation of dental plaque. In this case, the microbial cells become empty, although in some places the initial microbial structure is observed, masked by fine-grained material containing polyhedral and lamellar crystals. After 2-3 months, mineralized substances predominate in the dental calculus, forming entire fields of needle-shaped prismatic and cubic crystals. The adhesive surface of the stone, as well as the surface of tooth enamel and cement, after removing tartar, is usually covered with a layer of crystalline agglomerates and a thin granular mass.

Jones, using electron microscopy, found that the onset of tartar formation is usually associated with the presence of depressions on the surface of the enamel, causing tartar to form more quickly in the crevices between the mineralized ends of Sharpey's fibers, in carious depressions of cement and other pockets of the tooth surface. These data indicate that complete removal of tartar is associated with the need to destroy the enamel surface. However, Canis et al believe that such a tight attachment of tartar to the enamel is only one way of its deposition. Most often, the cuticle is located between tartar and enamel.

In just 5 minutes After thorough cleaning of the surface of the molars, about 1 million microbes are determined per 1 mm2 of surface. These are mainly facultative pleomorphic spherules and S. sanguis. There are either no gram-negative forms at all or very few of them in young plaque. Three phases of microbial film maturation are described.
1st phase: 2 days after cessation of care, proliferation of gram-positive cocci and micrococci occurs.
2nd phase: after 2-4 days, fusobacteria and filaments appear in significant numbers.
3rd phase: after 4-9 days, spirochetes and spirilla appear.

Microbial composition of plaque depending on the phase of its maturation:
1st phase: the bacterial film consists of Streptococcus spp., Neisseria, Nocardia predominates, while in the 3rd phase, after 9 days, Streptococcus spp., Veilonella are determined, and Corynebacterium predominates. Fusobacterii are present in greater numbers in a 9-day plaque than in a young plaque. The growth of anaerobic species, such as Veyonella and Fusobacteria, depends on the previous growth of aerobes and facultative representatives and a purely mechanical increase in layer thickness. When its thickness becomes sufficient to isolate it from oxygen, then the reproduction of anaerobes begins.

From the peridantal pocket for periodontal inflammation From 10 to 200 mg of plaque can be isolated, almost entirely consisting of microbes. The total area of ​​the inner surface of the gum pockets on which microbes settle is on average 10-15 cm2. In addition, this surface is also covered with ulcers. It is characteristic that only with ulcerative gingivitis and aggressive periodontitis are bacteria detected inside the soft tissues. In ulcerative gingivitis, these are spirochetes of medium and large sizes, rarely other forms, mainly Porphiromonas gindivalis. In other forms of periodontitis and gingivitis, microbes do not actually penetrate deep into the tissue. The reason for this is the presence of a dense layer of leukocytes at the border between the epithelium of the pocket and microbial accumulations, which can quite reliably protect the underlying tissues from the penetration of pathogenic flora into them.

Tartar formation

Tartar is a mineralized dental plaque. Compaction of soft plaque due to precipitation of salts occurs in the period from 1 day to 2 weeks. after the formation of the plaque, but the first signs of calcification can be detected within 4-8 hours. The plaque is calcified by 50% during the first 2 days, and for the remaining days (up to the 12th day) calcification reaches from 60 to 90%. The entire mass of plaque is not necessarily calcified. In the early stages, plaque contains a small amount of minerals, which increases as the plaque turns into stone. The maximum concentration of mineral components is achieved within 2 days.

Source calcification of supragingival plaque is saliva, subgingival is gingival fluid. A characteristic feature of plaque is to accumulate minerals in its composition in a concentration that is 2-20 times higher than their content in saliva. It is noteworthy that in the mineralization process the main role is played not by calcium, but by phosphorus.

Calcification begins along the inner surface of the supragingival plaque and on the part of the subgingival plaque attached to the tooth. First, individual areas calcify, then they increase in size. As a result, they form massive accumulations of stone. As the stone forms, its mineral composition and the amount of covering microbial plaque changes: the number of filaments increases. As they grow, the foci of calcification merge into a single conglomerate, and thin microbial membranes become almost indistinguishable.

