CARIES, UNCARIOUS TEETH CHANGES. PULPIT. PERIODONTIT. GUMS AND PARODONTAL ILLNESSES: GINGIVITIS, PARADONTIUMS, PARADONTOLIZ
(Concordantly Yu.Pospishil, V.Vovk)
Every tooth anatomically consist of a crown, neck and root. A crown comes forward above the surface of gums, a root is sunk in a dental alveolus, a neck is the area of transition of tooth crown in a root.
A tooth is built from hard tissues – enamel, dentine and cement, and also soft tissue – pulp.
Sagital cut of lower medial incisor:
1 – enamel; 2, 6 – dentine: 3 – pulp; 4 – capillary net; 5 – pulp; 7 – spongy bone tissue of lower jaw: 8 – gums; 9 – ephithelial attachment: 10 – cell-free cement; 11 – periodont; 12 – cellular cement.
A dentine makes the hardcore of tooth and localized in a crown, to the neck and root. The dentine of crown is covered an enamel, dentine of root – by cement. Into hard tissues of tooth filled pulp cavity which includes the cavity of crown and channel of root. The last is opened opening on the apex of root through which vessels and nerves pass to pulp. Teeth are fastened in dental alveoli a dental ligament – periodont. Hermetic of dental alveolus is provided dense accretion of epithelium of gums with the neck of tooth.
A dentine is hard tissue, which makes basis of root, crown and neck of tooth and is under an enamel and cement. He includes 70% inorganic and 30% organic matters. The inorganic components of dentine are phosphoric acid salts of calcium and magnesium, and also fluorine calcium. The organic matter of dentine is formed by collagen fibers bands (collagen 1 type), between which a basic matter lies. In radial direction a dentine is pierced by dentinal tubes, which contained the dentinoblast processes.
The cellular bodies of dentinoblastes lie in the peripheral area of pulp. Dentinoblastes are producings of organic matrix – dentinum. The blood capillaries are absent in a dentine also, and his trophism is provided by the dentinoblast processes. The body of dentinoblast has a prolate cylinder form. The long ramified procesus departs from his narrowed apical part. The cytoplasm of dentinoblast is basofil, fine-grained, a nucleus is displaced in basal part. Dentinoblastes have developed mitochondrial apparatus, granular cytoplasm net, the Goldj’s complex elements.
At the damage of tooth by pathological process dentinoblast activated, as a result in an adjoining to the defect area the secondary dentine accumulates from the side of pulp. The secondary dentine is always marked off primary a dark line. He differenced primary also by the degree of mineralization and structure. The small accumulations of the second dentine in a pulp have the name of denticles or stone of pulp. Enamel covers the crown of the tooth. It is the hardest tissue of human organism. She includes 96-97% inorganic and a 3-4% organic tissue. Phosphorus acid salts of calcium prevail among inorganic compounds of enamels, which as crystals of hydroxyapatit formed the hardcore of enamel. Carbonate and calcium ftorydum are other inorganic components of enamel. Proteins-glycoproteins are the mainly organic component of enamel. They formed a filament matrix. The enamel is cell-free tissue which is formed as a result of activity of specific cells – ameloblastes (enameloblastes, adamantoblastes). Ameloblastes have a cylinder form, oval nucleus, well developed mitochondrial apparatus, granular cytoplasm net and elements of Goldj’s complex. Specific extension of ameloblast apical part has the name of Tom’s extension and provides the secretion of synthetic activity products of cell. Time of ameloblast life is limited by the period of the tooth hystogenesis. After the cutting of teeth the ameloblastes perish and only them reductive apical part (Tom’s extension) is saved in composition of cuticle of enamel. That is why the damaged enamel does not recommence. Structural and functional unit of enamel is an enamel prism which pierces all layer of enamel. Every prism is the product of vital functions of one cell – ameloblast. A prism forma reminds the lens with the extended middle part and slim ends. Ameloblast synthesize filaments which are calcified by calcium hydroxyapatitum. They form an enamel prism. There are pores between the enamel prisms, and micropores between hydroxyapatitum crystals. They all provide diffusion. Penetrating of enamel is insignificant. Only small molecules of water, ions, vitamins, monosakharidi, amino acid can diffuse in an enamel. Penetrating of enamel grows under act of acids, alcohol, at the calcium deficit, phosphorus, fluorine. Without regard to considerable hardness, an enamel can be damaged as a result of decalcification action of acidsecretion bacteria which propagate oneself in composition food remains on-the-spot crown of the tooth and can be the nosotropic factor of caries development. Hydroxyapatitum durability increases In the fluorine presence. There are base of anticaries effect of fluorine tooth-pastes, drinking-water, vitamins and others.
Cement is hard tissue which covers the dentine of tooth root. The cement structure like coarsefibers bone tissue, but different by blood vessels absent. His nutrition is provided by diffusion from periodont blood vessels. Cement includes 65% mineral matters (phosphorus acid and carbonate salts of calcium), 23% organic compounds (fibers of 1 type collagens and basic intercellular matter) and 12% water. The collagen fibers have a longitudinal and radial orientation. Radial fibers proceed in periodont and farther in the periosteum of dental alveolus (Sharpeev’s fibers). From an opposite side they meet with the radial fibers band of dentine. Distinguish two varieties of cement – cell-free (primary) and cellular (secondary). Cell-free cement lies nearer to the neck of tooth. He is formed only the collagens fibers and gluey matter. Cellular cement lies on the apex of root, and in multirooted teeth also between the root forks. To his composition, except the collagen fibers and basic intercellular matter, the cells of cement entry also. The last develop from cementoblasts, which in the tooth hystogenesis process, synthesize actively a collagens and components of organic matrix of cement. Cementoblasts localized superficially in adjoining to periodont layers in the formed tooth, and that is why new formation of cement, as well as bone tissue, takes place the apposition way. Cementocytes structure and function remind the osteocytes of bone tissue. They have a poligonal form, lie in cavities (lakuna), and their procesuses go in the ductule of basic matter of cement. Processuses of nearby cementocytes have the anastomoses between itself, and also with the procesuses of dentinoblast.
Pulp is soft tissue, which fills the cavity of tooth and provides a trophies, innervations, immune defenses and regeneration of his tissues. It is formed by magnificent connecting tissue, and likes a mesenchyma structure – connecting tissue of embryo. Pulp contains numerous star fibroblasts, reticular fibers, immature fibers of collagens, grate capacity intercellular matter, haemocapillaries (blood to them go from periodont arterioles through opening of root apex of tooth) and nervous fibers.
