1.1. PERIOSTITIS OF THE JAWS
Periostitis is an inflammatory process with a focus of inflammation in the periosteum. The causes of the disease are teeth with chronic foci of inflammation in the pulp or periodontium, suppuration of an odontogenic inflammatory cyst, difficult eruption of both temporary and permanent teeth, trauma. According to the clinical course and the pathomorphological picture, acute periostitis (serous and purulent) and chronic (simple and ossifying) are distinguished.
Acute serous periostitis manifested by the smoothness of the transitional fold, severe pain on palpation. The mucous membrane over the inflamed periosteum is hyperemic, edematous. The process is localized in the area of the "causal" tooth and one or two adjacent teeth, it manifests itself more often from the vestibular surface of the alveolar process. Perifocal changes in the form of collateral edema are noted in the adjacent soft tissues.
At acute purulent periostitis swelling of the transitional fold due to the formation of a subperiosteal abscess, a symptom of fluctuation (with destruction of the periosteum and the spread of pus under the mucous membrane), pathological mobility of the "causal" tooth is determined. Perifocal edema is expressed in the soft tissues surrounding the focus of inflammation; in the place of direct contact with the subperiosteal abscess, inflammatory infiltration of soft tissues with skin hyperemia is observed.
At chronic periostitis an increase in bone volume is observed due to the layering of excess young bone on the jaw surface in the form of layers with varying degrees of axial
fication. The focus of chronic infection in the bone, trauma are a source of additional pathological irritation of the periosteum, which in children is already in a state of physiological irritation. With simple chronic periostitis, the newly formed bone, after adequate treatment, undergoes reverse development, with ossifying, bone ossification develops in the early stages and ends, as a rule, with hyperostosis. On radiographs lower jaw young bone tissue is defined in the form of a delicate strip outside the cortical layer of the bone. In the later stages of the disease, the layering of the newly built bone is clearly expressed. X-ray examination of the upper jaw rarely gives a clear picture that helps diagnose.
1.2. ODONTOGENIC OSTEOMYELITIS
JAWS
Acute osteomyelitis of the jaw bones. Depending on the way of penetration of the infection into the bone and the mechanism of development of the process, three forms of osteomyelitis of the facial bones are distinguished: odontogenic, hematogenous and traumatic. Odontogenic osteomyelitis occurs in 80% of all cases, hematogenous - in 9%, traumatic - in 11%. In children under 3 years of age (more often in the first year of life), predominantly hematogenous osteomyelitis develops, from 3 to 12 years old - odontogenic in 84% of cases. The following forms of the disease are distinguished: acute and chronic osteomyelitis, which is subdivided, depending on the clinical and radiological picture, into 3 forms: destructive, destructive, productive and productive.
Acute osteomyelitis- purulent infectious and inflammatory disease of the jaw bone (all its structural components), accompanied by bone lysis by purulent exudate, violation of its trophism and leading to osteonecrosis. For the clinic of acute osteomyelitis, general symptoms are manifest. The disease begins acutely, with a rise in body temperature to 38-39 ° C, accompanied by chills, general weakness, malaise. In children of younger and pubertal age, with a rise in body temperature, convulsions, vomiting and disturbance of the function of the gastrointestinal tract may appear, which indicates irritation of the central nervous system as a result of high general intoxication of the body. With odontogenic etiology, the disease is characterized by diffuse inflammation around the causative tooth, pathological mobility of it and adjacent intact teeth is observed. Pus can be discharged from the gingival pockets, subperiosteal abscesses are formed, which, as a rule, are localized on both sides of the alveolar ridge and jaw bone. Osteomyelitis is accompanied by pronounced inflammatory changes in the soft tissues of the face, inflammatory infiltration with hyperemia and edema of the skin develops in the adjacent tissues. Regional lymphadenitis is always present. Acute osteomyelitis is characterized by the formation of abscesses or phlegmon, more often adenophlegmon develop. In advanced cases, in older children, acute odontogenic osteomyelitis is complicated by peri-maxillary phlegmon.
X-ray examination in the early days of the disease does not reveal signs of changes in the jaw bones. By the end of the week, a diffuse rarefaction of the bone appears, which indicates its melting by purulent exudate. The bone becomes more transparent, the trabecular pattern disappears, becomes thinner and the cortical layer is interrupted in places.
Acute odontogenic osteomyelitis of the upper jaw is much less likely to acquire a chronic course in comparison with processes in the lower jaw, since the anatomical and physiological features of its structure contribute to the rapid breakthrough of abscesses and the relief of the osteomyelitis process.
Chronic osteomyelitis- purulent or proliferative inflammation bone tissue characterized by the formation of sequesters or no tendency to recover
and an increase in destructive and productive changes in the bone and periosteum. In chronic odontogenic osteomyelitis of the jaw bones, the rudiments of permanent teeth are involved in the process, which "behave" like sequestrants and maintain inflammation. Depending on the severity of the processes of death or construction of bone substance, three clinical and radiological forms of chronic osteomyelitis were identified: destructive, destructive-productive, productive. The lower jaw in children is affected by odontogenic osteomyelitis much more often than the upper one.
Chronic forms of odontogenic osteomyelitis are most often the outcome of acute odontogenic osteomyelitis, and the chronization of the process in children occurs in a shorter time frame than in adults (the process is interpreted as chronic in children as early as 3-4 weeks from the onset of the disease). However, chronic osteomyelitis can develop without a previous clinically pronounced acute stage, which determined its name as primary chronic (productive form of chronic odontogenic osteomyelitis).
Destructive form of chronic osteomyelitis observed in children younger age, emaciated, weakened by a common infectious disease, i.e. with reduced immune resistance of the organism. Symptoms of acute inflammation subside, however, the symptoms of general intoxication of the body remain pronounced and accompany the entire period of the disease. The lymph nodes remain enlarged and painful. Internal and / or external fistulas appear with purulent discharge and protruding granulations. A delay in the outflow of exudate can cause an exacerbation of inflammation (the clinic of which is similar to acute osteomyelitis). X-ray examination determines the areas of resorption of spongy and cortical substances. Bone destruction is rapid and diffuse. The final boundaries of the lesion are established at a later date: by the end of the 2nd - the beginning of the 3rd month from the onset of the disease. The destructive form is accompanied by the formation of large, total sequesters, pathological fractures. The periosteal structure of the bone in all stages of the destructive form is weakly expressed, the endosteal structure is not radiologically determined.
Destructive-productive form of chronic odontogenic osteomyelitis observed in children 7-12 years old and is the most frequent outcome of acute odontogenic osteomyelitis. The clinic is similar to the clinic of the destructive form of chronic osteomyelitis. X-ray examination reveals small foci of bone rarefaction, the formation of many small sequesters. In the periosteum, there is an active construction of bone substance, which is determined on radiographs in the form of (often layered) bone stratification. Signs of endosteal bone remodeling appear at a later date - rarefaction foci alternate with areas of osteosclerosis, and the bone acquires a rough-spotted pattern.
Productive (primary chronic) form of odontogenic osteomyelitis develops only in childhood and adolescence, more often in children 12-15 years old. Sensitization of the organism and a decrease in its protective properties are of great importance in the emergence of primary chronic forms. Not the least role is played by the irrational use of antibiotics (small doses, short courses), the wrong tactics for treating pulpitis and periodontitis, etc. Since it takes a long time from the onset of the disease to its manifestation (4-6 months), its diagnosis is very difficult. In the oral cavity, there may be no "causal" temporary teeth, and peri-coronitis (a common cause of damage) by the beginning of the process is already completed by the eruption of intact teeth. Usually productive (hyperplastic) osteomyelitis occurs unnoticed by the patient. The classic signs of osteomyelitis - fistulas and sequesters - are absent. In a separate area of the jaw, a deformation appears, slightly painful on palpation. The deformation grows slowly and over time can spread to several parts of the jaw. The process can last for years and is accompanied by frequent (up to 6-8 times a year) exacerbations. During the period of exacerbation, infiltrates of the surrounding soft tissues, trismus, painful on palpation, may appear. During the period of exacerbation, regional lymph nodes are also enlarged, painful on palpation, but periadenitis, abscesses and peri-maxillary phlegmon rarely develop.
The X-ray picture is characterized by an increase in the volume of the jaw due to pronounced endosteal and periosteal bone formation. Sequesters are not determined.
In the affected area, there is an alternation of foci of rarefaction with fuzzy boundaries and zones of osteosclerosis. The bone acquires a variegated, rough-spotted, so-called marble pattern. The cortical layer is not visible and, depending on the duration of the disease, merges with ossified periosteal layers, which most often have longitudinal layering. This form of osteomyelitis is characterized by retrograde infection of intact teeth in the lesion focus (ascending pulpitis and periodontitis).
1.3. HEMATOGENIC OSTEOMYELITIS
JAWS
Hematogenous osteomyelitis of the facial bones in children develops against the background of a septic state of the body and is one of the forms of septicopyemia that occurs against a background of low resistance. The source of infection can be inflammatory diseases of the umbilical cord, pustular lesions of the child's skin, inflammatory complications of the postpartum period in the mother (mastitis, etc.). This disease is found in newborns and children 1 month of life (77.4%), at the age of 1-3 years (15.2%) and from 3 to 12 years (7.36%) (Roginsky V.V., 1998) ...
Hematogenous osteomyelitis of the facial bones is more often localized in the zygomatic and nasal bones, the zygomatic and frontal processes are affected on the upper jaw, and the condylar process on the lower jaw.
In the acute phase of the disease, regardless of the localization of the primary lesion in newborns and children infancy an extremely difficult general condition develops and the general intoxication of the body is most pronounced. Despite the timely initiated and actively carried out therapy, new purulent foci often appear in various bones of the skeleton or other organs. In severe forms of the disease, bone damage is accompanied by the development of phlegmon. In many children, the disease is accompanied by septic pneumonia. After surgical opening of abscesses or the formation of fistulas, the general condition of the child does not improve immediately. With intensive therapy, the threat to life disappears by the end of the 3-4th week from the onset of the disease.
In the acute stage, cure is possible in few children. More often hematogenous osteomy-
litas becomes chronic and proceeds with the formation of extensive sequesters, including dead tooth rudiments. The regenerative processes in the bone are weakly expressed.
Outcomes depend on the clinical form of hematogenous osteomyelitis and the timing of the initiation of rational therapy. After suffering chronic hematogenous osteomyelitis, children have defects and deformities of the jaws associated with their underdevelopment or extensive bone sequestration. With osteomyelitis of the lower jaw, a defect or underdevelopment of the condylar process is formed, followed by impaired growth of the entire lower jaw or the development of primary bone lesions of the TMJ (see Chapter 4.1).
1.4. LYMPHADENITIS
One of the first places in frequency among inflammatory processes is lymphadenitis. Lymphadenitis in the maxillofacial region in children is extremely rare primary diseases. They accompany odontogenic, stomatogenic diseases, diseases of the upper respiratory tract, acute respiratory infections, acute respiratory viral infections, childhood infectious diseases, and in these cases are considered as one of the symptoms of the underlying disease. Lymphadenitis can be caused by hypothermia, trauma, routine vaccinations.
According to the clinical course, acute lymphadenitis (serous, in the stage of periadenitis, purulent) and chronic (hyperplastic, in the stage of exacerbation) are distinguished.
Acute serous lymphadenitis proceeds violently with a pronounced general reaction and local symptoms. The body temperature rises. General signs of intoxication appear, which are more pronounced in young children (1-3 years old). In the initial stage, local symptoms are characterized by a slight increase in lymph nodes, pain on palpation, the lymph node remains mobile, dense, the skin color is not changed. Then (2-3 days from the onset of the disease) soft tissues are involved in the process, the inflammation spreads beyond the lymph node capsule, which is interpreted as periadenitis. At the site of the lymph node, a dense, sharply painful infiltration is palpated. Subsequently, the lymph node melts
purulent exudate, which is clinically manifested by a focus of softening with a symptom of fluctuation (acute purulent lymphadenitis). Lymph nodes on the lateral surface of the neck, submandibular and parotid regions are more often affected.
Chronic hyperplastic lymphadenitis characterized by an increase in the lymph node - it is dense, mobile, not welded to the surrounding tissues, painless or slightly painful on palpation. More often, the etiology of this form of lymphadenitis is nonontogenic. In these cases, several regional lymph nodes are palpated.