Start time stone formation and the rate of its formation varies significantly among different people, at different periods of life, in different parts of the dentition. The average increase in stone quantity is 0.1-0.15% dry weight per day. The time during which the stone volume reaches its maximum ranges from 10 weeks. up to 6 months

Reducing stone mass After reaching maximum volume, known as the phenomenon of stone reversion, it can be explained by the fact that large stone formations are destroyed by the pressure of food, lips and tongue.

In this regard to prevent stone formation The use of toothpastes is useful, as they reduce calcium in the composition of the stone and its connection with phosphorus.

Diet plays an important role, primarily due to its effect on functional masticatory system activity. To do this, it is recommended to increase the consumption of roughage (vegetables and fruits that have not been subjected to heat treatment). It is necessary to reduce the proportion of foods rich in mono-, di- and oligosaccharides, as well as starch, since their consumption contributes to the active growth of microbial associations and a decrease in enamel resistance, but this is only valid in the case of inadequate hygienic care. In the case of high-quality hygienic care, this factor is not as significant as is commonly thought - the main role belongs to the load factor on the masticatory apparatus.

Dental caries (caries - decay) is one of the most pressing problems in dentistry. According to the scientific group of the World Health Organization, dental caries is “a localized pathological process of external origin, resulting in 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 most of the population in Europe, America and other regions.

In most developing countries, caries is less common, and often even in older people all teeth are completely healthy. But in these countries, over the past 10-20 years, the problem of caries has sharply worsened, especially where they began to eat more carbohydrates and refined foods. Thus, dental caries has become a pandemic.

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.

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

After this, a new so-called bacterial theory was put forward. The search began for a specific causative agent of caries. This role was assigned to many microbes inhabiting the oral cavity. The idea of ​​the predominant role of the entire genus Lactobacillus in caries, regardless of their species, has been firmly established for a long time. At the same time, facts accumulated that indicated 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 caries does not develop in all people, nor 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 matter of the enamel with metal ions (primarily calcium ions). The authors of this theory believe that oral acids even protect teeth from caries. However, the chelation theory also has significant drawbacks. One of the main ones is that the authors studied caries from a purely biochemical point of view and did not take into account the clinical manifestations of the pathological process.

The currently existing 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 known that are important in the occurrence of caries. These factors can have both general and local effects. These include social conditions, profession, constitutional characteristics of the body, disorders of the trophic functions of oral tissues, etc.

For the caries process to occur, 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, but there are different interpretations of the mechanism of action of carbohydrates. Some researchers (A.E. Sharpenak, 1964) believe that excess 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. Thus, when a cariogenic diet was administered to experimental animals directly into the stomach through a fistula, no development of the carious process was observed.

Indisputable proof of the role of microorganisms in the occurrence of caries should be considered the studies of Orlandi (1955), conducted on germ-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. Nonsterile (control) rats rapidly developed carious lesions, whereas gnotobiotes did not. When all the animals were transferred to normal 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 themselves cannot cause caries. However, a high carbohydrate content in food in the absence of microorganisms also cannot lead to caries. Caries develops with the simultaneous action of both factors.

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

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

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

Descended epithelial cells play a certain role in the formation of dental plaque. They attach to the surface of the tooth within an hour of cleaning it. By the end of the day, the number of attached cells increases noticeably. It has been established that epithelial cells adsorb microorganisms on their surface.

Cariogenic microorganisms are found in dental plaque, of which the most important are Streptococcus mutans, Lactobacillus acidophilus, Actinomyces viscosus. It appears 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 where caries is most frequently localized (in the fissure area, on the proximal surfaces of the teeth). Before the development of carious lesions in these areas, S. mutans constitutes 30% of the total microflora.

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

to demineralization of enamel. 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 the carious process, as well as the effectiveness of local treatment.