Anatomic pulp is divided into koronkovu and root, each of which has some features of the structure. In koronkoviy pulp the fibres of collogens are very thin and does not form bunches. In root pulp the fibres of collogens are thicker, form pinches and prevail above compact placed near each other cells. Histological in composition pulp distinguish three layers: peripheral, intermediate and central. A peripheral layer contains the immature fibres of collogens and bodies of dentinoblastiv. Intermediate are fibres of преколагенові and bodies of predentinoblastiv. A poor on cellular elements layer – so-called cell-free area of Veylya, which contains nakedly, lies between the layers of dentinoblastiv and predentinoblastivby vnim appearance retikulyarni and collogens fibres and procesuses of fibroblastiv. Vascular and nervous interlacements, fibred structures and various cellular elements – fibroblasti, makrofagi, are noncommunicative in the central layer of pulp, adipotsiti, bazofili (labrotsiti, mastotsiti, cells of Erlikha) of tissues, plazmotsiti, peritsiti, leucocytes. In pulp sometimes there are denticles (stone of tooth). It – formations of the rounded or wrong form are built from a dentine or dentinoid tissue of tverdi sizes to 2 –
Periodont is dense connecting tissue which provides fixing of tooth in the alveolus of overhead or lower jaw. That is why he is named yet a dental copula. Periodont is built from the thick bunches of fibres of collogens, two-bit of retikulyarnikh, elastic and oksitalanovikh fibres between which the layers of magnificent connecting tissue bed with vessels and nerves. From one side of his fibres of collogens grow in in cement of root of tooth, from opposite – in the periosteum of dental alveolus.
Areas of attachment of fibres on either side are periodontu in the state of permanent alteration: the areas of rezorbtsii alternate here with the areas of appozitsii. It remodelyuvannya which is carried out with participation of osteoclasts and osteoblastiv testifies to the permanent change of position of tooth in the process of life and gistofiziologichnim serves pid’runtyam of ortodontichnogo treatment (correction of anomalies of position of tooth). Retikulyarni fibres lie between the pinches of collogens and repeat their direction. Elastic fibres are related mainly to the walls of vessels of bloods. Described the oxytalan of fibre in prishiykoviy and bilyaverkhivkoviy areas to periodontu comparatively recently. They got the name through high firmness to the action of acids. After amino acid composition and structure to the oxytalan of fibre near to toimmature elastic, their direction mainly coincides with direction of fibres of collogens, and part from them is related to the adventitia. Round the apex of tooth a net is formed the oxytalan of fibre. It is set that with the increase of the functional loading on a tooth the amount of oksitalanovikh fibres grows in periodonti. The cellular elements of pe-riodontu are various: fibroblasti, bazofili of tissues, plazmotsiti, osteoblasti, osteoclasts. In addition, in magnificent connecting tissue there are accumulations of ephithelial cells which have the name of ephithelial tailings (aits) of Malasse periodontu. In periodonti it is possible to find out also the distopichni accumulation of cement – tsementikli. They are homogeneous (without a certain structure) and structured (have a nucleus with stratifications of cement round him). Germetizm provided periodontu dense connection of multi-layered flat epithelium of bottom of gingival crack with the cuticle of enamel of neck of tooth. Violation of safety of зубо-gingival connection can result to in to infekuvannya periodontu and developmentinflammatory process in him (pe-riodontit), and also in other navkolozubnikh tissues (paradontit).
ILLNESSES OF HARD CLOS OF TOOTH
Among the diseases of hard tissues of tooth (enamel, dentine, cement) a caries and separate uncarious defeats have most value.
CARIES
A caries is a disease which develops after prorizuvannya of teeth and shows up demineralizing and making progress destruction of hard tissues of tooth with formation of defect as a cavity.
It is known that a caries for a man met as early as the XII century to our era. Since then and to to now he became extraordinarily widespread. From data of VOOZ today to a 90% population of earth is ill a caries. A caries meets in any age, but mainly for children and teenagers, identically often for the persons of different floor.
Etiology and pathogeny. A dental caries is a «infection» of hard tissues of tooth, caused oxyntic bacteria. Already in the first scientific researches of caries was noticed to large influence kisplumb line and microorganisms on development of disease. In «Pathology of mouth cavity» opisuet’ caries as «microbal illness of kal’tsifikovanikh tissues of tooth, which shows up demineralizing of inorganic and destruction of organic substance of tooth».
At the study of caries such basic theories of development of this disease were offered: acid, proteolitichna, combined.
The acid theory of development of caries was offered in 1882 years by pione in research of caries of Міller. After this theory of acid of bacteria at first dekal’tsinuyut’ inorganic components of enamel, then damage a glikoproteinoviy matFig. Bacteria are fixed to the cuticle of enamel in which find protecting from the bactericidal components of saliva and product dekal’tsinuyuchi acids. Coming from modern positions, an acid theory explains development of caries on the lateral surfaces of crown of the tooth (labelial, tongues, middle, peripheral), where a cuticle is stored (nasmitova shell).
Proteolitichna theory. After this theory of bacterium of spochatku damage the glikoproteinoviy matrice of enamel, then dekal’tsinuyut’ enamel. This theory explains development of caries on the masticatory surfaces of teeth in enamel folds (fisurakh) and fossulas. In folds and fossulas of enamel there are areas with mionectic maintenance of inorganic component (enamel plates and pinches), which in some teeth penetrate through all layer of enamel. As acids of bacteria more frequent accumulate exactly in folds and fossulas of enamel, they conduce at first to the damage of albuminous components of enamel in the places of enamel plates and bunches, and farther to decalcifying of inorganic component.
The combined theory asserts that both foregoing theories correct, only an acid theory explains development of caries on the smooth, lateral surfaces of crown of the tooth, and proteolitichna is development of caries of enamel folds and fossulas of masticatory surface of tooth.
After any of these theories organic acids (in a tomu number milk) which product a bacterium damage hard tissues of tooth. What in a greater amount and more great while onsurfaces of tooth will be a bacterium and formed the bacteria of acid, the more so there will be a damage of hard tissues of tooth.
Such factors are instrumental in the damage of tissues of tooth, as: dental raid, odontolith, the features of feed of habitants of the developed countries (soft meal, use of sugar), hyposecretion of saliva, diminishing in saliva of maintenance of parotinu, violation of mineral exchange, are certain, in particular such, which conduce to diminishing of maintenance in the teeth of calcium, phosphorus, fluorine. A caries develops more frequent at some endocrine diseases, pregnancy, in periods of change of baby teeth, sexual ripening.