Chronic abscessing lymphadenitis characterized by the appearance of a focus of hyperemia and thinning of the skin over the enlarged lymph node, palpation is determined by the symptom of fluctuation, indicating purulent fusion of the node. Spontaneous opening of an abscess with the formation of a fistula is also possible. The general condition of children with chronic forms of lymphadenitis does not change.
1.5. ABSCESS
Abscess- a focus of accumulation of pus, resulting from the melting of tissues with the formation of a cavity in the soft tissues. An abscess in the face is caused by damage or inflammation of the skin of the face, the mucous membrane of the mouth, lips, nose, eyelids. Less often, abscesses in children occur due to the spread of infection from the odontogenic focus. The formed abscess is a bulging, domed, brightly hyperemic area. The skin above it is thinned. Palpation is sharply painful, fluctuation is easily detected. The general condition is disturbed slightly. More difficult are abscesses located deep in the tissues - periopharyngeal, paratonsillar, infratemporal space, tongue. They are accompanied by severe intoxication, dysfunction of chewing, swallowing, breathing, trismus. In the focus of inflammation, an infiltrate is formed, in the area of which the skin or mucous membrane is hyperemic, tense. In the center of the infiltrate, fluctuation is determined. The boundaries of the altered tissues are clearly delineated. Often, the skin or mucous membrane in the area of the abscess swells above the surface.
1.6. PHLEGMON
1.7. FURUNCLE
Phlegmon- acute purulent diffuse inflammation of the subcutaneous, intermuscular and interfascial loose fatty tissue. V childhood phlegmon often develops as a complication of acute purulent lymphadenitis (adenophlegmon) or accompanies odontogenic osteomyelitis (osteophlegmon). Adenophlegmon is observed in children from the very early age- from 2 months and older. The most common localization of adenophlegmon is the buccal, supra- and submandibular, less often the submental and parotid-masticatory regions. The source of infection can be teeth, ENT organs, traumatic injuries, including post-injection, due to violation of the rules of asepsis. With phlegmon, an increase in the level of intoxication of the body is noted in combination with pronounced local symptoms - a diffuse inflammatory infiltrate is determined, spreading to several anatomical areas. In the center of the inflammatory infiltrate, foci of softening with fluctuations are determined. The skin of the affected area becomes dense, tense, hyperemic. The rapidity of development of phlegmon in children is facilitated by a weak connection of the dermis with the basement membrane and subcutaneous fat layer, good blood supply. These are the main reasons for the development of purulent-necrotic processes of a diffuse nature in children. Immaturity of the immune system also contributes to the development of inflammation and prevents the limitation of the focus.
Osteophlegmon aggravates the course of acute odontogenic osteomyelitis and sharply increases the general intoxication of the body. With osteo-phlegmon, the spread of a purulent inflammatory process occurs as a result of melting of the periosteum and the breakthrough of purulent exudate into soft tissues.
In newborns and infants, a formidable complication of hematogenous osteomyelitis of the upper jaw is the formation of phlegmon in the cavity of the orbit or retrobulbar space. In acute odontogenic osteomyelitis, superficial phlegmon develop more often. Phlegmon of deep intermuscular spaces in childhood are rare (with long-term untreated bone processes).
Furuncle- acute purulent-necrotic inflammation of the hair follicle and the associated sebaceous gland with the surrounding fiber, caused by pyogenic microbes - staphylococci. The development of the boil is facilitated by skin trauma with subsequent infection. Predisposing factors are increased activity of sweat and sebaceous glands of the skin, vitamin deficiency, metabolic disorders, weakening of the immune system. A furuncle can occur on any part of the skin where there is hair, more often in the neck, lips and wings of the nose.
The development of a boil begins with the appearance of a dense painful infiltrate with a diameter of 0.5-2 cm of bright red color, towering above the skin in the form of a small cone. With a favorable course, on the 3-4th day, a focus of softening is formed in the center of it, which can open up on its own with the appearance of pus. At the site of the autopsy, a greenish area of necrotic tissue is found - the boil shaft. In the future, together with pus and blood, the rod is rejected. The skin tissue defect is replaced by granulations. After 2-3 days, healing occurs with the formation of a scar. With an uncomplicated course, the boil development cycle lasts 8-10 days.
The furuncle in the area of the lips and wings of the nose, as a rule, is difficult. Inflammatory edema spreads to the surrounding tissues of the face. There is severe radiating pain. Body temperature is high. There is a likelihood of developing such severe complications as meningitis, mediastinitis, sepsis, therefore, treatment of children with facial boils should be carried out in a hospital setting.
In weakened children, the disease may be sluggish, with a weak inflammatory reaction, and with excessive accumulation of pus, the necrotic rod may melt and an abscess (abscessing furuncle) may occur.
1.8. INFLAMMATORY DISEASES OF THE SALIVARY GLANDS
1.8.1. PARITIS OF NEWBORNS
The disease is rare. The etiology and pathogenesis of the disease are not well understood. It develops more often in premature or debilitated children with concomitant somatic pathology. The cause of the development of mumps may be the introduction of infection through the excretory duct of the salivary gland or by hematogenous route.
The disease develops acutely, more often in the 1st week of a child's life. It begins with the appearance of dense diffuse inflammatory infiltrates of one or two parotid-chewing areas, accompanied by a pronounced general intoxication of the body. After 2-3 days, purulent or purulent-necrotic melting of the gland occurs. The spread of pus to the temporomandibular joint area is possible, which can lead to the death of growth zones on the lower jaw and, as a result, to ankylosis of the TMJ, underdevelopment of the lower jaw.
History;
Palpation;
X-ray of the facial bones;
Ultrasound examination;
Blood and urine analyzes.
Mumps of a newborn is differentiated from:
Adenophlegmonous.
1.8.2. PAROTITIS
The causative agent of mumps is a filterable virus Pneumophilus parotidis. The mumps virus is rapidly inactivated when exposed to high temperatures, ultraviolet radiation, weak solutions of formalin, lysol, alcohol. The source of infection is a sick person. The transmission of infection occurs by airborne droplets, as well as through objects contaminated with the patient's saliva (dishes, toys). The virus is found in saliva at the end of the incubation period (18-20 days) and in the first 3-5 days of illness, as well as in the blood. Possible primary virus damage to the meninges, testicles and pancreas.
The disease often manifests itself between the ages of 5 and 15 years. Even before the appearance of distinct clinical signs you can find an increased content of amylase in the blood serum and diastase in the urine, disappearing only after the 10th day of illness. The onset of the disease is characterized by an increase in body temperature to 38-39 ° C and the appearance of swelling of the parotid salivary gland on one or both sides. It is also possible to involve the submandibular and sublingual salivary glands in the process, while extensive edema of the cervical tissue is possible. The skin over the inflamed glands is tense, shiny, but usually retains its normal color. The appearance of swelling of the parotid gland is accompanied by pain radiating towards the ear or neck, aggravated by chewing and swallowing. The swelling of the affected glands increases for the first 3-5 days, then begins to decrease by the 8-10th day. Sometimes the resorption of the infiltrate is delayed for several weeks. Occasionally, the disease is accompanied by bradycardia, followed by tachycardia. Often enlarged spleen. ESR is usually increased. Damage to the nervous system (meningitis, encephalitis) is often observed, sometimes with paralysis of the cranial and spinal nerves; sometimes accompanied by mental disorders.
Orchitis is a common complication. Oophoritis with mumps is less common. Mastitis is also described, accompanied by swelling and tenderness of the mammary glands.
The diagnosis is based on:
Complaints;
Epidemiological history;
Clinical examination (palpation of the salivary glands, pancreas, genitals);
Visual examination of saliva;
Ultrasound of the salivary glands.
Mumps should be differentiated from:
Various types of sialoadenitis;
Chronic nonspecific parotitis in the acute stage;
Infectious mononucleosis;
Buccal abscess;
Lymphadenitis;
Hematogenous osteomyelitis;
Lymphangioma in the stage of inflammation;
Adenophlegmonous.
1.8.3. CHRONIC PARENCHYMATIC PAROTITIS
The etiology of the disease has not been clarified.
The process is characterized by a primary chronic onset and latent inflammation in the parotid salivary glands.
The disease often manifests itself in children 3-8 years old. The peculiarity of chronic nonspecific parenchymal mumps is the duration of the course. Exacerbations can occur 6-8 times a year. Characterized by a deterioration in the general condition, the appearance of pain and swelling in the parotid glands on one or both sides. The appearance of hyperemia and skin tension is possible.
On palpation of the parotid-masticatory region, an enlarged, painful (slightly painful), dense, lumpy gland is felt. When massaging the parotid gland, a viscous jelly-like saliva with an admixture of pus or fibrin clots is released from the salivary duct.
In the course of the disease, triclinic-radiological stages are distinguished: initial, clinically pronounced and late. In each of the stages, a period of exacerbation and remission, as well as an active and inactive course, are distinguished. With an active course of the process, the disease is characterized by a pronounced inflammatory reaction of the OUSH. The duration of an exacerbation with an active course is from 2-3 weeks to 2 months, the number of exacerbations varies from 4 to 8 times a year.
With an inactive course, an exacerbation of chronic parenchymal parotitis occurs without pronounced local and general symptoms of inflammation with a smaller number of exacerbations per year (from 1 to 3).
The diagnosis is made on the basis of the following data:
Complaints;
History;
Clinical examination, including palpation of the salivary gland;
Visual examination of the secretion of the salivary gland;
Clinical analysis of blood and urine;
X-ray examination of the OUSG with preliminary contrasting of the ducts of the gland with water-soluble contrast agents: verografin, urografin, omnipak (sialography, orthopantomosialography);
Studies of purulent discharge from the salivary gland for sensitivity to antibiotics (during an exacerbation);
Cytological examination of saliva smears and punctate OUSH during remission;
Ultrasound.
Chronic parenchymal parotitis should be differentiated from mumps, lymphadenitis, specific lymphadenitis in the parotid-masticatory region, with chronic osteomyelitis of the lower jaw, lymphangioma and cysts in the parotid region, neoplasms.
1.8.4. CYTOMEGALIA
Cytomegaly is a viral disease that affects the salivary glands, predominantly of newborns and infants under 6 months of age. The causative agent is human cytomegalovirus (cytomegalovirus hominis), which belongs to the herpes virus family. Sources of infection: virus carriers and patients. The virus is excreted in saliva, breast milk. Cytomegalovirus can cross the placenta and cause intrauterine damage to the fetus at any stage of its development. Infection in the first weeks of pregnancy can cause spontaneous abortion or the formation of congenital defects (for example, cleft lip and palate). Infection at a later date can lead to damage to the central nervous system, liver, and gastrointestinal tract. Fetal infection can occur when an infected woman passes through the birth canal. The place of primary fixation of the virus is the salivary glands. The parotid glands are more commonly affected than the submandibular, sublingual salivary glands, and regional lymph nodes.
In the salivary gland, narrowing and even blockage of small salivary ducts is determined by giant epithelial cells protruding into their lumen. In the nucleus and cytoplasm of these cells, there are clearly visible inclusions. Similar giant cells in cytomegaly are found in saliva, urine and feces.
With the local course of cytomegaly, the salivary glands swell due to inflammation and the formation of small cysts. In the generalized course of the disease, the pathological process can affect the lungs, kidneys, pancreas, brain and other organs. After suffering cytomegaly in
children may experience congenital heart defects and large vessels, cutaneous angiomas, myocarditis.
In infants, in rare cases, there is a skin lesion in the form of large-lamellar peeling, long-standing diaper rash or non-healing ulcers. In some cases, the disease can develop as sepsis.
The prognosis was previously considered absolutely unfavorable. Currently, mild forms are diagnosed, proven virologically, with a favorable outcome.
The diagnosis is based on:
Parental complaints;
History;
Clinical examination;
Clinical analysis of blood and urine;
PCR and serological diagnostics. CMV infection of the salivary glands in children should be differentiated from:
Herpetic infection;
Fungal inflammation (actinomycosis, candidiasis);
Echinococcal infection;
HIV infection;
Hemolytic disease of the newborn;
Toxoplasmolysis.
1.8.5. Submandibular salivary glands salivary disease in children
The mechanism of calculus formation is not fully understood. In the occurrence of salivary stone disease great importance has a violation of calcium metabolism, sometimes trauma or the ingress of a foreign body into the excretory ducts of the salivary glands is noted.
The main diagnostic symptom is the detection of calculus, pain that occurs when eating, associated with impaired saliva outflow. Sialodochitis and sialodenitis are accompanying symptoms... The listed symptoms increase with the age of the child.