Immunological studies also provide evidence of the participation of microflora in the development of caries. Thus, in monkeys immunized with S. mutans, caries did not develop within two years after immunization 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 structure of all its layers is destroyed. With initial lesions of dentin, microorganisms are found that, 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 dental tissues, 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 in inflammatory processes in the oral cavity

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

1) odontogenic inflammation;

2) inflammation of gum tissue during periodontitis;

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

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

The etiological factor of inflammatory diseases of the maxillofacial region in 96-98% of cases is odontogenic infection, i.e. the spread of microorganisms from the tooth cavity during 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, the source of infection of bone tissue is suppurating periodontal cysts, alveolitis, and only in 2-4% of cases a non-odontogenic infection occurs, that is, the penetration of microorganisms into the maxillofacial area by hematogenous, lymphogenic 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 effects of microbes, their metabolic products and the decay of organic dentin matter.

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

The routes of penetration of microorganisms can be different. The most common route is from the carious cavity through the dentinal tubules. In this case, the localization of the carious cavity becomes important. Carious lesions of the cervical and proximal surfaces contribute to the involvement of both coronal and root pulps in the inflammatory process, whereas with caries of the masticatory surface, the root pulp is not always and not immediately affected.

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

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

Acute pulpitis initially has a focal character and occurs as a serous inflammation. Most often it is caused by viridans and non-hemolytic streptococci of group D and streptococci that do not have group C-antigen, as well as lactic acid bacteria. Later, in most cases, abscesses form, and rapid purulent melting of the coronal part of the pulp occurs. During this period, mainly staphylococci with virulence factors, beta-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 occurs according to the hyperergic type, that is, 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 rapid, 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 death of the pulp within several days. In non-sensitized animals, resorption of inflammatory foci is observed.

Acute pulpitis can become chronic, and with tissue decay, it can become gangrenous. In the necrotic pulp, anaerobic microorganisms with pronounced proteolytic properties are found in large quantities. These include peptostreptococci, bacteroides, spirochetes, actinomycetes, and vibrios. Along with obligate anaerobes, there are facultative anaerobes and microaerophiles - group D streptococci, beta-hemolytic streptococci of groups F and G, and pathogenic staphylococci. Putrefactive bacteria can also be added - representatives of the unstable microflora of the oral cavity - bacteria from the genus Proteus, chlosgridia, bacilli. .

Microflora in periodontitis. The periodontium is a complex anatomical formation located between the root of the tooth and the wall of its socket. 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 source of inflammation in the pulp or gum. Purulent inflammation occurs as a result of the penetration of microorganisms into the periodontium.

A characteristic feature of purulent periodontitis is the sharp predominance of streptococcal flora over staphylococcal flora. In the initial stages of inflammation, viridans and non-hemolytic streptococci lacking 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 to chronic periodontitis, the main role is played by anaerobic streptococci (Peptostreptococci) and representatives of other groups of these microorganisms.

Characteristic of periodontitis is the detection of not individual types of microbes, but their associations. Typically, streptococci are isolated together with veillonella, lactobacilli, corynebacteria, and yeast-like fungi. Actinomycetes, bacteroides, fusobacteria, vibrios, and spirochetes are found in apical granulomas.

In people suffering from chronic periodontal inflammation, a state of hypersensitivity to streptococcal antigens isolated from the site of inflammation was identified using skin allergic tests.

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

Microflora in odontogenic purulent inflammation (periostitis, osteomyelitis, soft tissue abscesses, phlegmon). With purulent periodontitis, the exudate may not be released 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 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 unfavorable conditions, acute purulent osteitis turns into a purulent-necrotic process, i.e., osteomyelitis. Any disease from the group of acute odontogenic infections can be complicated by abscesses and phlegmons.

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 foci in pure culture or in combination with other coccal flora, for example, beta-hemolytic streptococcus. The course of phlegmon can be complicated by the penetration of clostridia, the causative agents of anaerobic gas infection, into the tissue. This significantly aggravates the course of the disease and worsens the prognosis.