Such factors slow progress of caries, as: remineraliza-tsiya of hard tissues of tooth due to the receipt of salts from saliva, education as «barrier» of transparent and regenerator dentine.
Morphogeny of carious defeat. By a caries an enamel is usually struck at first, farther dentine, rarer cement of tooth. The morphogeny of caries in different hard tissues of tooth has the features.
Caries of enamel. Karies of smooth surface of enamel develops mainly on the lateral surfaces of crown of the tooth. The area of damage of enamel has a form of cone basis of which orientovana to the surface, apex – in direction to dentinal-enamel connection.
When the area of carious defeat spreads from an enamel on a dentine, at first struck the area of dentine had only. In such case restoration of tooth can be conducted with the minimum loss of his healthy tissues.
The caries of enamel in the area of enamel folds and fossulas develops on the masticatory surface of teeth. The area of damage of enamel has a form of cone also, but his basis orientovana to dentinal-enamel connection, and verkhivka- to the masticatory surface of tooth. At distribution of carious defeat from an enamel on a dentine the vast area of dentine is immediately damaged. Restoration of tooth in such case needs considerable loss of his healthy tissues.
The caries of dentine makes progress far quick in comparing to the caries of enamel. It is conditioned tim, that dentine less kal’tsifikovaniy porivnyanno with an enamel (70% and 96% accordingly) and contains dentinal tubulis which microorganisms and products of their vital functions spread for. At the same time progresses of caries in a dentine slow such processes of regenerators, as education transparent and reparativnogo dentine. A transparent dentine, or «sklerozovaniy», appears as a result of surplus deposit in a dentine, in particular in education of dentinal tubulis, salts of calcium. The tubulis of such dentine zvuzheni, a structure is homogeneous. After a kind he is transparent comparatively with the unchanged dentine. Reparativniy, zamisniy, or the second dentine does not have the vporyadkovano placed dentinal tubulis. Narrowing of dentinal tubulis in a transparent dentine and placing of lacking amenities of dentinal tubulis in a reparativnomu dentine slow distribution of microorganisms and products of their vital functions in a dentine.
The caries of cement develops, as a rule, for senior people in which the root of tooth and cement takes off all the clothes contacts with the liquid of mouth cavity. As soon as and surfaces of cement of sformuet’sya albuminous shell, bacteria damage cement. Microorganisms get to cement, above all things, through openings which remain in place of the blasted sharpeevskikh fibres of periodontal’noy copula. A defeat a caries in such case begins on the wide surface of cement round the root of tooth.
Pathoanatomy. After character of kliniko-morfologichnikh displays select 4 stages development of caries: stage of spot, superficial, middle and deep caries. Ran across a caries can be rapid and slow.
Stage of spot. On-the-spot enamel a white opaque spot which after a kind reminds a lime appears (chalky spot). A pathological process shows up dismineralizatsieyu and demineralizing of enamel in a subsuperficial layer. Maintenance of calcium, phosphorus, fluorine and other mineral matters diminishes in the area of spot. At first salts of calcium disappear from intervals between prisms, later – from prisms.
Intervals between prisms become wider, the contours of prisms are worn away, become fine-grained, transforming into necrotic mass. In investigation of it an enamel in the place of spot loses homogeneity, brilliance, becomes soft, more penetrating. A chalky spot can become pigmentovanoy (vid yellow to the darkly brown color) due to exogenous pigments or accumulation in the spot of tirozinu with subsequent formation of melaninu. Enamel dentinal connection on this stage is not broken. A cariosity can go out slowly, accompanied remineralizatsiyu. Then a spot acquires clear contours.
A superficial caries Shows up demineralizing and destruction of enamel within the limits of dentinal-enamel connection. Salts of calcium disappear from enamel prisms, a matter collapses between prisms, prisms look more rel”efnimi and transversal cut into strips as a result of uneven dissolution of salts of calcium. Farther prisms become placed lacking amenities and fully lose a structure. In the areas of defect enamels accumulate microorganisms which quickly spread the softened mizhprizmennoy matter and cracks, that utvoryuyut’sya between the stored prisms.
At rapid progress of caries a process spreads on a dentine, remineralizatsiya (zvapninnya) develops at slow motion, a rozm’yagshena enamel becomes hard.
Middle caries. Dentinal-enamel connection collapses on this stage, a cariosity passes to the dentine. Dentinal tubulis broaden, filled plenty of microorganisms. Under act of toxins of microorganisms dystrophy and necrosis develop in the procesuses of odontoblasts. A shell which covers dentinal tubulis from within collapses also. It is instrumental in penetration of products of vital functions and microorganisms in the tubulis of dentine are deeper located, strengthens his demineralizing and softening.
Middle caries.
Bottom of carious cavity. Dentinal tubulis are extended.
On this stage a carious cavity is formed (hollow). The area of defeat has a form of cone, oriented basis to the surface, by an apex – inlayer of tooth. In the wall of bottom of carious cavity it is possible to select three areas: softened dentine, transparent dentine and zamisnogo dentine. The area of the softened dentine is formed a soft anhistic dentine which quite does not contain a calcium and which plenty of microorganisms is in. It follows to examine formation of transparent and zamisnogo dentine as a display of reparativnoy regeneration.
Deep caries. In the softened dentine appears largenesses, as a cavity, carious cavity. Between the bottom of carious cavity and pulp the skim of dentine is saved only, or a carious cavity spreads on pulp.
Anatomic localization of carious defeat. More frequent. comparatively with the teeth of lower jaw, the teeth of supramaxilla are struck a caries. In a lower jaw the best krovopostachannya, teeth easier clear up vid tailings of meal, that in the turn prevents development of terms for the origin of caries. Struck a caries more frequent first large root teeth are molyari on which ismost loading is at mastication. The second after frequency of defeat a caries are second large root teeth, third are small native (premolyari) and overhead chisels, fourth are dog-teeth. The frontal teeth of lower jaw are struck rarely. In molyarakh and premolyarakh a caries begins usually on masticatory surfaces in folds and fossulas of enamel or on the contacting between itself surfaces of teeth. Rarer struck the caries of schochni surface of teeth and quite rarely – tongues. Relatively rarely there is a caries of neck of tooth and caries of cement.