The diagnosis is made on the basis of general clinical examination methods (complaints, anamnesis, examination of the child, palpation of the gland, visual examination of secretions, clinical analysis of blood and urine, X-ray examination of the submandibular salivary glands, ultrasound).
Salivary stone disease of the submandibular salivary glands is differentiated with a retention cyst of the sublingual salivary gland, hemangioma and lymphangioma of the sublingual region, sialodochitis, with an abscess of the maxillofacial groove.
Rice. 1.1. Child 3 years old. Exacerbation of chronic Rice. 1.2. Child 5 years old. Exacerbation of chronic periodontitis of tooth 84, acute periodontitis of tooth 54, acute purulent purulent periostitis of the lower jaw on the right; periostitis of the upper jaw on the right
Rice. 1.3. Enlarged panoramic radiograph of the lower jaw of a 9-year-old child. Chronic ossifying periostitis of the lower jaw on the right in the area of the teeth 46, 47
Rice. 1.4. Child 6 years old. Exacerbation of chronic periodontitis of tooth 64, acute serous periostitis of the upper jaw on the left
Rice. 1.5. Child 5 years old. Exacerbation of chronic periodontitis of tooth 75, acute serous periostitis of the lower jaw on the left
Rice. 1.6. Child 6 years old. Exacerbation of chronic periodontitis of tooth 75, acute purulent periostitis of the lower jaw on the left: a - condition in the oral cavity; b- orthopantomogram
Rice. 1.7. The child is 13 years old. Chronic destructive-productive osteomyelitis of the lower jaw on the right: a- appearance child; b- orthopantomogram. The foci of destruction of bone tissue in the region of the branch, angle and body of the lower jaw on the right are determined; v - view of the body of the lower jaw on the right at the stage of the operation
Rice. 1.8. The child is 13 years old. Chronic productive osteomyelitis of the lower jaw on the right. Disease duration 6 months: a- the appearance of the child; b- general X-ray of the bones of the facial skeleton in a direct projection
Rice. 1.9. Child 15 years old. Chronic productive osteomyelitis of the lower jaw on the left. Disease duration 2 years: orthopan tomogram. Areas of osteosclerosis are noted due to the previously repeatedly transferred inflammatory process without signs of sequestration. The cortical plate is not clearly visible. The characteristic marble pattern of the bone
Rice. 1.10. Chronic destructive osteomyelitis of the lower jaw in the sequestration stage. Dental volumetric tomogram of a 16-year-old child. The bone tissue of the lower jaw in the area of missing teeth 45-48 has a heterogeneous structure. In the projection of the missing tooth 46, an irregularly shaped focus of destruction of bone tissue is determined, up to 5.5 x 4.5 x 3.5 mm in size, in the cavity of which additional compaction of bone tissue (bone sequestration) is visualized. The cortical plate of the lower jaw in the region 46 is not traced along its entire length. On the vestibular and lingual surfaces of the lower jaw in the region of 45-48, there are pronounced linear periosteal layers
Rice. 1.11. Chronic destructive-productive osteomyelitis of the lower jaw. Dental volumetric tomogram of a 12-year-old child. There is a change in the bone structure (against the background of osteosclerosis of the lower jaw on the right, multiple foci of destruction of various sizes and shapes are revealed) and layered periosteal layers
Rice. 1.12. Chronic destructive-productive osteomyelitis of the lower jaw. Multispiral computed tomogram of a 17-year-old child (a, b- axial projection; v- 3D reconstruction). In the body of the lower jaw, multiple foci of destruction of bone tissue are visualized, ranging in size from 2.5 to 9.8 mm. On the lingual and vestibular surfaces, there are linear and fringed periosteal layers, more pronounced in the area of the lower jaw body in the projection of the missing teeth 36-46, there are areas of sharp compaction (from 173 to 769 N units) of soft tissues, up to their calcification
Rice. 1.13. Chronic destructive-productive osteomyelitis of the lower and upper jaws. Multispiral computed tomograms of a 9-year-old child: a- axial cut; b- MPR in coronary projection; v- MPR in sagittal projection; G- 3D reconstruction. The bone structure of the entire lower jaw, upper jaw, main bone, both zygomatic bones and zygomatic arches is markedly changed due to the presence of different-sized foci and foci of rarefaction and osteosclerosis, with uneven, indistinct contours, practically not delimited from the unchanged surrounding bone tissue, violating the integrity of the cortical plates ... The volume of the above bones is increased (more in the lower jaw), the ratio is not changed. In both TMJs, the ratios are not disturbed, the articular heads are swollen, and the integrity of the contours is broken in places. In the left maxillary sinus and cells of the ethmoid labyrinth, soft tissue contents with a density of about 16 units. N
Rice. 1.14. Child 4 years old. Acute serous lymphadenitis of the left submandibular region: a- the appearance of the child; b- Ultrasound, B-mode: the lymph node of low echogenicity, the cortex is thickened; v- Ultrasound, CDK mode: strengthening of the vascular pattern in the projection of the gate of the lymph node
Rice. 1.15. Ultrasound, CDK mode: a lymph node of a rounded shape, reduced echogenicity, heterogeneous structure, along the periphery - a hypoechoic rim (edema zone). Acute lymphadenitis at the stage of periadenitis
Rice. 1.16. Child 6 years old. Acute purulent lymphadenitis of the right submandibular region
Rice. 1.17. Child 5 years old. Acute purulent lymphadenitis of the left submandibular region
Rice. 1.18. Child 15 years old. Chronic hyperplastic lymphadenitis of the submental region
Rice. 1.19. Child 1.5 years old. Abscessing lymphadenitis of the left submandibular region after an acute respiratory viral infection: a - appearance; b- Ultrasound, B-mode: the echogenicity of the lymph node is reduced, in the projection the fluid area (abscess zone) is determined; v- Ultrasound, CDK mode: in the projection of the lymph node, there is an increase in the vascular pattern, the abscess zone is avascular
Rice. 1.20. Abscessing lymphadenitis of the right submandibular region with the development of adenophlegmon. Ultrasound, CDK mode: the lymph node capsule is intermittent, fluid areas are determined in the surrounding tissues
Rice. 1.21. Child 15 years old. Specific lymphadenitis (actinomycotic) of the right submandibular region
Rice. 1.22. Child 4 years old. Abscess of the left infraorbital region after an insect bite
Rice. 1.23. Child 14 years old. Abscess of the lateral surface of the neck on the right: a- the appearance of the child; b- Ultrasound, B-mode: a zone of reduced echogenicity with uneven contours is determined, in the projection - liquid areas
Rice. 1.24. Child 14 years old. Lower lip abscess: a, b - the appearance of the child; v- Ultrasound, B-mode: the formation of reduced echogenicity with the presence of a liquid section is determined
Rice. 1.25. Child 16 years old. Abscess of the right submandibular region
Rice. 1.26. Child 10 years old. Odontogenic phlegmon of the right submandibular region: a, b- the appearance of the child; v- orthopantomogram
Rice. 1.27. Child 7 years old. Furuncle of the left infraorbital region
Rice. 1.28. Infiltration of the left buccal region with signs of abscess formation. Ultrasound, B-mode: a zone of reduced echogenicity with the presence of a liquid area is determined
Rice. 1.29. Child 16 years old. Abscessing furuncle of the right zygomatic region
Rice. 1.30. Child 6 years old. Exacerbation of chronic parenchymal left-sided parotitis
Rice. 1.31. The child is 13 years old. Exacerbation of chronic left-sided parenchymal parotitis
Rice. 1.32. Chronic left-sided parenchymal parotitis, initial clinical and radiological stage. Orthopanthosialogram of a 9-year-old child
Rice. 1.33. Chronic bilateral parenchymal parotitis, initial clinical and radiological stage. Orthopanthosialogram of a 6-year-old child
Rice. 1.34. Chronic bilateral parenchymal parotitis, pronounced clinical and radiological stage. Ortho-pantomosialogram of a 7-year-old child
Rice. 1.35. Chronic right-sided parenchymal parotitis, pronounced clinical and radiological stage. Orthopanthosialogram of a 15-year-old child
Rice. 1.36. Chronic bilateral nonspecific parotitis, remission. Ultrasound, CDK mode: the salivary gland is enlarged, reduced echogenicity with the presence of small cysts; vascularization is not changed
Rice. 1.37. Chronic bilateral nonspecific parotitis, exacerbation. Ultrasound, CDC mode: in the projection of the parenchyma of the gland, vascularization is enhanced.
Rice. 1.38. Salivary stone disease of the left submandibular salivary gland. X-ray of a 10-year-old child (axial projection)
Rice. 1.39. Salivary stone disease of the right submandibular salivary gland. X-ray of a child 11 years old (axial projection)
Rice. 1.40. Salivary stone disease of the left submandibular salivary gland. Ultrasound, B-mode: the duct of the gland is enlarged, calculus is determined in its lumen
Rice. 1.41. Salivary stone disease of the right submandibular salivary gland. Sialogram of a child 8 years old. Expansion of the duct, calculus at the mouth of the duct is determined
Rice. 1.42. Salivary stone disease of the left submandibular salivary gland. Multispiral computed tomography of a 16-year-old child (a - MPR in sagittal projection; b- axial projection; v- 30-reconstruction). In the soft tissues of the oral cavity along the lingual surface of the lower jaw in the area of the frontal group of teeth and in the area of the corner, calculi 2.5 and 8.5 mm in size, with clear wavy contours, with a density of 1826 units are visualized. N
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Introduction
Inflammatory diseases of the maxillofacial region are one of the pressing problems of dentistry. Most of them are odontogenic. The severity of the course depends on the causative agent of the disease.
Despite the development of new methods for combating purulent infection, the number of patients with inflammatory diseases has an aggressive tendency to increase and the emergence of formidable complications. They not only lead to temporary disability of patients, but also due to the occurrence of serious complications can be fatal.
Inflammations in the maxillofacial region are predominantly odontogenic, associated with pathological processes in the dentoalveolar segment, ranging from complicated caries, difficult teething, periodontitis, etc. Inflammatory processes of tonsillogenic, rhinogenic, hematogenous and other genesis are also found in the maxillofacial region ... purulent infection complication of caries
Classification of inflammatory diseases of the maxillofacial region
The classification of odontogenic inflammatory diseases of the maxillofacial region and neck, proposed by A.M. Solntsev and A.A. Timofeev (1989).
Odontogenic inflammatory diseases
Jaws:
1. Periodontitis (acute, chronic, exacerbated)
2. Periostitis (acute, chronic, exacerbated)
3. Osteomyelitis (acute, chronic, exacerbated)
4. Alveolitis (acute, chronic)
5. Sinusitis (acute, chronic, exacerbated)
Soft tissue:
1. Lymphadenitis (acute and chronic)
2. Inflammatory infiltrate
3. Abscesses
4. Cellulitis
5. Subcutaneous granuloma of the face
6. Pericoronaritis (uncomplicated and complicated forms)
Complications of Odontogenic Inflammatory Diseases
1.Phlebitis and thrombophlebitis, thrombosis of the sinuses of the brain
2.Mediastinitis
3.Sepsis (acute and chronic)
4. Other complications: meningitis, pneumonia, brain abscess, etc.
Specific inflammatory diseases of the PMO
Actinomycosis
Tuberculosis
Syphilis
The severity of the course of acute inflammation depends as much on the type of pathogen as on the degree of sensitization and the level of nonspecific reactivity of the organism. Depending on the ratio of these factors, there are 3 types of clinical course of inflammatory processes:
1.with sufficient tension of the nonspecific reactivity of the organism, a low level of sensitization and high virulence of microflora, the inflammatory reaction is compensatory in nature and proceeds according to the tipunormergic;
2. with a low level of nonspecific immunity, pronounced sensitization of the body and low virulence of microflora, a hyperergic form of inflammation develops;
3. at a low level of nonspecific reactivity and sensitization of the body to microflora, which has a weakly expressed virulence, the inflammatory reaction proceeds as a hypoergic one.
In hyperergic and hypoergic forms, inflammation turns from a protective reaction into a pathological one.
Inflammatory diseases of odontogenic etiology
Periodontitis
Periodontitis- inflammation of the tissues located in the periodontal gap. Periodontitis is a connective formation that covers the root of the tooth and fills the gap between the root and the inner wall of the alveoli. The width of the periodontal gap on the lower jaw is 0.15-0.22 mm. slightly more on the top (0.20 -0.25 mm).
