1.1. PERIOSTITIS OF THE JAW BONES
Periostitis is an inflammatory process with the 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 pathomorphological picture, periostitis is distinguished between acute (serous and purulent) and chronic (simple and ossifying).
Acute serous periostitis manifested by smoothness of the transitional fold, pronounced pain on palpation. The mucous membrane over the inflamed periosteum is hyperemic and edematous. The process is localized in the area of the “causal” tooth and one or two neighboring teeth, and 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 the bulging of the transitional fold is determined due to the formation of a subperiosteal abscess, a symptom of fluctuation (with the destruction of the periosteum and the spread of pus under the mucous membrane), pathological mobility of the “causal” tooth. In the soft tissues surrounding the source of inflammation, perifocal edema is expressed; at the site of direct contact with the subperiosteal abscess, inflammatory infiltration of soft tissues with skin hyperemia is observed.
At chronic periostitis There is an increase in bone volume due to the layering of excess young bone on the surface of the jaw in the form of layers with varying degrees of ossification.
fication. A source of chronic infection in the bone or trauma are a source of additional pathological irritation of the periosteum, which in children is already in a state of physiological irritation. In simple chronic periostitis, the newly formed bone undergoes reverse development after adequate treatment; in ossifying periostitis, bone ossification develops in the early stages and ends, as a rule, in hyperostosis. X-rays of the lower jaw reveal young bone tissue 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 visible. X-ray examination of the upper jaw rarely provides a clear picture to aid diagnosis.
1.2. ODONTOGENIC OSTEOMYELITIS
JAW BONES
Acute osteomyelitis of the jaw bones. Depending on the route of 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 (usually in the first year of life), predominantly hematogenous osteomyelitis develops; from 3 to 12 years of age, odontogenic osteomyelitis develops in 84% of cases. The following forms of the disease are distinguished: acute osteomyelitis and chronic, which is divided depending on the clinical and radiological picture into 3 forms: destructive, destructive-productive and productive.
Acute osteomyelitis- a purulent infectious-inflammatory disease of the jaw bone (all its structural components), accompanied by bone lysis with purulent exudate, disruption of its trophism and leading to osteonecrosis. For the clinic of acute osteomyelitis, the manifestations are general symptoms. The disease begins acutely, with a rise in body temperature to 38-39 ° C, accompanied by chills, general weakness, and malaise. In young children and puberty, when the body temperature rises, convulsions, vomiting and dysfunction 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, and pathological mobility of it and the intact teeth adjacent to it is observed. Pus may be released from the gum pockets, and subperiosteal abscesses may form, which are usually localized on both sides of the alveolar process and jawbone. Osteomyelitis is accompanied by pronounced inflammatory changes in the soft tissues of the face; inflammatory infiltration with hyperemia and swelling of the skin develops in the adjacent tissues. Regional lymphadenitis is always present. Acute osteomyelitis is characterized by the formation of abscesses or phlegmons; adenophlegmons develop more often. In advanced cases in older children, acute odontogenic osteomyelitis is complicated by perimandibular phlegmon.
X-ray examination in the first days of the disease does not reveal signs of changes in the jaw bones. By the end of the week, diffuse thinning of the bone appears, which indicates its melting by purulent exudate. The bone becomes more transparent, the trabecular pattern disappears, the cortical layer becomes thinner and in places is interrupted.
Acute odontogenic osteomyelitis of the upper jaw becomes much less likely to become chronic compared to processes in the lower jaw, since the anatomical and physiological features of its structure contribute to the rapid breakthrough of abscesses and relief of the osteomyelitic process.
Chronic osteomyelitis- purulent or proliferative inflammation of bone tissue, characterized by the formation of sequesters or lack of tendency to recovery
and the increase in destructive and productive changes in the bone and periosteum. In chronic odontogenic osteomyelitis of the jaw bones, the process involves the rudiments of permanent teeth, which “behave” as sequesters and support inflammation. Depending on the severity of the processes of death or construction of bone substance, three clinical and radiological forms of chronic osteomyelitis are identified: destructive, destructive-productive, productive. The lower jaw in children is affected by odontogenic osteomyelitis much more often than the upper jaw.