Caries of neck of tooth
Caries of cement
Caries of lateral surface
Caries of contact surface
Circular caries
Children at the wrong formed teeth and violations of exchange of calcium have such variants of caries.
1. Circular caries at which a carious defeat is localized in the area of neck of tooth, engulfing her circular. Such caries develops quickly and a transparent dentine does not appear here.
2. An early, subenamel caries develops directly under the layer of enamel.
5. Retrograde caries. Development of carious defeat begins from the side of pulp. A dentine is damaged at first, then enamel. Such caries can develop at festerings pulpits, when an exciter gets in pulp a gematogennim way, at traumas and anomalies of odontogeny.
UNCARIOUS DEFEATS
Before the uncarious defeats of hard tissues of tooth take: wedge-shaped defects, fluorosis, erosion and acid necrosis of teeth.
WEDGE-SHAPED DEFECTS
Wedge-shaped defects are -це defects of hard tissues of neck of tooth, more frequent in all ikol and premolyariv which is placed on the vestibular surface of teeth. A disease develops as a result of trophic violations in the organic matter of enamel and dentine, that often develop for patients with parodontozom, diseases of gastroenteric highway, endocrine system.
Wedgethe ovidni defects of teeth develop by years. As a result of formation of reparativnogo dentine pulp remains marked off and atrophy and sclerosis develop in her.
FLUOROSIS
A fluorosis is a disease which develops at protracted and surplus postupanni in the organism of fluorine and shows up the defeat of many organs, including teeth. A disease develops in endemic regions, where maintenance of fluorine in water and food products anymore vid 2 mg/l (norm 0. 7-1. 2 mg/l).
In teeth at a fluorosis the processes of forming and calcinousis of enamel are violated. Select four degrees of flyuoroznogo defeat of teeth:
And a degree is a very weak defeat. On the lip and tongue surfaces of teeth no more than on 1/3 their areas are observed poorly expressed separate shallow farforopodibni or chalky spots and ribbons;
A ІІ degree is a weak defeat. Farforopodibni and chalky spots and ribbons occupy the areas of crown of the teeth near a half. There are separate pigmentovani spots, but urazhennya is localized only in an enamel;
ІІІ degree – a defeat is moderato expressed. More than on the half of surface of teeth spots are placed which meet between itself;
The IV degree is a heavy defeat. On-the-spot teeth separate and plural erosions of enamel of different form appear. They can be colourless or pigmentovani (vid yellow brown to the black). As a result of violation of mineralizatsii of hard tissues of tooth at III and the IV degrees of flyuoroznogo defeat teeth become fragile, easily worn away and collapse.
Erosions of teeth
Erosions of teeth are making progress chashepodibnoy forms of diminishing of enamel and dentine on the vestibular surface of teeth, at first chisels. and then ikol and premolyariv of supramaxilla. Reason of disease is not known. Develops for the people of middle ages. The chronic ran across with the gradual defeat of all plenty of teeth. Defects are very sickly.
Acid necrosis of hard tissues of tooth.
Acid necrosis of hard tissues of tooth is a professional disease which develops in lyudey, which contact on a production with inorganic acids.
A hit in the mouth cavity of acids results in the decline and remineralizing properties of saliva. It in same queue is instrumental in rapid destruction (to elimination) of hard tissues tooth.
A disease develops slowly with the defeat of crowns of many teeth. In connection with permanent formation of reparativnogo dentine at this disease a pulpit does not develop.
ILLNESSES OF PULP AND PERIAPICAL CLOS OF TOOTH
In pulp there can be various reactive changes under act of general and local factors. Inflammation of pulp is separately selected (pulpit).
REACTIVE CHANGES OF PULP
Among reactive changes pulpes distinguish disorders of blood- and lymphokinesis, atrophy, necrosis, dystrophy, denticles and vnutrishnepul’parni cysts.
Disorders of blood- and lymphokinesis. There are anemia in pulp, povnokriv’ya, hemorrhages, thrombosis, embolism, was swollen. They arise up as as a result of local, andk and general processes. Hemorrhages in pulp can be reason of development of pulpit.
Atrophy of pulp. An amount and sizes of cells diminishes foremost, at first odontoblastiv, and then pul’potsitiv. On such background expressly sklerozovana spoluchnotkaninna basis of pulp concernes as a net (sitkopodibna atrophy of pulp).
Necrosis. Can develop at a festering pulpit, if a cavity is closed. In the cases when there is connection of cavity of pulp and carious cavity, possibly penetration of anaerobic gnilostnoy flora and origin of gangrene of pulp.
Dystrophy. In odontoblastakh more frequent in all there is gidropichna and fatty dystrophy. In stromi of pulp – mukoidne and fibrinoidne swelling of fibres of collogens, hyalinosis of vessels and actually connecting tissue. Sometimes in pulp, especially at atrophy processes, the shallow little bodies of amyloids concerne. Considerably more frequent there is kal’tsinoz (petrifikati of pulp) which results in violation of processes of exchanges, that vplivait is on the state of hard tissues of tooth, and at presence of caries worsens his flowing.
Denticles. It is round or oval educations which are localized or freely disposed in pulp or pristinkovo, uniting from dentinomas, or in the middle of mass of dentine (interstitsial’ni denticles). Denticles more frequent in all meet in molyarakh of the second teeth. Depending on a structure the highly developed distinguish and niz’korozvineni denticles. The structure of highly developed denticles is near to the structure of zamisnogo dentine and characterized the presence of dentinal tubulis. Niz’korozvineni denticles are built from amorphous salts, have a layer structure and does not contain dentinal tubulis. Interstitsial’ni denticles are located in a dentine or it is isolated vid the bulk of dentine, or dentinal tubulis pass in the ductule of denticles. Especially often denticles meet at chronic pulpits and illnesses of paradontium.
Intra pulp cyst. There are poodinoki and plural. Arise up as a result of different patologichnikh processes in pulp.
PULPIT
A pulpit is inflammation of endodontium. Characterized ordinary for an inflammatory process components – al’teratsieyu, eksudatsieyu and proliferatsieyu.
Etiology and pathogeny. Reasons of pulpit can be various, but most frequent is an infection. A pulpit rarely arises up in aseptic terms. As a rule, a pulpit develops as complication of middle and deep saprodontia, when microbes or toxins get in pulp through dentinal tubulis or directly through narrow polosku of the softened dentine of bottom of carious cavity, and also at its penetration.