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

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

Tuberculous lesions of the oral cavity are usually secondary. They can be observed when the pathogen disseminates by hematogenous route.

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

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

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 facilitated by injuries to the skin and mucous membranes (bruise 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 can also occur. In this case, actinomycetes that grow on grasses, cereals, and soil enter the body. Possible airborne infection.

In the oral cavity there are favorite places for actinomycetes to penetrate into the depths of tissue: inflamed gums near wisdom teeth or near decayed tooth roots, pathological periodontal pockets, root canals of teeth with necrotic pulp, ducts of the salivary glands, tonsils.

For the disease to occur, the penetration of the actinomycete into the tissue is not enough. An important role is played by the reactivity of the macroorganism, as well as previous sensitization by waste products of actinomycetes.

The incubation period for actinomycosis is two to three weeks, but a longer incubation period is possible - 12 months. and more. The disease can be acute, more often chronic, 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 through the subcutaneous tissue and connective tissue, as well as hematogenously.

The clinical picture of actinomycosis is varied and is associated with its localization. The appearance of bluish-red and then purple infiltrates of dense consistency is characteristic. In the infiltrates, small multiple foci of fluctuation are found, 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 drusen has a characteristic structure and consists of interwoven threads; along the periphery of the drusen, the threads thicken, forming pear-shaped “flasks”. In their development, druses undergo several stages. At first they look like tender lumps, later they become calcified dense bodies, often without 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 detected.

With actinomycosis, as a rule, there is the addition of a secondary purulent infection caused by staphylococci, streptococci, and 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, secreting hyaluronidase, contribute to the spread of the process. The addition of pyogenic flora worsens the course of actinomycosis, aggravates the process, and changes its clinical picture.

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

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

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

3.3. Microflora in periodontal tissue diseases

The periodontium is a complex of tissues that have genetic and functional similarities: periodontium, alveolar bone with periosteum, gums and tooth tissue. Periodontal tissues are constantly exposed to bacterial, temperature and mechanical influences. The integrity of the periodontium is a reliable protection of the body from the effects of adverse factors. When the internal environment is disrupted, caused by local (microbes, toxins, enzymes, trauma, overload, etc.) or general factors (hypovitaminosis, diseases, metabolic disorders, neurotrophic disorders), structural and functional changes in periodontal tissue develop, which leads to reduction of barrier functions and 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 diseases has increased sharply. 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 over 40 years of age, periodontal disease is more common than caries.

Periodontal diseases are extremely diverse - from short-term reversible gingivitis, which can develop as a result of poor oral hygiene, stress or short-term nutritional disorders, to acute periodontal abscess and chronic irreversible periodontitis, ultimately leading to loss of dental function.

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

Gingivitis manifests itself as redness, swelling of the gums, and bleeding when brushing your teeth. The etiological factors of gingivitis are varied. Local factors include tartar, defects in fillings 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 the cardiovascular system, gastrointestinal tract, dysfunction pituitary gland, thyroid gland).

The mechanism of development of inflammatory phenomena in marginal periodontal tissues is closely related to impaired tissue and vascular permeability. Essentially, increasing 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 the enamel with the gum tissue. It is customary to distinguish between supra- and subgingival plaque.

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

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

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

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

Against the background of altered reactivity of the body after illnesses, intoxications, and vitamin deficiency, ulcerative gingivitis can develop. In this case, the gingival margin ulcerates, which is accompanied by an increase in temperature, enlargement of the submandibular lymph nodes, and the appearance of bad breath.

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

Among the numerous factors affecting periodontal tissue, the first and most important place is occupied by microbial irritants, which are part of dental plaque. In recent years, the assessment of its role in the development of periodontal diseases has increased dramatically. Particular attention was paid to the study of the composition and specificity of microorganisms, the mechanisms of formation and attachment of dental plaque to the structural components of the tissues of the oral cavity and their pathogenic potential. The participation of microorganisms in the development of inflammation of periodontal tissues is generally recognized. As a generally accepted term, “dental plaque” means the accumulation on the surface of a tooth of colonies of microorganisms that live in the oral cavity. WHO interprets the concept of “dental 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. The number of bacteria per unit volume of dental plaque is very large and depends on the age of the person, his attitude to oral hygiene, diet, iatrogenic factors, and the influence of risk factors (smoking, etc.).