Chronic forms of odontogenic osteomyelitis are most often the outcome of acute odontogenic osteomyelitis, and the process becomes chronic in children in a shorter period of time than in adults (the process can be interpreted as chronic in children already at 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 (the productive form of chronic odontogenic osteomyelitis).
Destructive form of chronic osteomyelitis observed in young children, exhausted, weakened by a general infectious disease, i.e. with reduced immune resistance of the body. Symptoms of acute inflammation subside, but symptoms of general intoxication of the body remain pronounced and accompany the entire period of the disease. Lymph nodes remain enlarged and painful. Internal and/or external fistulas appear with purulent discharge and bulging granulations. A delay in the outflow of exudate can cause exacerbation of inflammation (the clinical picture of which is similar to acute osteomyelitis). X-ray examination reveals areas of resorption of spongy and cortical substances. Bone destruction occurs quickly and diffusely. The final boundaries of the lesion are established at a later date: by the end of the 2nd - beginning of the 3rd month from the onset of the disease. The destructive form is accompanied by the formation of large, total sequestration and pathological fractures. The periosteal bone structure in all stages of the destructive form is weakly expressed, the endosteal structure is not determined radiologically.
Destructive-productive form of chronic odontogenic osteomyelitis observed in children 7-12 years old and is the most common outcome of acute odontogenic osteomyelitis. The clinic is similar to the clinic of the destructive form of chronic osteomyelitis. X-ray examination reveals small areas of bone loss and the formation of many small sequesters. In the periosteum, active construction of bone substance occurs, which is determined on radiographs in the form of (often layered) bone layers. Signs of endosteal bone restructuring appear at a later date - foci of rarefaction alternate with areas of osteosclerosis, and the bone acquires a coarsely spotted pattern.
Productive (primary chronic) form of odontogenic osteomyelitis develops only in childhood and adolescence, most often in children 12-15 years old. Sensitization of the body and a decrease in its protective properties are of great importance in the occurrence of primary chronic forms. Not the least important role is played by the irrational use of antibiotics (small doses, short courses), incorrect treatment tactics for pulpitis and periodontitis, etc. Since a long time passes from the onset of the disease to its manifestation (4-6 months), its diagnosis can be very difficult. There may be no “causal” temporary teeth in the oral cavity, and peri-coronitis (a common cause of damage) by the beginning of the process is already completed with the eruption of intact teeth. Typically, productive (hyperplastic) osteomyelitis occurs unnoticed by the patient. Classic signs of osteomyelitis - fistulas and sequestra - are absent. A deformation appears in a separate area of the jaw, slightly painful on palpation. The deformity increases 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, painful on palpation, and trismus may appear. During the period of exacerbation, regional lymph nodes are also enlarged and painful on palpation, but periadenitis, abscesses and peri-maxillary phlegmons rarely develop.
The X-ray picture is characterized by an increase in jaw volume due to pronounced endosteal and periosteal bone formation. Sequesters are not identified.
In the affected area there is an alternation of rarefaction foci with unclear boundaries and zones of osteosclerosis. The bone acquires a variegated, coarsely 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 affected area (ascending pulpitis and periodontitis).
1.3. HEMATOGENIC OSTEOMYELITIS
JAW BONES
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 the 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%), aged 1-3 years (15.2%) and from 3 to 12 years (7.36%) (Roginsky V.V., 1998) .
Hematogenous osteomyelitis of the facial bones is most often localized in the zygomatic and nasal bones, the zygomatic and frontal processes are affected in the upper jaw, and the condylar process in the lower jaw.
In the acute phase of the disease, regardless of the location of the primary lesion, newborns and infants develop an extremely severe general condition and the most pronounced general intoxication of the body. Despite timely initiation and active therapy, new purulent foci often appear in various skeletal bones 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 child’s general condition 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 osteomyelitis
lithitis becomes chronic and proceeds with the formation of extensive sequestration, including dead rudiments of teeth. Restorative processes in the bone are weakly expressed.