The origin of pulpit sometimes is not related to the caries, but predefined penetration of infection through the apikal’niy opening of tooth at an inflammatory process in periodonti (ascending pulpit). There are also very liquid reports about the cases of origin of pulpit by a gematogennim and lymphogenic way at a sepsis. A pulpit can also cause trauma of tooth, action of physical factors (for example, thermal and mekhanichthem at treatment of tooth under a crown) but chemical factors, including medicinal at treatment of tooth (for example, matters for stopping). Intensity and character of inflammation in pulp depends not only on microbes but also vid the state of local and general reactivity of organism. An inflammatory process in pulp flows in a cavity, limited hard tissues, that predetermines him a feature, namely to the zatrudnennya outflow as a result of narrowity of root-canals and small of the apikal’nogo opening. It results in the expressed inflammatory hyperemia edema which strengthens dystrophic changes and can entail necrosis. As a result of those reasons arise up and clinical features of pulpit which show up foremost a megalgia.
Pathoanatomy. A pulpit is divided into sharp, chronic and chronic with sharpening. In addition, distinguish diffuse (total) and vognischeviy, which depending on localization can be crown or root.
SHARP PULPIT
Sharpa pulpit is divided into serosal and festering. Such division is conditional enough clinically, as a serosal pulpit as a rule in a few hours passes to festering. A sharp pulpit begins as serosal vognischeviy near a carious cavity. Thus there is hyperemia in pulp, was swollen, single leucocytes, limfotsiti, sometimes eritrodiapedez. In a few hours the expressed neutrophilic infiltration, and also dystrophic changes of nervous fibres, develops with disintegration of mielinu. There is vognischeviy festering pulpit. Macroscopically here is a little abscess (rarer two) of yellow green color, located in giperemovaniy to koronkoviy pulp. Microscopically an abscess consists of leucocytes and cellular detritus. Directly round an abscess there is an edema, hyperemia, polimorfnoklitinna inflammatory infiltration. At progress of illness from an abscess in koronkoviy pulp festering inflammation spreads on all koronkovu and root pulp and a diffuse festering pulpit develops orphlegmon of pulp. At penetration from a carious cavity there can be a gangrene of pulp in pulp of anaerobic flora of cavity of mouth. Thus macroscopically pulp has the appearance of grey black mass with a putrid smell, and microscopically -безструктурної of nekrotizovanoy tissue which contains the crystals of fat acids and microbes often. General duration of sharp pulpit makes 3-5 days.
Complication and consequences. They depend on character of inflammation and his distribution. A serosal pulpit can resolve at the removal of his reason. A festering pulpit, as a rule, ends with death of pulp and passing to the chronic form.
Chronic pulpit
A chronic pulpit more frequent in all develops gradually, as an independent form, but can arise up and as a result of sharp pulpit. Distinguish a gangrenous, granulating (hypertrophy) and fibrotic chronic pulpit.
A gangrenous pulpit mainly arises up as a result of sharp after partial necrosis of pulp. In will savegranulation tissue which marks off dead the masses appears part of pulp her. A gangrenous pulpit can arise up and as a result of chronic granulating pulpit at his sharpening. Thus develops staz and thrombosis of vessels of granulation tissue which results in its necrosis.
Granulating (hypertrophy) a pulpit characterized chronic productive inflammation. There is excrescence of granulation tissue which spreads on all koronkovu, and quite often and on root pulp. Granulation tissue can spread and on a carious cavity with education the polypus of pulp. A polypus is soft, red color, bleeds easily. Surface of him – with ulcers or epitelizovana due to the epithelium of gums. At a granulating pulpit there can be rozsmoktuvannya of areas of dentine which results makrofagami of, in expansion of pul’parnoy cavity. Together with rezorbtsieyu of dentine can be observed and the opposite phenomenon is formation of hard tissue, similar on a bone, and dentine -so-called osteodentine. Characteristic is also formation of petrifikativ and dentikl.
A fibrotic pulpit is characterized substituting for more greater part of tooth by connecting tissue with plenty of fibres of collogens and vognischevimi infil’tratami from limfotsitiv, makrofagiv and plazmatichnikh cells. The amount of cells diminishes in course of time, fibres of collogens of gialinizuyut’sya, petrifikati and niz’korozvineni denticles appear often.
Complication and consequences. Chronic forms end with atrophy, sclerosis, hyalinosis, kal’tsinozom, formation of denticles. Frequent complication of pulpit is periodontit.
Chronic fibrotic pulpit. Fibroz and vognischeva (makrofagami) infiltration limfotsitami.
Apical granuloma as complication of pulpitis
PERIODONTIT
Periodontit (or peritsementit) is inflammation which is localized directly iavkolokoreneviy the spoluchnotkaninniy shell of tooth – periodonti.
Etiology and pathogeny. Reason of periodontitu can be an infection, trauma, chemical matters, there are medications in a tomu number. Especially large value of infection, in fact she not only is the most frequent reason of illness but also joins in with other pathogenic factors. Basic part is here acted by streptococci. Ways of penetration of infection can be different. Most frequent is a внутрішньозубний (niskhidniy) way, when periodontit arises up as complication of pulpit which results in development of apikal’nogo periodontitu. Rarer there is a pozazubniy (pin) way from surrounding tissues (at stomatitakh, traumas of tooth and gums) of -розвивається marginal’niy periodontit. Very rarely periodontit arises up at lymphogenic or gematogennomu distribution of infection (ascending way).
Periodontit more frequent in all arises up for childrenand people of young age, why the magnificent promotes and spoluchnotkaninna is very vascularized navkolokoreneva shell in such age. In addition, children have more wide root-canals and apikal’ni openings of teeth. More frequent in all periodontit develops in a lower jaw, and his localization answers first, second and third molyaram (to 70% cases).
Pathoanatomy. Distinguish vognischeviy and diffuse periodontit. The diffuse mainly develops from vognischevogo – apikal’nogo or marginal’nogo. From an apikal’noy area an inflammatory process can spread on a periodontal’niy crack to gums, and from marginal’noy – on periodontal’niy connecting tissue can attain to the apex of tooth. After motion periodontit is divided
into sharp, chronic and chronic with sharpening.