The oral cavity is home to over 90 types of microorganisms, among which streptococci and anaerobic bacilli predominate. According to the latest data, more than 70% of the colonies are formed by streptococci, 15% by Veillonella and Neisseria, the rest of the microflora is diphtheroids, lactobacilli, staphylococci, leptotrichia, fusobacteria, actinomycetes, yeast-like fungi, etc.

The microflora of dental plaque is quantitatively and qualitatively variable. The main role in the development of inflammation is played by streptococci and staphylococci.

A significant place is given to bacteroides, fusobacteria, veillonella, and spirochetes. In the dental literature, special attention is paid to the study of the species specificity of microorganisms living in the oral cavity, their influence on the development and progression of periodontal diseases (K. CHibosh, I. Houlet, 1975; 81o18 et al., 1978; XV. Mooge and al., 1982). Back in the 17th century, an oral spirochete was discovered and described in ulcerative necrotizing gingivitis. Later, not only was this “find” confirmed, but also a large number of other species and groups of microorganisms that were constantly present in the oral cavity were discovered (R. Sagganga, 1990; etc.). According to research data, gram-positive and gram-negative cocci, as well as gram-positive bacilli, fusobacteria, spirochetes, actinomycetes, etc., were particularly pathogenic.

The diverse composition of microflora in clinically healthy and inflamed periodontal tissues is presented in Fig. 4.2. The species specificity of dental plaque microorganisms is variable and depends on endogenous and especially exogenous factors.

Thus, the intensity of plaque formation depends on the microflora of the oral cavity, desquamation of the epithelium of the mucous membrane, the composition of saliva and its viscosity, the level of self-cleaning processes, the anatomical structure of the teeth, diet, ability to brush teeth and interdental spaces, gums, tongue, etc.

Dental plaque is not washed off with saliva even when rinsing the mouth, since its surface is covered with a mucous semi-permeable gel in the form of a mucoid film, which blocks the neutralizing effect of saliva on microorganisms.

The chemical composition of plaque varies greatly in different areas of the mouth and in different people depending on age, sugar intake, etc. It is known that calcium and phosphorus in dental plaque are formed mainly by saliva.

The content of phosphorus, sodium and potassium in young people in 2-3-day dental plaque is higher than in saliva. In general, the concentration of inorganic salts in dental plaque increases over time. About 40% of the dry mass of inorganic plaque material is oxyapatite. The pH value has a great influence on the adsorption of phosphorus in dental plaque (at 7.0-7.4 it accelerates). Plaque can mineralize over time.

The number of microorganisms in the oral cavity, which is in a state of dynamic interaction with the antibacterial factors of saliva - immunoglobulins, antimicrobial enzymes, and endogenous low-molecular bacteriostatic substances, has a certain significance in the pathogenesis of periodontal diseases. As is known, the main habitat of microorganisms in the oral cavity is the gingival groove, the dorsal surface of the tongue (their maximum number), pits, fissures on the surface of the teeth, areas on the gum mucosa, etc. There is convincing evidence that the development of periodontal diseases directly depends on the number of dental plaque and general microbial contamination of the oral cavity and inversely proportional to the effectiveness of hygiene measures.

As a rule, with the development of gingivitis and periodontitis, tissue invasion of the periodontium by microorganisms is accompanied by transient bacteremia.

Rice. 4.2. Microbiology of dental plaque and relationship with periodontal diseases.