Outcomes depend on the clinical form of hematogenous osteomyelitis and the timing of initiation of rational therapy. After suffering from chronic hematogenous osteomyelitis, children are left with defects and deformations of the jaws associated with their underdevelopment or extensive sequestration of the bone. With osteomyelitis of the mandible, a defect or underdevelopment of the condylar process is formed, followed by impaired growth of the entire mandible 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 occupied by lymphadenitis. Lymphadenitis in the maxillofacial area in children is extremely rarely a primary disease. They accompany odontogenic, dental diseases, diseases of the ENT organs, 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, injury, or routine vaccination.
According to the clinical course, acute lymphadenitis is distinguished (serous, in the stage of periadenitis, purulent) and chronic (hyperplastic, in the acute stage).
Acute serous lymphadenitis proceeds violently with a pronounced general reaction and local symptoms. Body temperature rises. General signs of intoxication appear, more pronounced in young children (1-3 years). In the initial stage, local symptoms are characterized by a slight enlargement of the lymph nodes, pain on palpation, the lymph node remains mobile, dense, and the skin color is not changed. Then (2-3 days from the onset of the disease) soft tissues are involved in the process, inflammation spreads beyond the capsule of the lymph node, which is interpreted as periadenitis. At the site of the lymph node, a dense, sharply painful infiltrate 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). The lymph nodes of the lateral surface of the neck, submandibular and parotid areas are most often affected.
Chronic hyperplastic lymphadenitis characterized by an enlarged lymph node - it is dense, mobile, not fused with surrounding tissues, painless or slightly painful on palpation. More often, the etiology of this form of lymphadenitis is non-odontogenic. In these cases, several regional lymph nodes are palpated.
Chronic abscess lymphadenitis characterized by the appearance of a focus of hyperemia and thinning of the skin over the enlarged lymph node; a symptom of fluctuation is determined by palpation, indicating purulent melting 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 facial area occurs due to damage or inflammation of the facial skin, mucous membrane of the mouth, lips, nose, and eyelids. Less commonly, abscesses in children occur due to the spread of infection from an odontogenic focus. The formed abscess is a bulging, dome-shaped, brightly hyperemic area. The skin over it is thinned. Palpation is sharply painful, fluctuation is easily detected. The general condition is slightly disturbed. Abscesses located deep in the tissues are more severe - peripharyngeal, paratonsillar, subtemporal, tongue. They are accompanied by severe intoxication, dysfunction of chewing, swallowing, breathing, and trismus. An infiltrate is formed at the site of inflammation, in the area of which the skin or mucous membrane is hyperemic and tense. A fluctuation is determined in the center of the infiltrate. The boundaries of the changed tissues are clearly defined. Often the skin or mucous membrane in the area of the abscess bulges above the surface.
1.6. PHLEGMON
1.7. FURUNCLE
Phlegmon- acute purulent diffuse inflammation of subcutaneous, intermuscular and interfascial loose fatty tissue. In childhood, phlegmon often develops as a complication of acute purulent lymphadenitis (adenophlegmon) or accompanies odontogenic osteomyelitis (osteophlegmon). Adenophlegmon is observed in children from a 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 areas. The source of infection can be teeth, ENT organs, traumatic injuries, including post-injection injuries, due to violation of aseptic rules. With phlegmon, there is an increase in the level of intoxication of the body 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 fluctuation are determined. The skin of the affected area becomes dense, tense, and hyperemic. The rapid development of phlegmon in children is facilitated by a weak connection of the dermis with the basement membrane and subcutaneous fat layer, and good blood supply. These are the main reasons for the development of diffuse purulent-necrotic processes in children. Immaturity of the immune system also contributes to the development of inflammation and prevents the focus from being limited.
Osteophlegmon aggravates the course of acute odontogenic osteomyelitis and sharply increases the general intoxication of the body. With osteophlegmon, the spread of a purulent inflammatory process occurs as a result of the melting of the periosteum and the breakthrough of purulent exudate into the soft tissue.
In newborns and infants, a serious complication of hematogenous osteomyelitis of the upper jaw is the formation of phlegmon in the orbital cavity or retrobulbar space. In acute odontogenic osteomyelitis, superficial phlegmons develop more often. Cellulitis of deep intermuscular spaces is rare in childhood (with long-term untreated bone processes).