Periodontitis consists of bundles of collagen fibers, in between which there are layers of loose connective tissue, as well as elastic, tissues come vessels and nerves, and there is also a variety of cellular composition; cementoblasts, osteoblasts, osteoblasts, fibroblasts, plasma and mast cells, macrophages, epithelial cells, which are the remains of tooth-forming epithelium.
The periodontium performs various functions: barrier, fixing, shock-absorbing, plastic, reflexogenic.
Depending on the etiological factor that caused the development of periodontitis, they are divided into infectious, chemical (toxic, drug) and traumatic. At the site of localization of the inflammatory process, periodontitis is distinguished apical (apical) and marginal (marginal).
In clinical practice, infectious apical periodontitis is most common.
Periodontitis is the initial stage of the spread of odontogenic infection, which is characterized by both mild and the most severe and dangerous manifestations.
The most acceptable and widespread is the classification of I.T. Lukomsky (1955), which, depending on the clinical picture and pathological changes, divides all periodontitis:
Acute periodontitis:
1.serious (limited and diffuse)
2.purulent (limited and spilled)
Chronic periodontitis:
1..granulating
2.granulomatous
3.fibrous
· Chronic periodontitis in the acute stage.
Clinical picture acute periodontitis quite characteristic and mainly determined by local manifestations. The general reaction of the body is not expressed, although an increase in temperature, a feeling of discomfort, slightly pronounced changes in the blood picture, and immune reactions are possible.
For acute purulent periodontitis, due to the development of the inflammatory process in the exudative stage, acute persistent pains are characteristic, aggravated by the slightest load on the tooth, a symptom of a "grown tooth", percussion is sharply painful, pain can be irradiated along the corresponding nerve fibers of the trigeminal nerve. There may be edema and hyperemia of the mucous membrane in the area of the affected tooth. X-ray and electro-dental examinations are not informative. Clinical symptoms are sufficient to establish a diagnosis.
Periodontitis treatment includes conservative methods drainage of the focus through the root canal, blockade with anesthetics with antibiotics, enzymes. More rational surgery, which consists in periostotomy (according to indications) and removal of the affected tooth. Anti-inflammatory, hyposensitizing, immunomodulating, antibiotic therapy is prescribed individually, more often in patients with concomitant diseases. It is advisable to use various types of physiotherapy aimed at improving the outflow and reparative processes: UHF therapy, laser, iontophoresis, etc. If possible, it is recommended to carry out delayed replantation of the affected tooth.
The outcome of untreated or unsatisfactorily treated acute periodontitis can be the development of either one of the forms of a chronic process, or an inflammatory focus in the surrounding tissues.
The most favorable course is fibrous periodontitis. There may be no clinical signs of inflammation. Radiographically, a uniform slight expansion of the periodontal gap is determined. Therefore, a number of authors consider fibrous periodontitis as acute periodontitis completed by scarring. Surgical treatment is usually not required. The tooth can be used for orthopedic purposes.
Granulomatous periodontitis manifests itself in the form of minor pain when chewing, percussion, more often it flows asymptomatically, and the granuloma formed in the area of the root apex (roots) is detected only radiographically. In case of violation of the integrity of the granuloma capsule, a decrease in the body's resistance, superinfection, an exacerbation of the process of the type of acute periodontitis is possible. In the process of further development of the granuloma, through the stage of cystogranuloma, it can develop into a radicular cyst.
At the same time, granulomatous periodontitis is a focus of chronic infection, which is important for patients with concomitant diseases of the heart, liver, kidneys, during pregnancy, etc. Depending on the place of the tooth in the dentition, the degree of its destruction, treatment may consist in its removal, immediate or delayed replantation, hemisection, root apex resection.
The most aggressive and dangerous is the granulating form of chronic periodontitis, which is characterized by the growth of granulation tissue beyond the alveoli with resorption of bone and marrow tissue of the alveoli, which served as a basis for a number of researchers, as mentioned above, to consider periodontitis as the initial phase of osteomyelitis. In connection with this type of growth, fistulous holes appear on the mucous membrane of the alveolar process and even on the skin with a slight discharge of pus and subsequent scarring, which can be repeated several times. Formation of submucosal and subcutaneous odontogenic granulomas is possible.
Odontogenic periostitis
A more severe type of development of an odontogenic inflammatory process is acute periostitis.
Acute purulent periostitis is an acute purulent inflammation of the periosteum of the alveolar processes of the jaws, sometimes extending to the periosteum of the jaw body. According to the literature, acute purulent periostitis accounts for 20% to 40% (28-52%) of complications of odontogenic infection. The reason for its development is more often the exacerbation of granulomatous periodontitis, complications in inflammatory processes in the area of impacted and semi-uretinated teeth.
The process mainly develops on the lower jaw in the area of the chewing teeth. It is possible that the infection spreads not only throughout, but also through the system of blood and lymphatic vessels, due to which acute periostitis may be accompanied by inflammation of the lymph nodes.
Clinical manifestations of periostitis, in addition to pronounced local phenomena of an acute purulent process - hyperemia of the mucous membrane, edema and tissue infiltration from the vestibular or oral side up to the formation of subperiosteal abscesses, swelling of soft tissues, mobility and painful percussion of the tooth - are also characterized by a violation of the general condition in the form fever, weakness, loss of appetite, etc.
Changes in the blood picture, immune parameters, etc. are also noted.
Treatment of acute purulent periostitis is usually surgical. The incision must be carried out with the obligatory dissection of the periosteum for 3-5 teeth with the center in the area of the causative tooth. An important condition is to ensure sufficient drainage of the focus. Medication and physiotherapy are carried out individually, depending on the prevalence of the process, the nature of its course, the patient's age, concomitant diseases. The tactics regarding the causative tooth are also individual, although most authors are inclined in favor of its extraction.
With timely started and adequate treatment, the disease ends with recovery on the 3rd - 5th day from the moment of treatment.
Chronic periostitis is rare and is characterized by excessive formation of periosteal layers, which are removed, if indicated, by surgery.
Sharp odontogenic osteomyelitis of the jaws
Classification. Depending on the nature of the clinical course, some authors distinguish three stages of osteomyelitis: acute, subacute and chronic.
Depending on the common inflammatory process, there are:
Limited
Focal
Spilled (diffuse) osteomyelitis.
It is believed that the process, which is localized in the alveolar process within 2-3 teeth, should be considered as limited. When it spreads to the body of the jaw or a branch, it is as focal. Diffuse osteomyelitis is characterized by affection of half of the entire jaw.
VI Lukyanenko, depending on the severity of the clinical course of osteomyelitis, there are three degrees of severity: mild, moderate and severe.
The clinical picture of odontogenic osteomyelitis of the jaws is quite diverse. The onset of acute odontogenic osteomyelitis is usually preceded by infectious diseases (ARVI, flu, tonsillitis, etc.), allergic diseases (allergic rhinitis) and para-allergic reactions (hypothermia, overheating, physical overstrain).
In the initial stage of acute odontogenic osteomyelitis, clinical manifestations are similar to exacerbated chronic or acute purulent periodontitis, i.e. pain is usually localized in the area of the "causative" tooth. With the growth of inflammatory phenomena, the intensity of the pain increases and is permanent. The pain in the "causal" tooth intensifies even when the tongue is touched. The tooth becomes, as it were, higher than the others, there is a sharp pain when the teeth are closed and therefore the patient keeps his mouth half-open. With the further development of the disease, patients are no longer able to localize pain sensations and note that the entire half of the jaw or head hurts, and the pain radiates to the ear, temple, back of the head, eyes, depending on the localization of the inflammatory focus.
In some cases, with acute osteomyelitis, local symptoms for the first 2-3 days are poorly expressed, and the rapidly progressive deterioration of the general condition of the patient comes to the fore. The patient complains about feeling unwell, headache, general weakness, bad dream, an increase in temperature, sometimes a rise in temperature is preceded by a strong chill. Usually a patient with acute purulent osteomyelitis of the jaw is pale, lethargic, facial features are sharpened.
In patients with acute odontogenic osteomyelitis, the pulse increases in proportion to the rise in body temperature, The body temperature of patients can be from subfebrile (within 37-37.5 ° to quite high (up to 38-40 °), especially in children. The nature of the temperature reaction depends on state of general immunological reactivity of the organism (IPR) The absence of a temperature reaction in the presence of other septic phenomena should be regarded as a poor prognostic sign, especially in debilitated patients.
Important for judging the severity of the disease is not only a general increase in body temperature, but also temperature fluctuations between morning and evening hours. If these fluctuations exceed 1.5-2 °, then this indicates the further spread of the inflammatory process or the existence of an unrecognized purulent focus.
A sick tooth in the first hours, and sometimes during the first days from the onset of the disease, is well fixed, but later its mobility is manifested. If the process is not limited to the limits of one hole, then loosening of the adjacent intact teeth is also observed, and the percussion of these teeth also causes a painful reaction. The painful reaction to percussion and mobility gives an idea, along with other objective signs, about the prevalence of the inflammatory process. Looseness of all teeth on one side of the jaw indicates diffuse bone damage.
The gums adjacent to the teeth and the transitional fold of the mucous membrane become swollen and painful when palpated. There is a thickening of the jaw periosteum and an increase in collateral edema of the soft tissues of the face, and sometimes the neck. Regional lymph nodes enlarge and become painful. At the beginning of the process, palpation of the lymph nodes is possible, but later it becomes difficult due to edema and infiltration of the tissue surrounding the lymph node. Suppuration of lymph nodes in adults with acute odontogenic osteomyelitis is not observed, while in children it happens.
Following the mobility of the teeth, pus appears from the gingival pockets, and it also accumulates under the periosteum of the alveolar process or the body of the jaw on both sides of the vestibular and lingual. The alveolar process is muffin enlarged.
On days 2-3 from the onset of the disease, patients develop a fetid odor from the mouth, the appearance of plaque on the mucous membrane of the gums, tongue, teeth. The saliva is thick, viscous.
When X-ray examination of the jaw at the onset of the disease, only a picture of apical periodontitis appears without visible changes from the side of the jaw body. Radiologically destructive changes in the jaw bone tissue are usually detected only 2-3 weeks after the onset of acute odontogenic osteomyelitis, when the formation of sequesters begins.
In acute odontogenic osteomyelitis, changes in the composition of the blood of patients are almost always observed. Treatment. There are many schemes nowadays treatment measures, which are used for odontogenic osteomyelitis of the jaws.
First of all, it is necessary to remove the "causal" tooth, if it has not been removed earlier. Usually, removal is not difficult, since as a result of the inflammatory process, the ligamentous apparatus of the tooth melts. After the extraction of the tooth, the wound remains open and the patient is prescribed abundant irrigation of the oral cavity with a warm solution.
In addition, an opening of the associated abscesses and phlegmon should be performed.
Antibiotic therapy is prescribed: first, antibiotics of a broad spectrum of action or osteotropic action (lincomycin), and after clarifying the nature of the microflora and its sensitivity to antibiotics, the most effective one is chosen. In combination with antibiotics, sulfonamides are prescribed.
In order to reduce vascular permeability - 10% solution calcium chloride 10 ml intravenously. Antihistamines (desensitizing therapy) - diphenhydramine, suprastin, diazolin, etc. Detoxification therapy.
Symptomatic therapy: pain relievers, antipyretics.
Acute odontogenic sinusitis
Acute inflammation of the mucous membrane of the maxillary sinus is always accompanied by its edema, which leads to narrowing or complete closure of the opening that communicates the maxillary sinus with the middle nasal passage (ostium maxilla) and to the cessation of the outflow of exudate.
According to the etiology, maxillary sinusitis is divided into: odontogenic, traumatic, rhinogenic, hematogenous, vasomotor, allergic. According to the clinical course, one - and bilateral maxillary sinusitis is subdivided:
Catarrhal
Purulent
Chronic:
Exudative
Catarrhal
Serous
Purulent
Productive
Parietal-hyperplastic
Polypoid
Cystic
The process of inflammation begins with catarrhal changes occurring in the mucous membrane: edema, hyperemia, multicellular infiltration. Subsequently, the infiltration increases: foci of purulent expansion of the infiltrate are formed, acute purulent sinusitis develops. Patients complain of lethargy, weakening of the sense of smell, pain that grows in intensity, first localized, and then radiating to the frontal, temporal and occipital regions. Pain in the alveolar ridge of the upper jaw, which simulates pulpitis or neuritis.