Using bacteriological, immunological and ultrastructural methods, the presence of microbes in the intercellular substance, inside epithelial cells, and in the connective tissue of the gums was established. Dental plaque, moving as it grows under the gingival margin, causes tissue irritation due to microorganisms and their toxins, which subsequently leads to changes or damage to the epithelium of the gingival sulcus and inflammation of adjacent tissues. Of particular pathogenetic importance in periodontal diseases is the gingival sulcus (gingival crevice). This is a narrow, slit-like space between the tooth and the gum, located from the edge of the free gum to the attachment epithelium. It is this area that is the reservoir of microorganisms that make up the dentogingival and subgingival plaque.

When a groove depth exceeds 3 mm, it is considered pathological and is often called a gingival pocket. Plaque can cause the development of hyperplastic gingivitis against the background of hormonal disorders (during pregnancy, in adolescence 11-17 years old) and with a low level of hygiene. The occurrence of such gingivitis is facilitated by crowding of teeth, malocclusion, lack of chewing load on a group of teeth, caries in the cervical area, overhanging edges of fillings, movement of teeth during orthodontic treatment against the background of poor hygienic dental care. Many foreign and domestic authors have presented indisputable facts indicating that in gingivitis and progressive forms of periodontitis, periodontal plaque is the main source of changes in periodontal tissues.

To identify different types of microorganisms within bacterial aggregates, it is important to take into account their localization and the state of surrounding tissues. The term “bacterial plaque” is identical to “dental plaque”, as it refers to the accumulation of microorganisms located on the surface of the teeth and along the gum margin and tightly associated with these areas. Depending on the location of dental plaque, supragingival and subgingival plaque are distinguished. In dental practice, it is important to take into account that microorganisms in the tissues of the oral cavity are found both isolated and in the form of bacterial aggregates. Clinically, it is necessary to clearly diagnose supra- and subgingival plaque, taking into account their mechanism of formation and distinctive features that play a key role in periodontal development.

Characteristics of supragingival plaque

The microflora of supragingival (dental) plaque of healthy gums in the cervical surface of the tooth consists of 90% gram-positive cocci and also includes a small number of gram-negative cocci. Normally, minor supragingival bacterial plaque is a whitish or yellowish thin layer localized along the gingival margin of the teeth. In addition, it is constantly present in the fissures of occlusal surfaces, recesses, cracks, pits of teeth, on crowns, along the edges along restoration fillings.

Supragingival plaque initially consists of microorganisms and destroyed epithelial cells, leukocytes and macrophages adhering to the intracellular matrix. Organic and inorganic components make up more than 20% of plaque, the rest is water. Plaque formation begins with the adhesion of bacteria to the pellicle or tooth surface (enamel, cementum, dentin). Its growth is enhanced due to the adhesion and increase in the number of new bacteria, the accumulation of bacteria and their metabolic products. It has been proven that the composition of bacterial plaque quickly changes and after 3-8 hours streptococci dominate in it, and after 2 days not only the growth of all types of bacteria is noted, but also an increase in their pathogenic activity in relation to surrounding tissues (I. 81o18, 1987; R Peleyen, 1991, etc.). In patients who do not maintain hygiene, in the next 3-4 days the processes of proliferation of fusobacteria begin to prevail, and on the 5-9th day spirilla, spirochetes, and gram-positive rods appear in the supragingival dental plaque, constituting 50% of the total microflora (Fig. 4.3). However, complete removal of plaque is unattainable and a few hours after the attempt is made, it reappears. However, microbial plaque becomes pathogenic only after a certain time required for its maturation.

According to the results of studies by K. Syaosh (1975), R. Saggapha, E. Keppeu (1981) and others, the duration of maturation of bacterial plaque varies from 1 to 3 days, on average it is 48 hours.

If plaque is not removed during this period, it becomes potentially harmful to healthy gums. Therefore, reducing the amount and weakening the pathogenicity of bacterial plaque can only be achieved by careful adherence to oral hygiene.

Rice. 4.3. The role of microorganisms in the development of gingivitis in the absence of oral hygiene (1_1ps1g1e, 1993).