Furuncle- acute purulent-necrotic inflammation of the hair follicle and the associated sebaceous gland with surrounding tissue, caused by pyogenic microbes - staphylococci. The development of a boil is promoted by skin trauma with subsequent infection. Predisposing factors are increased activity of the sweat and sebaceous glands of the skin, vitamin deficiency, metabolic disorders, and weakened immunity. A boil can occur on any area of the skin where there is hair, most 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, bright red, rising above the skin in the form of a small cone. If the course is favorable, on the 3-4th day a focus of softening forms in the center, which can open on its own with the appearance of pus. At the autopsy site, a greenish area of necrotic tissue is found - the core of the boil. Later, along 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. In an uncomplicated course, the development cycle of the boil lasts 8-10 days.
Furuncles in the area of the lips and wings of the nose, as a rule, are severe. Inflammatory swelling spreads to the surrounding tissues of the face. There is severe radiating pain. Body temperature is high. There is a possibility of developing such severe complications as meningitis, mediastenitis, sepsis, therefore treatment of children with facial boils should be carried out in a hospital setting.
In weakened children, the disease may proceed sluggishly, with a weak inflammatory reaction, and with excessive accumulation of pus, the necrotic core may melt and an abscess (abscessing boil) may occur.
1.8. INFLAMMATORY DISEASES OF THE SALIVARY GLANDS
1.8.1. MUMPS OF NEWBORN
The disease is rare. The etiology and pathogenesis of the disease have not been sufficiently studied. It develops more often in premature or weakened 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 hematogenously.
The disease develops acutely, most 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-masticatory areas, accompanied by severe general intoxication of the body. After 2-3 days, purulent or purulent-necrotic melting of the gland occurs. It is possible for pus to spread to the area of the temporomandibular joint, which can lead to the death of growth zones on the lower jaw and, as a result, to ankylosis of the TMJ and underdevelopment of the lower jaw.
History;
Palpation;
X-rays of facial bones;
Ultrasound examination;
Blood and urine tests.
Mumps of the newborn is differentiated from:
Adenophlegmon.
1.8.2. PAROTITIS
Mumps is caused by a filterable virus Pneumophilus parotidis. The mumps virus is quickly inactivated when exposed to high temperature, ultraviolet irradiation, weak solutions of formaldehyde, Lysol, and alcohol. The source of infection is a sick person. Transmission of infection occurs through airborne droplets, as well as through objects contaminated with the saliva of a patient (dishes, toys). The virus is detected 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. Primary damage by the virus to the meninges, testicles and pancreas is possible.
The disease most often manifests itself between the ages of 5 and 15 years. Even before the appearance of clear clinical signs, one can detect increased levels of amylase in the blood serum and diastase in the urine, which disappear 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 that the submandibular and sublingual salivary glands are involved in the process, and extensive swelling of the cervical tissue is possible. The skin over the inflamed glands is tense and 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, intensifying with 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 alternating with tachycardia. Often the spleen is enlarged. The ESR is usually increased. Often there is damage to the nervous system (meningitis, encephalitis), sometimes with paralysis of the cranial and spinal nerves; sometimes accompanied by mental disorders.
A common complication is orchitis. Oophoritis with mumps is observed less frequently. Mastitis, accompanied by swelling and tenderness of the mammary glands, has also been described.
The diagnosis is made 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 sialadenitis;
Chronic nonspecific parotitis in the acute stage;
Infectious mononucleosis;
Abscess of the buccal area;
Lymphadenitis;
Hematogenous osteomyelitis;
Lymphangioma in the inflammation stage;
Adenophlegmon.
1.8.3. CHRONIC PARENCYMATOUS MUMPS
The etiology of the disease is not clear.
The process is characterized by a primary chronic onset and latent inflammation in the parotid salivary glands.
The disease most often manifests itself in children 3-8 years old. The peculiarity of chronic nonspecific parenchymal parotitis lies in the duration of the course. Exacerbations can occur 6-8 times a year. Characteristic is a deterioration in the general condition, the appearance of pain and swelling in the area of the parotid glands on one or both sides. Hyperemia and skin tension may occur.