Acute periodontit
Sharp periodontit can be serosal and festering. At serosal periodontiti macroscopically navkolokoreneva shell of giperemovana, with an edema. Microscopically there is povnokriv’ya of vessels of bloodsshallow hemorrhages, was swollen, perivaskulyarna cellular infiltration from the two-bit of leucocytes, limfotsitiv and makrofagiv. In a small hole only on separate areas can be marked osteoclastic rezorbtsiya of bone tissue is poorly expressed. At liquidation of reason sharp serosal periodontit calms down. But more frequent he quickly passes to the sharp festering, localized mainly also in the area of apex of root of tooth. The festering melting of tissues can result in the origin of sharp abscess in the area of apex of tooth (apikal’niy abscess), or to diffuse festering infiltration of navkoloverkhivkovoy tissue with passing to the small hole of tooth, gums and transitional fold. Thus in soft tissues of cheek, transitional fold and sky perifokal’ne develops serosal inflammation with the expressed edema of tissues, which is named a gumboil (parulis). A sharp process in periodonti lasts vid 2-3 days to 2 weeks and ends with convalescence or passing to the chronic form.
Chronic periodontit
Chronic peeriodontit divide into basic three kinds: granulating, granulematozniy and fibrotic. Granulematozniy – depending on the type of granulemi, in the turn, divided into three kinds: simple granulema, difficult (or ephithelial) granulema and kistogranulema.
Granulating periodontit. At him granulation tissue appears in the area of apex of tooth. As a rule, he arises out of sharp, when an apikal’niy abscess does not develop, and exsudate inflammation passes to productive. Although sometimes an abscess can precede him. In such cases after evacuation of pus from an abscess ooritsyakh excrescence of granulation tissue passes in periodonti. Macroscopically at granulating periodontiti there is rozrikhlena tissue of red color in periodonti. At microscopic research typical is excrescence of granulation tissue with plenty of capillaries and cellular elements as accumulations of limfotsitiv, monotsitiv, plazmatichnikh cells and moderate amount of leucocytes. At sharpening of khronichnogo of granulating periodontitu the amount of leucocytes grows. At the protracted flowing of disease among other cellular elements it is often possible to look after the groups of foamy ksantomnikh cells. According to the areas of excrescence of granulation tissue intensive osteoclastic rezorbtsiya of bone tissue of alveolar procesus of jaw and rozsmoktuvannya of cement passes at granulating periodontiti. Rezorbtsiya of bone tissue passes both outside periodontu and in bone-cerebral spaces, where granulation tissue penetrates. Microscopically here along the beams of bones evidently plenty of osteoclasts. It is sometimes possible to look after smooth rezorbtsiyu of bone tissue: a compartement without osteoclasts, filled cellular-fibred tissue, appears in a bone beam. At progress of chronic granulating periodontitu rezorbtsiya of bone tissue grows, resolves on this area and kortikal’niy layer of jaw with passing of inflammatory process to adjoining soft tissues. It can leadbefore formation of no-rits’: on gums, skin pokrovakh of cheeks, chin and even on a neck. It is necessary to mark that at granulating periodontiti, except for intensive rezorbtsii of bone tissue, simultaneously there is formation of bone tissue in the alongside located areas. It is often possible to see under a microscope, as in the same bone beam from one side, outside peritsementu, osteoclastic or smooth rezorbtsiya passes, and from the second is osteoblastic formation of bone. At fading of pathological process (mainly as a result of treatment) there is ripening of granulation tissue, appearance in her of fibroblastiv and excrescence of fibred tissue, and also formation of new beams of bones from the side of the stored bone tissue. At stratification of new bone tissue on already existing a striola which is more intensive painted gematoksilinom and named the line of agglutination appears between old and new bone tissue. With fading of granulating peritsementitu education passes alsoto cement of tooth, built on the type of the second. Sometimes there is surplus formation of cement tissue of root of tooth of -гіперцементоз (except for chronic periodontitu he is observed also at parodontozi, functional overload of tooth, trauma).
Granulematozniy periodontit shows up formation of granulem in an area apexes of root, which are named apikal’nimi granulemami. Distinguish the followings types of apikal’nikh granulem: 1) simple granulema, 2) difficult, or ephithelial, granulema, 3) kistogranulema.
Simple granulema is a knot of grey or siro-rozhevogo color which is densely connected by fibrotic tissue with the apex of tooth macroscopically. That is why at an odontectomy granulema, as a rule, retires together with a tooth. Histological simple granulema consists of ordinary granulation tissue for peripheries of which there is fibrotic tissue as a dense capsule.
Apical simple granulema. Granulation tissue.
A degree of maturity of granulation tissue can be different depending on duration of existence of granulemi. At of long duration existence fibroblasti prevail in her, placed there are foamy cells, crystals of cholesterol and fat acids, surrounded bagatoyadernimi giant cells. In cases of sharpening of inflammatory process in granulemi plenty of leucocytes appears among the cells of granulation tissue, and sometimes there can be suppuration of granulemi.
Action of reason which caused granulemu halted, chronic inflammation goes out slowly, granulation tissue grows into fibred connecting tissue and there is scarring of granulemi. Bone tissue of alveolar procesus in accordance with localization of granulemi is reserved, that well concernes roentgenologic.
Difficult (ephithelial) granulema macroscopically looks the same as simple. She also is densely connected by fibrotic tissue with the apex of tooth. Pri microscopic research difficult granulema consists of granulation tissue, pierced in different directions thin and wide enough tyazhami of flat epithelium. In thin tyazhakh ephithelial cells are as compared to wide tyazhami anymore vityagneni, that have a fusiform form. The origin of epithelium in granulemakh most authors binds to excrescence at chronic inflammation of tailings of epithelium from zarodishevogo of emalevogo organ, which as shallow hearths are in periodonti (aits of Malasse). However there are other points of view of origin of ephithelial tyazhiv – growings in of epithelium in tissue of granulemi from gums, or germination after motion of norits’. In accordance with localization of ephithelial granulemi, as well as at outage of granulemi, there is a defect of bone tissue of alveolar procesus.
CYSTOGRANULEMA
CYSTOGRANULEMA
CHRONIC PERIODONTITIS COMPLICATION
CHRONIC PERIODONTITIS COMPLICATION
Cystogranulema develops from difficult apikal’noy granulemi and is a cavity, covered a flat epithelium. In the central areas of wide ephithelial tyazhiv passesdystrophy and disintegration of ephithelial cells is with the origin of cracks, which, meeting, form a cavity. Round an epithelium which covers kistogranulemu, there is granulation tissue. Fibrotic tissue appears on periphery of granulemi, what granulema is fastened on the root of tooth. An end of apex of tooth, as a rule, is in the cystophorous cavity of granulemi. A cavity in the center of kistogranulemi as a result of piling up of exsudate from granulation tissue is gradually multiplied, achieving largenesses. Thus prikoreneva appears or radikulyarna cyst.