It must be emphasized that the oral cavity is a biological environment in which microorganisms tend to adhere to hard and uneven surfaces. The phenomenon of stickiness (adhesion) of bacteria is based on physicochemical mechanisms determined by the relationship between the structure of bacteria and the active components of saliva (K Rege, 1970; etc.).

Bacteria from the oral cavity can be removed by the flow of saliva, gingival fluid during chewing and desquamation of gum epithelial cells and during hygiene measures (T. L. Pilat, 1984; E. M. Melnichenko, 1990). According to modern views, the increase in the initial adhesion of microorganisms is proportional to the growth of bacterial plaque, which doubles in volume during the first day if hygiene rules are not followed or if individual oral care products are used incorrectly. It has also been established that periodontal plaque increases not only in thickness, but also in depth, as a result of which gum inflammation develops and increased secretion of gingival fluid is noted.

Supragingival plaque is not only an etiological factor in the initial forms of gingivitis, but also a pathogen that can potentially stimulate the formation of subgingival plaque (R. Sagganga 1975, etc.). The polysaccharides, enzymes, and enzymes they produce participate in the adhesion of microbes. Stagnant processes contribute to the retention of bacteria and the development of inflammation of periodontal tissue. It has been proven that some bacteria stick faster. The organic matrix of supragingival plaque consists mainly of carbohydrates, proteins (30% each) and lipids (about 15%). These components are part of the waste products of dental plaque bacteria and the cytoplasm of the cell membrane. An important component of supragingival plaque carbohydrates is dextran, which accounts for 9.5% of the total plaque volume. In addition, carbohydrates in the organic matrix are represented by galactose and methylpentose. The protein composition of the matrix is ​​replenished by glucoproteins from their main source - saliva.

Subgingival plaque is formed as a result of the accumulation of microorganisms in the gingival sulcus when supragingival plaque has already formed. The gingival sulcus is the main site of localization of accumulated bacteria in the form of plaque or tartar. Subgingival plaque differs from supragingival plaque in its composition, colonization of microorganisms, and mechanisms of bacterial fixation. The composition of subgingival plaque microorganisms is different in nature and functional significance and depends on the specificity of the supragingival plaque microflora (aerobes, fusobacteria, bacteroids, etc.). Depending on the anatomical and topographical sites of attachment of subgingival plaque in the gingival sulcus, tooth-attached and epithelial-attached plaque are distinguished.

Bacteria and other microorganisms of subgingival plaque are capable of penetrating, invading, and colonizing the gingival connective tissue through epithelially attached plaque. This is the mechanism for fixing bacteria on the surface of connective tissue. With dentally attached subgingival plaque, the microorganisms included in its composition are associated with the proximal surfaces of the teeth and the cement wall of the root in the area of ​​the gingival sulcus. The border of the tooth-attached subgingival plaque towards the apical part of the tooth is located at some distance from the place of attachment of the connective epithelium of the gums (Fig. 4.4).

The composition of microorganisms in dentally attached subgingival plaque is dominated by gram-positive bacilli and cocci; it also contains some strains of gram-negative cocci and bacilli. The composition of microorganisms in dentally attached subgingival plaque can change when it is impregnated with mineral components of saliva, which contribute to the formation of stones.

Rice. 4.4. Dental plaque associated with the tooth surface and periodontal tissues (R. A. Saggapga, 1990).

Thus, subgingival plaque also serves as an organic matrix for subsequent mineralization and formation of tartar. There are reliable facts confirming that microorganisms of epithelially attached subgingival plaque are able to penetrate deep into the tissue structures of the gums and bone. In addition, to understand the pathogenesis of periodontal diseases, the presence in the gingival sulcus of the so-called zone of unattached subgingival plaque is essential. It is these microorganisms, which are part of it and circulate freely in the gingival sulcus, that are a source of infection for the development of periodontal diseases. Subgingival plaque microorganisms, depending on the location of their attachment, are distinguished by their pathogenic specificity and can cause various pathological conditions - periodontal disease, starting with gingivitis, or approximal caries or root cementum (Table 4.1).