As a result of the cessation of the outflow of inflammatory exudate from the maxillary sinus, toxicosis develops: the body temperature rises to 37.5-39. S., chills, headache, malaise, loss of appetite appear. Patients note a feeling of heaviness in the corresponding half of the face, distention, difficulty breathing, sleep disturbance. Photophobia and lacrimation may occur.
At the initial stages of the development of the disease, there are no visible changes in the configuration of the patient's face. The color of the skin is not changed. The mucous membrane of the nasal passage on the side of the lesion is edematous and hyperemic, mucus and pus are separated from it, which intensifies when the head is tilted forward. Nose is stuffed. Palpation of the skin in the area of the anterior facial wall and percussion along the zygomatic bone may cause some pain. With the development of periostitis, edema of the cheek and both eyelids develops. On plain radiographs, a veil is determined in the area of the affected maxillary sinus.
With the development of purulent sinusitis, all symptoms worsen and become more pronounced. The process proceeds as a serious infectious disease. The intensity of spontaneous throbbing pains sharply increases, which can radiate to the alveolar ridge and to the eye area. The body temperature rises to 39 C., and with empyema of the maxillary sinus - up to 40 C. There is swelling of the tissues of the cheeks, the skin is shiny. Palpation of the skin of the corresponding half of the face and percussion on the zygomatic bone causes acute pain. Pain is also determined during percussion of the teeth, the roots of which are projected into the region of the maxillary sinus on the side of the lesion. Rhinoscopy reveals edema, sharp hyperemia of the mucous membrane, under the middle shell - pus. However, purulent discharge from the nostril is often absent. On the roentgenogram, intense shading of the affected sinus is determined, and with the development of empyema, pronounced darkening. With its puncture, purulent exudate is found. In the blood - pronounced leukocytosis with a shift of the formula to the left, increased ESR indices.
Treatment of a patient with acute odontogenic sinusitis is aimed at:
Eliminate the focus and generator of infection - "causal" tooth, granuloma, cyst, etc .;
Create an outflow for the exudate formed in the sinus; - to carry out antibacterial, detoxification, hyposensitizing, restorative and physiotherapy.
In addition, symptomatic treatment is prescribed. At the initial stages of the disease with catarrhal sinusitis and a satisfactory general condition of the patient, treatment can be carried out in a polyclinic. The "causal" tooth is removed, the nasal mucosa is lubricated with vasoconstrictor agents, thereby achieving the resumption of natural drainage of the sinus, and symptomatic and physiotherapy is prescribed. With an increase in inflammation and purulent sinusitis, when it is necessary to conduct, sinusitis, antibacterial and detoxification therapy, hospitalization of the patient is indicated. The prognosis with timely treatment is usually good. Complicated forms of the course are possible: the development of peri-maxillary abscesses and phlegmon, phlegmon of the retrobulbar space, thrombophlebitis of the veins of the face, meningitis and sepsis.
Chronic odontogenic maxillary sinusitis
Chronic sinusitis may be a consequence of the acute stage of its course or the result of chronic infection of peri-apical foci of inflammation.
In contrast to acute catarrhal sinusitis, with a similar chronic form of the course, edema and hyperemia are observed in a more limited area of the sinus mucosa. Nasal breathing, some discomfort towards the end of the day. With rhinoscopy, hypertrophy of the inferior turbinate and cyanosis of the mucous membrane of the nasal passage are found.
With purulent and polypous lesions, patients complain of rapid fatigue, a putrid odor, and periodic discharge of pus from the corresponding half of the nose. There is an increase in body temperature up to 37.5-37.8є С. In the blood there is a slight leukocytosis, increased ESR. Treatment of chronic sinusitis can be conservative and operative, but always provides for the rehabilitation of the patient's oral cavity. In chronic catarrhal sinusitis, this is usually enough to ensure the patient's recovery. With deeper changes in the mucous membrane of the maxillary sinus, sanitation of the oral cavity is not enough, but it has a positive effect on the healing process in the conditions of the subsequent surgical treatment the patient, which should be carried out in a hospital.
Conclusion
Acute odontogenic infection is one of the urgent problems of modern surgical dentistry. V last years there is an increase in the number of patients with acute odontogenic inflammatory diseases, often there is a severe, progressive course, complicated by acute respiratory failure, mediasthenitis, meningoencephalitis and other intracranial inflammatory processes, sepsis, septic shock.
Despite certain successes achieved in the treatment of acute odontogenic inflammatory diseases and their complications, the mortality rate continues to remain high, which indicates the need for early diagnosis, prognosis of the course and effective treatment.
Often, there is a change in the clinical picture of the disease, especially at the beginning of its development, which creates diagnostic difficulties. In recent decades, an aggressive course of diffuse phlegmons, osteomyelitis has been observed more often, and severe complications have appeared.
It is quite obvious that an increase in the frequency and severity of the course of inflammatory diseases led to a significant increase in temporary disability, and in some cases to disability of the analyzed category of patients. Thus, the problem under consideration has not only medical, but also important social significance.
List of used literature
1. Kozlov V.A. Dentistry. Textbook. - SPb: SpetsLit, 2003 .-- 477 p.
2. Basics of dentistry. Tutorial. Silin A.V., Kirsanova E.V., Surdina E.D., Leonova E.V., Yakovenko L.L., Tumanova S.A. - SPb: 2015 .-- 262 p.
3. Topographic anatomy and operative surgery: textbook. Kagan I.I., Chemezov S.V. - M .: GEOTAR-Media, 2011 .-- 672 p.
4. Surgical dentistry and maxillofacial surgery: national guidelines / comp. L.A. Kulakov; T.G. Robustova, A.I. Nerobeev. - M .: GEOTAR-Media, 2010 .-- 500s.
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In the maxillofacial region, a special group is made up of inflammatory diseases caused by specific pathogens: a radiant fungus, treponema pale, mycobacterium tuberculosis. Diseases caused by these pathogens (actinomycosis, syphilis, tuberculosis) are usually classified into a group of specific inflammatory processes.
ACTINOMYCOSIS
Actinomycosis, or radiant fungal disease, is an infectious disease resulting from the introduction of actinomycetes (radiant fungi) into the body. The disease can affect all organs and tissues, but more often (80-85% of cases) the maxillofacial region.
Etiology. The causative agents of actinomycosis are radiant fungi (bacteria). The culture of actinomycetes can be aerobic and anaerobic. With actinomycosis in humans, in 90% of cases, the anaerobic form of radiant fungi (proactinomycetes) is secreted, less often certain types of aerobic actinomycetes (thermophiles) and micromonospores. A significant role in the development of actinomycosis is played by a mixed infection - streptococci, staphylococci, diplococci and other cocci, as well as anaerobic microbes - bacteroids, anaerobic streptococci, staphylococci, etc. ...
Pathogenesis. Actinomycosis occurs as a result of autoinfection, when radiant fungi penetrate the tissues of the maxillofacial region, and a specific actinomycotic granuloma or several granulomas are formed. In the oral cavity, actinomycetes are found in dental plaque, carious dental cavities, pathological periodontal pockets, on the tonsils; actinomycetes make up the main stroma of dental calculus.
The development of the actinomycotic process reflects complex changes in the body's immuno-biological reactivity, nonspecific defense factors in response to the introduction of an infectious agent - radiant fungi. Normally, the constant presence of actinomycetes in the oral cavity does not cause an infectious process, since there is a natural balance between the immunological mechanisms of the body and the antigens of radiant fungi.
The leading mechanism for the development of actinomycosis is a violation of the immune system. For the development of actinomycosis in the human body, special conditions are needed: a decrease or violation of the immunobiological reactivity of the body, a factor of nonspecific defense in response to the introduction of an infectious agent - radiant fungi. Among the general factors that impair immunity, one can distinguish primary or secondary immunodeficiency diseases and conditions. Local pathogenetic causes are of great importance - odontogenic or stomatogenic, less often tonsillogenic and rhinogenic inflammatory diseases, as well as tissue damage that disrupt the normal symbiosis of actinomycetes and other microflora. With actinomycosis, disorders of specific immunity and phenomena of immunopathology develop, of which allergy is the leading one.
The entrance gate for the introduction of actinomycotic infection in case of damage to tissues and organs of the maxillofacial region can be carious teeth, pathological periodontal pockets, damaged and inflamed mucous membrane of the oral cavity, pharynx, nose, salivary gland ducts, etc.
Actinomycetes from the site of introduction are spread by contact, lymphogenous and hematogenous routes. Usually, a specific focus develops in well-vascularized tissues: loose tissue, connective tissue layers of muscles and bone organs, where actinomycetes form colonies - drusen.
The incubation period ranges from several days to 2-3 weeks, but it can be longer - up to several months.
Pathological anatomy. In response to the penetration of radiant fungi into the tissue, a specific granuloma is formed. Polynuclear cells and lymphocytes accumulate directly around the colonies of the radiant fungus - the actinomycete druses. On the periphery of this zone, granulation tissue rich in thin-walled small-caliber vessels is formed, consisting of round, plasma, epitheloid cells and fibroblasts. Giant multinucleated cells are occasionally found here. The presence of xanthoma cells is characteristic. Subsequently, in the central parts of the actinomycotic granuloma, cell necrobiosis and their decay occur. In this case, macrophages rush to the colonies of drusen of the radiant fungus, capture pieces of mycelium and migrate with them to the adjacent tissue with a specific granuloma. There, a secondary granuloma forms. Further, similar changes are observed in the secondary granuloma, a tertiary granuloma is formed, etc. Daughter granulomas give rise to diffuse and focal chronic infiltrates. On the periphery of a specific granuloma, granulation tissue matures and turns into fibrous tissue. At the same time, the number of vessels and cellular elements decreases, fibrous structures appear, and dense cicatricial connective tissue is formed.
Morphological changes in actinomycosis are in direct proportion to the reactivity of the organism - the factors of its specific and nonspecific protection. This determines the nature of the tissue reaction - the predominance and combination of exudative and proliferative changes. Of no small importance is the accession of a secondary pyogenic infection. Strengthening of necrotic processes, local spread of the process are often associated with the addition of purulent microflora.
Clinical picture the disease depends on the individual characteristics of the organism, which determine the degree of general and local reaction, as well as on the localization of a specific granuloma in the tissues of the maxillofacial region.
Actinomycosis most often occurs as an acute or chronic inflammatory process with exacerbations, characterized by a normal reaction. With a duration of the disease of 2-3 months or more, in persons burdened with concomitant pathology (primary and secondary immunodeficiency diseases and conditions), actinomycosis acquires a chronic course and is characterized by a hypergic inflammatory reaction. Relatively rarely, actinomycosis occurs as an acute progressive and chronic hyperblastic process with a hyperergic inflammatory reaction.
Often, the general hypergic chronic course is combined with local hyperblastic changes in tissues, expressed in cicatricial changes in tissues adjacent to the lymph nodes, similar to muscle hypertrophy, hyperostous thickening of the jaws.
Depending on the clinical manifestations of the disease and the characteristics of its course associated with the localization of a specific granuloma, it is necessary to distinguish the following clinical forms of actinomycosis of the face, neck, jaws and oral cavity: 1) cutaneous, 2) subcutaneous, 3) submucosal, 4) mucous, 5) odontogenic actinomycosis granuloma, 6) subcutaneous-intermuscular (deep), 7) actinomycosis of the lymph nodes, 8) actinomycosis of the jaw periosteum, 9) actinomycosis of the jaws, 10) actinomycosis of the oral cavity organs - tongue, tonsils, salivary glands, maxillary. (Classification of Robustova T.G.)
Skin form. Rare. Occurs both odontogenically and as a result of damage skin... Patients complain of minor pain and induration in a small area of the skin; when questioned, they indicate a gradual increase and hardening of the lesion or foci.
Actinomycosis of the skin proceeds without an increase in body temperature. On examination, inflammatory skin infiltration is determined, one or more foci that grow outward are revealed. This is accompanied by a thinning of the skin, a change in its color from bright red to brownish blue. On the skin of the face and neck, pustules or tubercles may predominate, their combination is found.
The cutaneous form of actinomycosis spreads along the length of the tissue.
Subcutaneous form characterized by the development of a pathological process in the subcutaneous tissue, as a rule, near the odontogenic focus. Patients complain of pain and swelling. From the anamnesis, it can be found out that the subcutaneous form arose as a result of a previous purulent odontogenic disease. Also, this form can develop with the breakdown of the lymph nodes and the involvement of subcutaneous tissue in the process.