Fibrotic periodontit – more frequent in all it is investigation of granulating periodontitu. His origin is predefined ripening of granulation tissue in default of sharpening of pathological process. In addition, reasons of fibrotic periodontitu can be small traumas or pressure on periodont of prosthetic appliances, or large deposits of tooth to the stone. Macroscopically at fibrotic periodontiti a considerable compression concernes to periodontu.Microscopically there is excrescence of fibrotic tyazhiv which мононуклеарні infil’trati is between, sometimes -ксантомні cells.
Complication and consequences. At heavy motion, in cases of suppuration of granulemi, inflammation from can spread periodontu on periost, and then and on marrow of alveolar escape. There is periostitis or and osteomielit of small hole of tooth. At the proper localization on a supramaxilla development of festering antritis is possible.
PARODONT’S ILLNESSES
A paradontium is a морфо-functional complex in composition of which enter: gums, periodont, bone alveolus. Before the diseases of parodonta belong: gingivitis, dental deposits, parodontit, parodontoz, idiopatichniy making progress parodontoliz, tumours and tumular processes.
The diseases of parodonta in most cases develop as a result of unbalance between bacterial symbiosis and tissues of mouth cavity which is the balanced biological system. In their development playa t’ role is both local and general (endogenous) factors, changes of reactivity of organism.
GINGIVITIS
Gingivitis is inflammation of mucus shell of gums without violation of safety of зубо-gingival connection. Gingivitis is divided after distribution on local and generalizovaniy, after motion – on sharp and chronic.
The most frequent reason of development of gingivitis are microorganisms, especially associations of streptococci which are in a dental raid. Local gingivitis can develop after the mechanical trauma of gums, under act of physical and chemical factors. Generalizovaniy gingivitis develops, as a rule, for patients with infectious and endocrine diseases, more frequent in all for children and persons of young age.
Pathoanatomy. After character of morphological changes select such forms gingivitis: catarrhal, ulcerous, hypertrophy. Sharp and chronic motion, hypertrophy – chronic motion, can have catarrhal and ulcerous gingivitis.
Catarrhal gingivitis of kharakterizuby et’sya infiltration by neutrophilic leucocytes, and in course of time limfotsitami, makrofagami, plazmatichnimi cells and hyperemia, edema, small gemoragiyami.
At an ulocace there are superficial ulcers of mucus shell, covered фібринозно-festerings tapes, under which intensive infiltration is by neutrophilic leucocytes, limfotsitami, makrofagami, plazmatichnimi cells, hyperemia and was swollen.
At hypertrophy gingivitis in gums productive inflammation develops with infiltration limfotsitami and plazmatichnimi cells, giper-keratozom and by the acanthosis of pokrovnogo of multi-layered flat epithelium. In periods of sharpening of hypertrophy gingivitis in gums find, except for the changes indicated higher infiltratioeutrophilic leucocytes, fat cells.
Chronic hypertrophy gingivitis is with sharpening. Diffuse polimorpho-cellular inflammatory infiltration, acanthosis of epithelium.
Complication and consequences: Sharp local or sharp generalizovaniy gingivitis at liquidation of reason which caused him is completed convalescence. After chronic catarrhal, ulcerous and hypertrophy gingivitises parodontit develops often.
DENTAL ADJOURMENTS
Before dental deposits take a dental raid and odontolith.
A dental raid consists of mucus, leucocytes, tailings of meal. There is plenty of microorganisms in him, including those which conduce to development of caries.
An odontolith appears a dental raid which a deposit of phosphate of calcium is in. More frequent in all he meets in the area of neck of tooth and gingival pocket. In color an odontolith can be white, brown, siro-zelenim. An odontolith assists development of periodontitu, parodontitu, to gingivitis.
PARODONTIT
Parodontit is inflammation of parodontum with subsequent destruction of peri-odontum, bone tissue of dental membranes and forming of gingival and periodontic pocket.
Fromand can be distributions of parodontitis local and generalization. Local parodontit can be sharp and chronic, develops for the people of different age. Generalizovaniy of parodontit has chronic motion with the periods of sharpening. He meets for people more senior 30-40 years.
Depending on the depth of well-educated parodontal’noy pocket select easy (to 3.
Etiology and pathogeny. Reason of parodontitu are associations of microorganisms which are in a dental raid and odontolith. Local and general factors assist development of disease. To the local factors take: anomalies of bite and odontogeny (them skuchenist’ and dystonia), anomaly of development of soft tissues of cavity of mouth (small prisinok company, short bridle of lips or its wrong attachment). To the general factors which assist development of parodontitu, take: saccharine diabetes, illness of Itsenko-kushinga, disease of privy parts, nervous systemsi, rheumatic illnesses, ulcerous illness, chronic hepatitis, atherosclerosis, hypertensive illness, avitaminosises, metabolic disturbances.
At presence of local and general factors and at their combination terms at which the bacteria of dental raid and odontolith conduce to development of gingivitis and parodontitu are created. Thus violated composition of saliva and liquid of mouth. They become more viscid. It, in the turn, is instrumental in yet greater formation of dental raid and odontolith.
The damage of bone tissue is conditioned an action biologically of active matters which appear in the area of inflammation: lizosomni enzymes of neutrophilic leucocytes, neurohumors of cells of the immune system.
Mainly local factors matter in development of local parodontitu, in development of generalizovanogo parodontitu are general factors in combination with local.
Pathoanatomy. A disease begins from the defeat of gingiva chronic catarrhal or hypertrophy gingivitis.
Chronic hypertrophy gingivitis is with sharpening. Diffuse polimorfnoklitinna inflammatory infiltration, acanthosis of epithelium.
Bazofilic the masses accumulate in education of gingival furrows in a far – nad’yasenniy and pid’yasenniy raid. In composition a raid there is plenty of microorganisms, zluschenikh ephithelial cells, leucocytes, necrotizing the masses. Gidropichna dystrophy, necrosis, zrogovinnya, develop in the epithelium of marginal’noy area of gums. In connecting tissue of gums mukoidne develop and fibrinoidne swellings, vaskuliti. зубо-gingival connection, circular copula of tooth, collapses as a result of inflammation, a зубо-gingival pocket is formed. Microorganisms and toxins get to the periodontal’nu crack, where in future inflammation develops also. A periodontal’na crack broadens.