Thus, in the epithelially attached subgingival plaque, microorganisms are mainly represented by gram-negative cocci and rods, which are able to penetrate and invade the underlying periodontal tissues and bone tissue, forming periodontal pockets. Depending on the composition of microorganisms in subgingival plaque (dentally attached, epithelially attached and non-attached) and the quantitative ratio of bacteria in it, various forms of periodontal diseases with a rapidly or slowly progressing course are clinically observed. The participation of subgingival plaque microorganisms in the formation of periodontal pockets is due to the ability of bacteria to penetrate into the connective tissue and depends on the pathogenic potential of the bacteria that are part of the epithelially attached subgingival plaque.

The Role of Diet in Plaque Formation

The mechanical impact of food and increased saliva flow during chewing reduce plaque formation. Saliva and salivation have a biological effect on gingival plaque.

In people suffering from dry mouth and eating soft foods, when the act of chewing is insufficient, supragingival plaque forms much faster. It has been established that supragingival dental plaque forms faster during sleep. Sweet foods promote the formation of supragingival dental plaque and affect its bacterial composition by increasing the amount of polysaccharides produced by the microflora.

A tendency to develop plaque more quickly has been noted in people who eat foods high in protein and low in fat.

A. S. Artyushkevich
Periodontal diseases

2.Somatic diseases, shifts in the functional state of organs and systems during the period of formation and maturation of dental tissues.

3. Extreme physical and neuropsychic effects on the body (stress).

4. Heredity, which determines the usefulness of the structure and chemical composition of tooth tissue.

Local factors:

1. Dental plaque and plaque.

2. Violation of the composition and properties of oral fluid.

3.Carbohydrate sticky food residues in the oral cavity.

Prevention of caries can be aimed at reducing the number of cariogenic microorganisms in the oral cavity. Mechanical removal of dental plaque is impractical, since new bacterial cells immediately settle on the cleaned surface, which leads to the rapid restoration of the microflora. The use of various bactericidal and bacteriostatic drugs is more effective. Good results are obtained using antiseptics, in particular 0.2% chlorhexidine. At the same time, the number of S. mutans cells in dental plaques decreases by 80-85%, and in saliva by 55%. By covering the tooth surface, chlorhexidine not only has a bactericidal effect on microorganisms, but also prevents their adhesion, thereby disturbing the microbial balance.

Fluorine and its compounds, especially the salts ZnF2 and CuF2, as well as the pentaatomic alcohol xylitol, which disrupts the process of glycolysis in bacteria, have an inhibitory effect on microorganisms. To prevent caries, chemical inhibitors are used that suppress certain metabolic reactions in S. mutans. For example, fluorine inhibits the action of enzymes involved in the process of glycolysis, which include: phosphatases, endolases and phosphoglyceromutases. This leads to inhibition of acid formation. N-lauryl sarcosinate and sodium hydroacetate have a similar effect.

Another way to reduce acid formation and accumulation of glucans is to replace sucrose with other carbohydrates, for example, xylitol compounds, the enzymatic breakdown of which does not form these products.

The main protective mechanism of local immunity of the oral cavity during caries is the ability of secretory IgA to prevent the adhesion of S. mutans. Recognition of the leading role of microbes of the "mutans" group as an etiological agent of caries made it possible to carry out experiments to obtain preparations for immunization against caries (killed vaccines, purified cell wall proteins, ribosomal antigens, glucosyltransferase, DNA). Studies conducted both on animals and on human volunteers have shown a certain effectiveness of such vaccination. Protection against caries as a result of passive transfer of secretory IgA and serum IgG has also been demonstrated.

Disadvantages of vaccination:

· these microbes contain cross antigens with the tissues of the heart, kidneys, skeletal muscles of humans and animals, which can cause various pathological reactions of an autoimmune nature;

· due to the commonality of antigens of mutans group streptococci with other oral streptococci, the production