The pathological process with this form of actinomycosis is characterized by a long, but calm course. The period of disintegration of a specific granuloma may be accompanied by minor pain and low-grade fever.
When viewed in the subcutaneous tissue, a rounded infiltrate is determined, at first dense and painless. During the disintegration of the granuloma, the skin is soldered to the underlying tissues, becomes bright pink to red, and a softening area appears in the center of the focus.
Submucosa form occurs relatively rarely, with damage to the oral mucosa - biting, foreign bodies, etc.
The form develops without a rise in body temperature. Painful sensations in the lesion focus are moderate. Depending on the localization, the pain may increase when opening the mouth, talking, swallowing. Further, there is a feeling of a foreign body, awkwardness. On palpation, a round-shaped dense infiltrate is determined, which is further limited. The mucous membrane above it is soldered.
Actinomycosis of the mucous membrane mouth is rare. Radiant fungus penetrates through damaged mucous membranes, traumatic factors are most often foreign bodies, sometimes - sharp edges of the teeth.
Actinomycosis of the oral mucosa is characterized by a slow, calm course, not accompanied by an increase in body temperature. The pain in the focus is insignificant.
On examination, a superficially located inflammatory infiltrate with a bright red mucous membrane above it is determined. Often there is a spread of the focus outward, its breakthrough and the formation of separate small fistulous passages, from which granulation bulges.
Odontogenic actinomycotic granuloma in periodontal tissues is rare, but difficult to recognize. This focus always tends to spread to other tissues. When granulomas are localized in the skin and subcutaneous tissue, a strand is observed along the transitional fold, going from the tooth to the focus in the soft tissues; with a submucous focus, there is no strand. The process often spreads to the mucous membrane, with the next exacerbation, it becomes thinner, forming a fistulous passage.
Subcutaneous-intermuscular (deep) form actinomycosis is common. In this form, the process develops in the subcutaneous, intermuscular, interfascial tissue, spreads to the skin, muscles, jaw and other bones of the face. It is localized in the submandibular, buccal and parotid-masticatory region, and also affects the tissues of the temporal, infraorbital, zygomatic regions, infratemporal and pterygo-palatine fossa, pterygo-jaw and periopharyngeal spaces and other areas of the neck.
With a deep form of actinomycosis, patients indicate the appearance of swelling due to inflammatory edema and subsequent infiltration of soft tissues.
Often the first sign is a progressive restriction of mouth opening, since the radiant fungi growing into the tissue infect the chewing and internal pterygoid muscles, as a result of which there is a restriction of mouth opening that worries the patient.
On examination, there is a cyanosis of the skin over the infiltrate; the softening foci arising in certain areas of the infiltrate resemble forming abscesses. A breakthrough of a thinned area of the skin leads to its perforation and the release of a viscous pus-like fluid, often containing small whitish grains - actinomycete druses.
Acute onset or exacerbation of the disease is accompanied by an increase in body temperature to 38 - 39 ° C, pain. After opening the actinomycotic focus, acute inflammation subsides. There is a board-like density of the peripheral sections of the infiltrate, areas of softening in the center with fistulous passages. The skin over the affected area is soldered, cyanotic. Subsequently, the actinomycotic process develops in two directions: there is a gradual resorption and softening of the infiltrate or spread to neighboring tissues, which sometimes leads to secondary damage to the bones of the face or metastasis to other organs.
Actinomycosis lymph nodes occurs with odontogenic, tonsillogenic, otogenic ways of spreading the infection.
The process can manifest itself in the form of actinomycotic lymphangitis, abscessing lymphadenitis, adenophlegmon, or chronic hyperplastic lymphadenitis.
The clinical picture of lymphangitis is distinguished by a superficially located flat infiltrate, at first dense, and then softening and soldering to the skin. Sometimes the infiltration is in the form of a dense cord extending from the affected lymph node up or down the neck.
Abscessive actinomycotic lymphadenitis is characterized by complaints of a limited, slightly painful dense node. The disease develops sluggishly, without an increase in body temperature. The lymph node is enlarged, gradually gets drunk with the adjacent tissues, tissue infiltration grows around it. With abscess formation, pain intensifies, body temperature rises to subfebrile, and malaise appears. After opening the abscess, the process undergoes reverse development, leaving a dense scar-altered conglomerate.
Adenophlegmon is characterized by complaints of sharp pain in the affected area, the clinic resembles a picture of phlegmon caused by a pyogenic infection.
With hyperplastic actinomycotic lymphadenitis, an enlarged, dense lymph node resembling a tumor or tumor-like disease is observed. It is characterized by a slow, asymptomatic course. The process can worsen and abscess.
Actinomycosis periosteum rare in comparison with other forms. It proceeds in the form of exudative or productive inflammation.
With exudative periostitis of the jaw, inflammation develops in the area of the tooth and passes to the vestibular surface of the alveolar process and the body of the jaw. Pain sensations are poorly expressed, the state of health is not disturbed.
Clinically, a dense infiltrate develops on the eve of the oral cavity, flattening of the lower fornix. The mucous membrane above it is red, sometimes with a bluish tinge. Then the infiltration slowly softens, is limited, pain appears. Percussion of the tooth is painless, it seems to "spring". When the lesion is opened, pus is not always released, the growth of granulations is often noted.
With productive actinomycotic periostitis, there is a thickening of the base of the lower jaw due to the periosteum. The process from the periosteum of the alveolar part passes to the base of the jaw, deforming and thickening its edge.
Radiographically, outside the alveolar part, the base of the jaw body and especially along the lower edge, loose periosteal thickenings of a heterogeneous structure are determined.
Actinomycosis of the jaws. The pathological process with a primary lesion of the jaws is often localized on the lower jaw and very rarely on the upper. Primary actinomycosis of the jaw can be in the form of a destructive and productive-destructive process.
Primary destructive actinomycosis of the jaw can manifest itself as an intraosseous abscess or intraosseous gum.
With an intraosseous abscess, patients complain of pain in the area of the affected bone. When the focus is adjacent to the canal of the lower jaw, sensitivity in the area of the chin nerve branching is disturbed. In the future, the pain becomes intense, acquiring the character of neuralgic. There is swelling of the soft tissues adjacent to the bone.
The bone gum clinic is characterized by a slow, calm course with little pain; accompanied by exacerbations, in which there is an inflammatory contracture of the masticatory muscles.
Radiographically, the primary destructive actinomycosis of the jaws is manifested by the presence in the bone of one or several merged round cavities, not always clearly contoured. With gumma, the focus may be surrounded by a zone of sclerosis.
Primary productive-destructive damage to the jaws is observed mainly in children, adolescents, the cause is an odontogenic or tonsillogenic inflammatory process. There is a thickening of the bone due to periosteal overlays, which progressively increases and thickens, simulating a neoplasm.
The course of the disease is long - from 1-3 years to several decades. Against the background of a chronic course, there are separate exacerbations, similar to those in the destructive process.
On the roentgenogram, a new bone formation is visible, coming from the periosteum, the compaction of the structure of a compact and spongy substance in the body region, a branch of the lower jaw. Separate foci of resorption are found; days of the cavity are small, almost punctate, others are large. More or less pronounced bone sclerosis in the circumference of these foci.
Actinomycosis of the oral cavity organs is relatively rare and presents significant diagnostic difficulties.
Clinic actinomycosis of the tongue can proceed in the form of a diffuse inflammatory process such as phlegmon or abscess. A slightly painful node appears on the back or tip of the tongue, which remains unchanged for a long time, and after 1-2 months. resolved by abscessing and opening outward with the formation of fistulas and swelling of abundant granulations.
Actinomycosis of the salivary glands can be primary and secondary. The clinic is diverse, depending on the length of the process in the gland and the nature of the inflammatory reaction, the following forms of actinomycosis of the salivary glands can be distinguished: 1) exudative limited and diffuse actinomycosis; 2) productive limited and diffuse actinomycosis; 3) actinomycosis of deep lymph nodes in the parotid salivary gland.
Diagnosis. The diagnosis of actinomycosis in connection with a significant variety of the clinical picture of the disease presents some difficulties. The sluggish and prolonged course of odontogenic inflammatory processes, the failure of the anti-inflammatory therapy carried out are always alarming in relation to actinomycosis.
The clinical diagnosis of actinomycosis should be supported by a microbiological examination of the discharge, an allergic skin test with actinolysate and other methods of immunodiagnostics, and pathological examination. In some cases, repeated, often multiple diagnostic studies are required.
Microbiological examination of the discharge should consist in the study of the native preparation, cytological examination of stained smears and, in some cases, in the isolation of a pathogenic culture by inoculation.
The study of the discharge in a native preparation is the simplest method for the determination of drusen and elements of radiant fungi. Cytological examination of stained smears makes it possible to establish the presence of actinomycete mycelium, secondary infection, and also to judge the reactivity of the organism by the cellular composition (phagocytosis, etc.).
Differential diagnosis. Actinomycosis is differentiated from a number of inflammatory diseases: abscess, phlegmon, periostitis and osteomyelitis of the jaw, tuberculosis, syphilis, tumors and tumor-like processes. Clinical diagnostics are assisted by microbiological studies, specific reactions, serodiagnostics. Morphological data play an important role in the differential diagnosis of tumors.
Treatment. Therapy of actinomycosis of the maxillofacial region should be comprehensive and include: 1) surgical methods of treatment with a local effect on the wound process; 2) impact on specific immunity; 3) an increase in the general reactivity of the body; 4) impact on concomitant purulent infection; 5) anti-inflammatory, desensitizing, symptomatic therapy, treatment of concomitant diseases; 6) physical methods of treatment and exercise therapy.
Surgical treatment of actinomycosis consists in: 1) removal of teeth, which were the entrance gate of the infection; 2) surgical treatment of actinomycotic foci in soft and bone tissues, removal of areas of excessively newly formed bone and, in some cases, lymph nodes affected by the actinomycotic process.
Care of the wound after opening the actinomycotic focus is of great importance. Its long-term drainage, subsequent scraping of granulations, treatment of the affected tissues with 5% iodine tincture, and the introduction of iodoform powder are shown. With the addition of a secondary pyogenic infection, the deposited administration of antibiotics is indicated.
With the normal course of actinomycosis, actinolizatotherapy is performed or specially selected immunomodulators are prescribed, as well as general strengthening stimulants and, in some cases, biologically active drugs.
Therapy of actinomycosis with a hypergic inflammatory reaction begins with detoxification, restorative and stimulating treatment. Actinolysate and other immunomodulators are prescribed strictly individually. In order to relieve intoxication, a solution of hemodez, rheopolyglucin with the addition of vitamins, cocarboxylase is injected intravenously. The complex of treatment of chronic intoxication includes multivitamins with trace elements, enterosorbents, drinking plenty of water with herbal infusion. Such treatment is carried out for 7-10 days at intervals of 10 days as part of 2-3 courses. After 1-2 courses, immunomodulators are prescribed: T-activin, thymazine, actinolizate, staphylococcal toxoid, levamisole.
With a hyperergic type of process with pronounced sensitization to the radiant fungus, treatment begins with general antibacterial, enzymatic and complex infusion therapy aimed at correcting hemodynamics, eliminating metabolic disorders, and detoxification. Prescribe drugs with desensitizing, tonic and tonic properties. In the complex of treatment, vitamins of group B and C, cocarboxylase, ATP are used. After a course of such treatment (from 2-3 weeks to 1-2 months), based on the data of the immunological study, a course of immunotherapy with actinolysate or levamisole is prescribed.
An important place in complex treatment is occupied by stimulating therapy: hemotherapy, the appointment of antigenic stimulants and general tonic agents - multivitamins, vitamins B 1, B 12, C, aloe extract, prodigiosan, pentoxil, methyluracil, levamisole, T-activin, thymalin. Treatment should be combined with the appointment of antihistamines, pyrazolone derivatives, and symptomatic therapy.
Forecast with actinomycosis of the maxillofacial region, in most cases, it is favorable.
Prevention. They sanitize the oral cavity and remove odontogenic, stomatogenic pathological foci. The main thing in the prevention of actinomycosis is to increase the general anti-infectious defense of the body.
Tuberculosis is a chronic infectious disease caused by mycobacterium tuberculosis. Tuberculosis is a vector-borne disease. In recent years, diseases of the jaws, facial tissues and oral cavity have become rare.