Already bone tissue of paradontium, pazushna, lakunarna and smooth rezorbtsiya develops in which, collapses on the early stages of development of disease. Lakunarna rezorbtsiya begins from the edge of comb of dental fossulasand shows up appearance of osteoclasts, placed in lakunakh. It results in horizontal rozsmoktuvannya of comb of small holes. At vertical rozsmokutvanni osteoclasts and hearths of rozsmoktuvannya of bone are placed on length of mizhzubnoy membrane from the side of paradontium. At the same time there is lakunarna rezorbtsiya of beams of bones in the body of bones of jaws. A parodontal’na pocket, which is filled homogeneous the masses, colonies of microorganisms, neutrophilic leucocytes, tailings of meal, is formed. At intensifying of disease the depth of parodontal’noy pocket is multiplied. . The external wall of parodontal’noy pocket and bottom is formed granulation tissue which is covered a multi-layered flat epithelium. Thus an epithelium achieves the apex of tooth. In granulation tissue a lot of neutrophilic leucocytes, plazmatichnikh cells, makrofagiv, limfotsitiv. From a parodontal’noy pocket, especially in the period of sharpening, a pus is selected (alveolar pioreya).
In course of time an osteoporosis develops in the alveolar procesuss of jaws, asiy it is possible to discover roentgenologic. As a result of roentgenologic research rezorbtsii of bone tissue of small holes of teeth select such degrees:
I degree – the edges of bones of small holes of tooth are diminished, on a height to 1/4 roots
tooth;
II degree – the edges of bones of small holes of tooth are diminished, on a height to 1/2 kore
nya tooth;
III degree – the edges of bones of small holes of tooth are diminished, on a height to 2/3 roots of tooth;
IV a degree is complete dissolve of bone tissue of small holes, the apex of root of tooth is placed in soft tissues of paradontium.
At parodontiti in a tooth there is rezorbtsiya of cement with forming of niches of cements and cement-dentinal. At the same time there is new formation of cement (gipertsementoz) and beams of bones. Dystrophy and atrophy develop in an endodontium.
Complication and consequences. Parodontit results in loosening and fall of teeth. Atrophy of alveolar escape of shelepi complicates protezuvannya. The hearths of festering inflammation in a paradontium can become inorotami infections and to result in development of sepsis.
PARODONTOZ
Parodontoz is a chronic disease of paradontium of initially dystrophic character. Among all diseases parodonta parodontoz makes 4-5% cases. Parodontoz quite often develops for patients with the uncarious defeats of hard tissues of tooth, in particular by erosion of enamel, wedge-shaped defects.
Reason of parodontozu is not clear. A background for his development are those diseases which assist development of parodontitu.
The basic display of parodontozu is retraktsiya of gums with baring of neck of tooth, but in default of before it to gingivitis and parodontitu. A defeat develops more frequent in all in the area of chisels and ikol. In bone tissue of teethridges there is a delay of change of structures of bones, bulge of trabekul, strengthening of line of agglutination of osteons with the next loss of ordinary structure of bone (the hearths of compression alternate with the hearths of osteoporosis), smooth rezorbtsiya of bone prevails. These changes are combined with a defeatmikro-tsirkulyatornogo river-beds are with development of hyalinosis and sclerosis of walls of shallow vessels with narrowing and complete obliteratsieyu of their road clearance, reduction of capillaries. There are also dystrophic changes of connecting tissue.
IDIOPATICHNIY MAKING PROGRESS PARODONTOLIZ
Idiopatichniy parodontoliz is a disease of unknowature with the constantly making progress lysis of all tissues of parodonta. Meets for children and teenagers with a neutropenia, by the syndrome of Papiyona-lefevra and patients on insulinzalezhniy saccharine diabetes. There is rapid formation of gingival and parodontal’noy pockets with alveolar pioreeyu, dicking and fall of teeth during 2-3. To put the milk lose, and farther the second teeth.
PARODONTOMI
Parodontomi are tumours and tumular processes of parodonta. The tumours of parodonta develop from soft tissues of parodonta, more frequent of high qualities. The feature of their motion is the frequent injuring from virazkuvannyam, by development of inflammation. Among the tumular processes of gums more frequent zustrichaet’sya epulis, rarer fibromatosis of gums.
Epulis
Epulis is education clear, which develops as a result of chronic irritation of tissues of gums a crown, stopping, root of the blasted tooth. Education develops more frequent in all on gums of chisels, ikol, rarer premolyariv and, as a rule, on a vestibular surface. Epulis has a mushroom-like, sometimes rounded form, by sizes vid 0, 5 to 2, 0 see in a diameter, rarely greater. Epulis is fixed a leg or wide basis to superalveolar tissues. Meets in age 20-40, more frequent in all for women. In a period pregnancy growth of epulisa can be accelerated. In color epulis can be blond, poorly red, sometimes brown.
Epulis
Epulis
After a histological structure select such types of epulisa:
* angiomatozniy;
* fibrotic;
* gigantoklitinniy.
Angiomatozniy of epulis after a structure reminds capillary gemangiomu. In him always find hemorrhages, vognto the ischa hemosiderosis.
Fibromatous epulis after a structure reminds a hard fibroma.
Gigantic cell epulis, or peripheral gigantic cell granuleoma, consists of connecting tissue with plenty of the thin-walled vessels of sinusoidnogo of type and generous or more small amount of giant cells as osteoclasts and shallow cells as osteoblastiv. In him there are plural dribnovognischevi hemorrhages, hearths of hemosiderosis, that is why macroscopically such epulis of brown color. The aits of ossiform tissue and primitive beams of bones can appear in this epulisi.
Gigantoklitinniy of epulis. Plenty of giant bagatoyadernikh cells (as osteoclasts).
Select also central gigantoklitinnu granulemu, which after a histological structure similar to peripheral gigantoklitinnoy granulemi, but placed in bone tissue of alveolus. The scopes of her are clear. Central and peripheral gigantoklitinni granulemi is often localized in a lower jaw and grow in direction of language.
On-the-spot epulisa ulcers, granulation tissue, infil’trovana limfotsitami and plazmatichnimi cells, appears in the place of which, develop often. In the place of such epulisu there can be rezorbtsiya of bone tissue of alveolus which conduces to dicking of tooth. In the epithelium of mucus shell which covers epulis, a parakeratosis, acanthosis, psevdoepiteliomatozna giperplaziya, develops.