Etiology. The causative agent of the disease is mycobacterium tuberculosis, - thin, straight or curved rods, 1..10 microns long, 0.2..0.6 microns wide. There are three types of tuberculosis bacteria: human (causes 92% of cases), bovine (5% of cases) and intermediate (3%).
Pathogenesis. The source of the spread of infection is more often a person with tuberculosis; the disease is transmitted by the alimentary route through the milk of sick cows. In the development of tuberculosis, the immunity and resistance of a person to this infection is of great importance.
It is customary to distinguish between primary and secondary tuberculous lesions. Primary damage to the lymph nodes of the maxillofacial region occurs when mycobacteria enter through the teeth, tonsils, the mucous membrane of the mouth and nose, damaged skin. Secondary damage occurs when the primary affect is localized in other organs or systems.
Pathological anatomy. Tuberculosis can affect any organ or organ system, while remaining a common disease. At the site of introduction of the pathogen, a tuberculoma is formed - a banal inflammation develops, acquiring a specific character in the proliferative phase. Around the inflammatory focus, a shaft of cellular elements is formed, in which, in addition to the cells characteristic of inflammation, there are epitheloid cells, the giant Pirogov-Langhans cell. In the center of the inflammatory focus, a site of caseous necrosis is formed. Another specific form of inflammation is a tubercle (tuberculous granuloma), morphologically similar to tuberculoma.
The clinical picture. In the maxillofacial region, lesions of the skin, mucous membranes, submucosa, subcutaneous tissue, salivary glands, and jaws are isolated.
Primary defeat lymphatic knots characterized by their single appearance or in the form of soldered into a package. The lymph nodes are dense, in the dynamics of the disease they become even more dense, reaching a cartilaginous or bone consistency. In patients of young age, the collapse of the node is often observed with the release of the characteristic cheesy secret. Primary tuberculosis of the lymph nodes is accompanied by general symptoms characteristic of the inflammatory process.
Secondary tuberculous lymphadenitis is one of the most common forms of this pathological process. It develops in the presence of a focus in other organs. The disease often proceeds chronically and is accompanied by low-grade fever, general weakness, and loss of appetite. In some patients, the process may have an acute onset, with a sharp increase in body temperature, symptoms of intoxication. There is an increase in lymph nodes, they have a dense elastic consistency, sometimes a bumpy surface, clearly contoured. Their palpation is slightly painful, sometimes painless. In some cases, there is a rapid disintegration of the focus, in others - slow suppuration with the formation of cheesy tissue decay. Upon the release of the contents, a fistula or several fistulas remain outside. In recent years, the number of cases of slow-flowing lymphadenitis has increased.
Tuberculosis of the skin and subcutaneous tissue... There are several clinical forms:
Primary tuberculosis of the skin (tuberculous chancre) - erosions and ulcers with a compacted bottom form on the skin. Regional lymph nodes are suppurating. After the ulcers heal, deforming scars remain.
Tuberculous lupus. The primary element is lupoma, which is characterized by the symptom of "apple jelly" - when pressed on any glass slide, a yellow zone is formed in the center of the element. Lupomas have a soft consistency, a tendency to merge, forming an infiltrate, with the resolution of which deforming scars are formed.
Scrofuloderma - most often formed in the immediate vicinity of the tuberculous focus in the jaws or lymph nodes, less often - when the infection spreads from distant foci. The development of an infiltrate in the subcutaneous tissue in the form of nodes or their chains, as well as merged gummy foci, is characteristic. The lesions are located superficially, covered with atrophic, thinned skin. The lesions open outward with the formation of single fistulas or ulcers, as well as their combinations. After opening, a bright red or red-violet color of the affected tissues is characteristic. When the pus is separated, a crust forms that closes the fistula or the surface of the ulcer. The process tends to spread to new tissue sites. After the lesions have healed, characteristic atrophic scars of a stellate shape are formed on the skin.
Dissimilated miliary tuberculosis of the face is the appearance on the skin of the face and neck of small painless nodules of red or brown color, which can ulcerate and heal with or without a scar.
Rosace-like tuberculoid - against the background of rosace-like redness and telangio-ectasia, pinkish-brown papules appear, rarely - with pustules in the center. The opened pustules are covered with a crust, heal with the formation of a scar.
Papulo-necrotizing tuberculosis. Soft, rounded papules with a diameter of 2-3 mm are formed on the skin, painless, cyanotic-brown in color. In the center of the papule, a pustule may form, containing necrotic masses that dry out into a crust. Perifocal inflammation is observed around the papule.
Tuberculosis defeat salivary glands is relatively rare. Tuberculosis bacteria spread to the gland by hematogenous, lymphogenous, or, less often, by contact. The process is more often localized in the parotid gland, while there may be a focal or diffuse lesion, with tuberculosis of the submandibular gland - only diffuse. Clinically, the disease is characterized by the formation of dense, painless or slightly painful nodes in the gland. Over time, the skin above them gets drunk. At the site of a breakthrough of the thinned skin area, fistulas or ulcerative surfaces are formed. From the duct of the gland, the secretion of saliva is scanty or not. With the decay of the focus and the emptying of its contents into the duct, flocculent inclusions appear in the saliva. Sometimes paralysis of facial muscles can occur on the affected side.
When radiography in the projection of the salivary gland in the chain of lymph nodes, foci of calcification are found. With sialography, a blurred pattern of the ducts of the gland and individual stripes corresponding to the formed cavities are noted.
Jaw tuberculosis occurs secondarily, as well as due to contact transition from the oral mucosa. Accordingly, they distinguish: a) bone lesions in primary tuberculosis complex; b) damage to the bone with active pulmonary tuberculosis.
Tuberculosis of the jaws is observed more often with damage to the lungs. It is characterized by the formation of a single focus of bone resorption, often with a pronounced periosteal reaction. On the upper jaw, it is localized in the region of the infraorbital edge or zygomatic process, on the lower - in the region of its body or branch.
At first, the tuberculous focus in the bone is not accompanied by pain, but as it spreads to other areas of the bone, periosteum, soft tissues, pains appear, and inflammatory contracture of the masticatory muscles. During the transition of the process from the depth of the bone to the adjacent tissues, infiltration, soldering of the skin with the underlying tissues, and a change in its color from red to bluish is observed. One or more cold processes are formed, which are prone to spontaneous opening with the separation of watery exudate and lumps of cheesy decay, fused to the affected bone, multiple fistulas with bulging granulations remain. Their probing allows you to find a focus in the bone, filled with granulations, sometimes small dense sequesters. Slowly, such foci are completely or partially scarred, leaving retracted, atrophic scars; tissue decreases, especially subcutaneous tissue. More often fistulas persist for several years, and some fistulas are scarred, and new ones appear nearby.
On the roentgenogram, bone resorption and single intraosseous foci are determined. They have clear boundaries and sometimes contain small sequesters. When the disease is old, the intraosseous focus is separated by the sclerosis zone from the healthy bone.
Diagnosis. Diagnosis of tuberculosis of the maxillofacial region consists of a number of methods and, first of all, of tuberculin diagnostics, which makes it possible to establish the presence of tuberculosis infection in the body. Tuberculin solutions are used in various methods (Mantoux, Pirke, Koch tests). A general study of patients is carried out using X-ray methods for examining the lungs. In addition, smears of pus from foci, imprints of cells from ulcers are examined, cultures are isolated to detect tuberculosis bacteria.
Differential diagnosis. Primary and secondary damage to the lymph nodes must be differentiated from abscess, lymphadenitis, chronic osteomyelitis of the jaw, actinomycosis, syphilis, as well as from malignant neoplasms.
Scrofuloderma is differentiated from cutaneous and subcutaneous forms of actinomycosis, cancer.
The defeat of the jaw bone by tuberculosis should be differentiated from the same processes caused by pyogenic microbes, as well as malignant neoplasms.
Treatment patients with tuberculosis of the maxillofacial area are in a specialized hospital. General treatment should be complemented by local: hygienic maintenance and oral hygiene. Surgical interventions are carried out strictly according to the indications: with the clinical effect of treatment and the delimitation of the local process in the oral cavity, in the bone tissue. Intraosseous foci are opened, granulations are scraped out of them, sequesters are removed, fistulas are excised and ulcers are sutured or their edges are refreshed for tissue healing by secondary intention under a tampon of iodoform gauze. Teeth with periodontal disease affected by tuberculosis must be removed.
Forecast with timely general anti-tuberculosis treatment, it is favorable.
Prevention. Application modern methods treatment of tuberculosis is the main one in the prevention of tuberculous complications in the maxillofacial region. Treatment of caries and its complications, diseases of the mucous membrane and periodontal disease should be carried out.
SYPHILIS
Syphilis is a chronic infectious venereal disease that can affect all organs and tissues, including the maxillofacial region.
Etiology. The causative agent of syphilis is pale treponema (spirochete), a spiral-shaped microorganism, 4..14 microns long, 0.2..0.4 microns wide. In the human body, it develops as a facultative anaerobe and is most often localized in lymphatic system... The spirochete is slightly resistant to external factors.
There is no congenital or acquired immunity to syphilis.
Pathogenesis. Infection with syphilis occurs through sexual contact. Pale treponema gets on the mucous membrane or on the skin, more often when their integrity is violated. Infection can also occur asexually (common syphilis) or in utero from a sick mother.
The clinical picture. The disease has several periods: incubation, primary, secondary and tertiary. With congenital syphilis, specific changes are observed in the tissues of the maxillofacial region.
The primary period of syphilis is characterized by the appearance on the mucous membrane, including in the oral cavity, of primary syphiloma or hard chancre. In the secondary period of syphilis, the mucous membrane of the oral cavity is most often affected, pustular and roseolous elements are formed.
A rare manifestation of syphilis in the secondary period is the defeat of the periosteum. It is characterized by a slow and sluggish course. The thickened periosteum acquires a pasty consistency, but the periosteal abscess does not form. Gradually, the areas of the periosteum are compacted, flat elevations appear.
The tertiary period of syphilis develops 3-6 years or more after the onset of the disease and is characterized by the formation of so-called gummas. Gummas can be localized in the mucous membrane, periosteum and bone tissue of the jaws. Manifestations of syphilis in the tertiary period do not always occur, in this regard, manifest or latent tertiary syphilis is distinguished.
With the formation of syphilitic gummas, a dense, painless knot first appears, which eventually opens with the rejection of the gummy core. The resulting ulcer has a crater-like shape, painless on palpation. Its edges are smooth, dense, the bottom is covered with granulations.
Syphilitic lesion of the tongue manifests itself in the form of gummy glossitis, diffuse interstitial glossitis.
The defeat of the periosteum in the tertiary period of syphilis is characterized by diffuse, dense infiltration of the periosteum. Further, the thickened periosteum is soldered to the mucous membrane, and in the area of the jaw body - to the skin; gum softens and opens outward with the formation of a fistula or ulcer in the center. The ulcer on the periosteum of the jaw gradually scarred, leaving thickenings on the surface, often of a roller-like shape. Teeth can be involved in the process, they become painful and mobile. The process of the periosteum can be transferred to the bone.
Changes in bone tissue in the tertiary period of syphilis are localized in the jaw, nasal bones, and nasal septum. The process begins with a thickening of the bone, which increases as the gum grows. The patient is disturbed severe pain, sometimes impaired sensitivity in the branching of the chin, infra- and supraorbital nasopalatine nerves. Subsequently, gum grows in one or several places to the periosteum, mucous membrane or skin, opens outward, forming fistulous passages. Sequesters are not always formed, they are small. Only the attachment of a secondary pyogenic infection leads to the death of more significant areas of the bone. In this case, the formation of messages with the nasal cavity and maxillary sinus is possible on the upper jaw.
After the disintegration of gum in the bone, the tissue gradually heals with the formation of coarse, dense, often tightening scars. Exostoses and hyperostoses develop in the bone.
The X-ray picture of gummy bone lesions is characterized by destruction foci of various sizes with clear even edges surrounded by sclerosed bone tissue.
Diagnosis. The clinical diagnosis of syphilis is confirmed by the reaction of Wasserman and others serological tests... Microbiological examination, as well as morphological examination of the affected tissues, is of great importance.
Differential diagnosis syphilitic lesions of the mouth, teeth and jaws presents certain difficulties. The ulcerative form of primary syphiloma on the lip may resemble a decaying cancerous tumor. Gums of the oral mucosa have common symptoms with traumatic ulcers. Gummy glossitis should be differentiated from tuberculous ulcers, cancerous lesions.
Syphilitic lesions of the periosteum and bone tissue should be distinguished from nonspecific and specific lesions of these tissues. The gummy process in the bone can simulate cancerous or sarcomatous diseases.
Treatment syphilis is carried out in a specialized venereal hospital.
With syphilis affecting the bone tissue of the jaws, periodic studies of the electrical excitability of the dental pulp are advisable, according to indications - trepanning of teeth with dead pulp and treatment according to the principle of therapy for chronic periodontitis. Moving teeth should not be removed; after treatment, they are strengthened quite well.
Active surgical treatment for lesions of the periosteum of the jaws with syphilis is not indicated even in the case of the formation of sequesters. They are removed after specific treatment against the background of a subsiding process.
The hygienic maintenance of the oral cavity is important. Tartar is removed, the sharp edges of the teeth are ground, and the oral cavity is sanitized.
Forecast with timely diagnosis, correct treatment and further dispensary observation, it is mostly favorable.
Prevention. In the prevention of syphilis, in addition to its social aspect, the hygienic maintenance of the oral cavity, the prevention of cracks and erosion in it is of great importance.
USED BOOKS:
1) "Surgical dentistry" - ed. Robustova. M. Medicine, 1996. With. 295-308.
2) "Surgical dentistry" under the editorship of V. A. Dunaevsky - M. Medicine, 1979. With. 221-224
3) "Guide to maxillofacial surgeon ai and surgical dentistry "- A.A. Timofeev. Kiev, "Chervona Ruta-Tours", 1997 With. 345-350.
A specialist in the field of surgical diseases and damage to teeth, oral cavity organs, face and neck, bones of the facial skeleton, in which complex treatment will be prescribed. The maxillofacial area, face, neck are areas that are very richly supplied with blood and innervated, therefore any inflammatory processes and injuries proceed violently and often painfully for the patient, leaving behind (especially with poor-quality treatment) gross deformations and defects. It is worth noting the proximity of these areas to the brain and mediastinal organs, which also speaks of the absolute need for timely treatment of inflammation on the face.What is the competence of the Oral and Maxillofacial Surgeon
Oral and maxillofacial surgeon who studies surgical diseases of the teeth, bones of the facial skeleton, oral organs, face and neck.What diseases does the Maxillofacial surgeon deal with?
Diseases can be divided into four groups, depending on the cause and clinical picture.1) Inflammatory diseases of the teeth, jaws, tissues of the face and neck, oral organs (periodontitis, periostitis, osteomyelitis of the jaw, abscesses, phlegmon, lymphadenitis, difficult teething, odontogenic inflammation of the maxillary sinus, inflammatory diseases of the salivary glands, temporomandibular joint ).
2) Injuries to the soft tissues of the face and neck, bones of the facial skeleton.
3) Tumors and tumor-like formations of the face, jaws, oral organs.
4) Congenital and acquired defects and deformities of the face, jaws and plastic surgery of the maxillofacial region (blepharoplasty, otoplasty, rhinoplasty, circular facelift, contour plastic).
What organs the doctor deals with Oral and maxillofacial surgeon
Teeth, face, neck, tongue.When to contact a Maxillofacial Surgeon
Periodontitis symptoms. The leading symptom of acute periodontitis is a sharp, constantly growing pain. Touching the tooth dramatically increases the pain. The tooth seems to be "higher" than others. These painful sensations are caused by the pressure of the accumulated exudate on the tissues and nerve receptors of the periodontal gap.The affected tooth is discolored and mobile. It may have a cavity or be intact.
Probing is painless and the response to percussion is severely painful. The mucous membrane in the area of the transitional fold is edematous, hyperemic, painful on palpation.
With the progression of the process, swelling of the soft tissues may occur, leading to asymmetry of the face, the general condition is disturbed (headache, weakness, malaise, body temperature rises to 38 - 39 ° C). There is an increase and soreness of regional lymph nodes.
Symptoms of periostitis - inflammation of the periosteum of the jaw - are well known to many children and adults: a sharply painful hard compaction appears on the gum near a tooth with dead pulp or the remaining root, rapidly increasing.
The swelling, becoming more pronounced, passes to the soft tissues of the face. Depending on the location of the diseased tooth, the lip and wing of the nose, cheek and lower eyelid swell, the temperature rises, and the person feels unwell. This disease is popularly known as flux.
Jaw osteomyelitis symptoms
spontaneous throbbing pain in the jaw, headache, chills, temperature up to 40 "C. An affected tooth with necrotic pulp (possibly with a filling) is found; he and the adjacent teeth are sharply painful, mobile. Edematous asymmetric face. The transitional fold is hyperemic and smoothed. Lymph nodes are enlarged, painful.
Osteomyelitis is often complicated by abscess, phlegmon. In the blood, neutrophipic leukocytosis; ESR increased. General condition of varying severity.
An abscess is a delimited accumulation of pus in various tissues and organs. An abscess should be distinguished from phlegmon (diffuse purulent inflammation of tissues) and empyema (accumulation of pus in body cavities and hollow organs).
General clinical manifestations of abscesses are typical for purulent-inflammatory processes of any localization: an increase in body temperature from subfebrile to 41 ° (in severe cases), general malaise, weakness, loss of appetite, headache.
In the blood, leukocytosis with neutrophilia and a shift of the leukocyte formula to the left is noted. The degree of these changes depends on the severity of the pathological process.
V clinical picture abscesses of various organs have specific signs due to the localization of the process. The outcome of an abscess may be a spontaneous opening with a breakthrough outward (abscess of subcutaneous tissue, mastitis, paraproctitis, etc.); breakthrough and emptying into closed cavities (abdominal, pleural, joint cavity, etc.); a breakthrough into the lumen of organs communicating with the external environment (intestine, stomach, bladder, bronchi, etc.). The emptied abscess cavity, under favorable conditions, decreases in size and undergoes scarring.
With incomplete emptying of the abscess cavity and its poor drainage, the process can become chronic with the formation of a fistula. A breakthrough of pus into closed cavities leads to the development of purulent processes in them (peritonitis, pleurisy, pericarditis, meningitis, arthritis, etc.).
Lymphadenitis is an inflammation of the lymph nodes.
Acute lymphadenitis almost always occurs as a complication of a local focus of infection - a boil, an infected wound or abrasion, etc. Causative agents of infection (usually staphylococci) penetrate into the lymph nodes with the flow of lymph through the lymphatic vessels, and often without inflammation of the latter, that is, without lymphagitis.
Purulent foci on the lower limb are complicated by damage to the inguinal, less often popliteal lymph nodes; on the upper limb- axillary, less often ulnar, on the head, in the oral cavity and pharynx - cervical.
When and what tests need to be done
- histological examination of biopsy;- general analysis blood;
- general urine analysis;
- analyzes for hormones;
What are the main types of diagnostics usually performed by a Maxillofacial surgeon?
- X-ray;- Intraoral radiography;
- Radiovisiographic examination of teeth and jaw bone tissue;
- Panoramic radiography;
- Tomography;
- Cephalometric X-ray of the face
- X-ray computed tomography;
- Magnetic resonance imaging;
- Three-dimensional visualization of the facial skull and soft tissues of the face. Implantation means the introduction into the body of materials of non-biological origin in order to replace the lost organ.
When implanting teeth, special implants are used, installed in the area of missing teeth.
A titanium "screw" is screwed into the bone onto which the crown is fixed. Materials for implants are titanium and its alloys, tantalum, various types of ceramics, sapphire, zirconium and other substances. All these materials are highly bioinert, that is, they do not irritate the surrounding tissues.
Benefits of implantation
Adjacent teeth are not sharpened;
- it is possible to restore a defect of any length;
- strength and reliability (the service life of implants is longer than with other types of prosthetics, since the very first implants, installed more than 40 years ago, continue to serve their owners);
- high aesthetics (the implant is practically indistinguishable from a healthy natural tooth).
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A maxillofacial surgeon is a doctor whose job is to research and treat diseases of the jaws and face. Let's look at what diseases the doctor treats, diagnostic methods and tips for maintaining health.
Oral and maxillofacial surgeon is the most popular, but at the same time difficult medical specialty to date. A person's face is his business card, it is the appearance that determines the individuality and provides a number of vital functions (breathing, speech, facial expressions, food intake). The doctor deals with the treatment of abscesses, periostitis, difficult teething, inflammation of the salivary glands and maxillary sinuses. The doctor helps with the treatment of injuries of the facial skeleton, tumors on the jaw bones, birth defects, pathologies and deformities.
In the course of treatment, the doctor uses multi-stage surgical methods to treat both children and adults. Particular difficulties in the process of surgical treatment arise with the maintenance of the normal respiratory process. The result of treatment of maxillofacial lesions depends on the tactics of its management (anesthesia, surgery, rehabilitation) and the professionalism of doctors.
Who is a Maxillofacial Surgeon?
Who is a maxillofacial surgeon is a qualified doctor who treats oral organs, damaged teeth, pathologies and deformities of the bones of the facial skeleton, neck and face. The area of the disease is innervated and supplied with blood, so all lesions are painful, leaving behind defects and serious deformities.
The maxillofacial surgeon, before treating the disease, conducts a detailed diagnosis of the patient. This is because the treatment area has proximity to vital organs and the brain. All this suggests that the maxillofacial surgeon must be a real professional, be able to recognize the symptoms of serious diseases and promptly treat inflammation and lesions of the maxillofacial region.
When should you see a maxillofacial surgeon?
When should I go to a maxillofacial surgeon for help, and what defects of the jaws and face require mandatory treatment? Let's take a look at the symptoms of conditions treated by a doctor that require immediate attention.
- Periodontitis - the disease is accompanied by a sharp and growing pain in the teeth. Painful sensations are associated with pressure on the nerve endings. Teeth that are affected by periodontitis change color and become mobile.
- Periostitis is an inflammation of the jaw that occurs due to the remaining tooth after root extraction, and is accompanied by a slight compaction on the gums, which gradually affects the soft tissues of the face.
- Osteomyelitis of the jaws - the symptoms of the disease are accompanied by throbbing pain in the jaw, chills, headache and high fever. The disease occurs due to the necrotic pulp of the tooth.
- An abscess is a purulent accumulation. The disease is accompanied by weakness, headaches, high fever and other symptoms that are typical of purulent-inflammatory processes.
- Lymphadenitis is a disease that causes inflammation of the lymph nodes. Most often affects the head, mouth and pharynx.
What tests do I need to take when contacting a maxillofacial surgeon?
Treatment of any disease is accompanied by tests that help diagnose the cause of the lesion and draw up the most effective treatment plan that matches the individual characteristics of the patient's body. The standard tests, which are mandatory for all patients, are general and biochemical blood tests, as well as general urine tests.
The maxillofacial surgeon can give a referral for histology, that is, scraping the skin from the affected area. If the disease occurs on the neck and or in the area of the lymph nodes, then the patient must be tested for hormones.
What diagnostic methods does a maxillofacial surgeon use?
Diagnostic methods help to determine the disease as accurately as possible, focusing on its symptoms and test results. Let's look at what diagnostic methods a maxillofacial surgeon uses. The most common method that allows you to visually see the extent of damage is X-ray and intraoral X-rays, which are given for lesions of the jaw and teeth.
In case of defects in teeth and bone tissue, the doctor conducts radiovisiographic diagnostics and radiography. To diagnose facial lesions, tomography, MRI, CT, cephalometric radiography are performed.
What does a maxillofacial surgeon do?
What does a maxillofacial surgeon do and what are the responsibilities of a doctor? The specialist is engaged in the diagnosis, treatment and prevention of diseases, lesions and pathologies of the maxillofacial region. The doctor corrects congenital deformities, malocclusion and performs aesthetic surgical treatment of the face and neck.
The maxillofacial surgeon deals with the treatment of emergency patients who come with injuries and disabilities that require medical care... As a rule, these are people who have suffered in accidents and accidents. The doctor diagnoses and treats planned patients, performs operations. The surgeon accompanies the patient until complete recovery.
What diseases does a maxillofacial surgeon treat?
A maxillofacial surgeon is a qualified physician who treats pathologies and defects in the maxillofacial area. Let's take a closer look at what diseases the doctor treats. All diseases are divided into certain groups, which depend on the causes of the lesions. The groups include tumors, inflammations, trauma, and acquired and birth defects.
Oral and maxillofacial surgeon is a qualified doctor whose task is to timely diagnose and correctly treat lesions of the jaws and face. For this, the doctor uses modern diagnostic techniques and methods of treatment.