When palpating the parotid-masticatory area, an enlarged, painful (mildly painful), dense, tuberous gland is felt. When massaging the area of the parotid gland, viscous jelly-like saliva mixed with pus or fibrin clots is released from the salivary duct.
During the course of the disease, triclinico-radiological stages are distinguished: initial, clinically pronounced and late. In each stage, there is a period of exacerbation and remission, as well as an active and inactive course. When the process is active, the disease is characterized by a pronounced inflammatory reaction of the thyroid gland. The duration of exacerbation during an active course ranges from 2-3 weeks to 2 months, the number of exacerbations varies from 4 to 8 times a year.
With an inactive course, exacerbation of chronic parenchymal parotitis occurs without pronounced local and general symptoms of inflammation with fewer exacerbations per year (from 1 to 3).
The diagnosis is made based on 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 thyroid gland with preliminary contrasting of the gland ducts with water-soluble contrast agents: verografin, urografin, omnipaque (sialography, orthopantomosialography);
Testing purulent discharge from the salivary gland for sensitivity to antibiotics (during an exacerbation);
Cytological examination of saliva smears and punctate of the uterine fluid 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. CYTOMEGALY
Cytomegaly is a viral disease that affects the salivary glands mainly in 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 and breast milk. Cytomegalovirus can penetrate 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 birth 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. Infection of the fetus can occur when an infected woman passes through the birth canal. The site of primary fixation of the virus is the salivary glands. The parotid glands are affected more often than the submandibular, sublingual salivary glands and regional lymph nodes.
In the salivary gland, narrowing and even blockage of small salivary ducts by giant epithelial cells protruding into their lumen is determined. There are clearly visible inclusions in the nucleus and cytoplasm of these cells. Similar giant cells with cytomegaly are found in saliva, urine and feces.
With local 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 from cytomegaly
Children may experience congenital heart defects and large vessels, skin angiomas, and myocarditis.
In infants, in rare cases, skin lesions are observed in the form of large-plate peeling, long-term diaper rash or non-healing ulcers. In some cases, the disease can occur as sepsis.
The prognosis was previously considered absolutely unfavorable. Currently, mild forms are diagnosed, proven virologically, with a favorable outcome.
The diagnosis is made 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 newborns;
Toxoplasmolysis.
1.8.5. SALILOSIS DISEASE OF THE SUBMANDIBLIAR SALIVARY GLANDS IN CHILDREN
The mechanism of stone formation is not entirely clear. In the occurrence of salivary stone disease, a disturbance of calcium metabolism is of great importance; sometimes injury or the entry of a foreign body into the excretory ducts of the salivary glands is noted.
The main diagnostic symptom is the detection of a calculus, pain that occurs when eating, associated with impaired flow of saliva. Sialodochitis and sialadenitis are associated symptoms. These symptoms increase with the age of the child.
The diagnosis is made on the basis of general clinical examination methods (complaints, medical history, 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 from a retention cyst of the sublingual salivary gland, hemangioma and lymphangioma of the sublingual region, sialodochitis, and an abscess of the maxillo-lingual 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 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. Child 13 years old. Chronic destructive-productive osteomyelitis of the lower jaw on the right: A- the appearance of the child; b- orthopantomogram. Foci of bone tissue destruction are identified in the area of the branch, angle and body of the lower jaw on the right; V - view of the body of the lower jaw on the right at the stage of surgery
Rice. 1.8. Child 13 years old. Chronic productive osteomyelitis of the lower jaw on the right. Disease duration 6 months: A- the appearance of the child; b- overview radiograph 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: orthopane tomogram. Areas of osteosclerosis are noted due to previously repeatedly suffered inflammatory process without signs of sequestration. The cortical plate is not clearly visible. Characteristic marble bone pattern
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 missing tooth 46, a focus of destruction of bone tissue of irregular shape measuring up to 5.5 x 4.5 x 3.5 mm is identified, in the cavity of which additional compaction of bone tissue (bone sequestration) is visualized. The cortical plate of the lower jaw in area 46 is not traced along its entire length. Pronounced linear periosteal layers are noted along the vestibular and lingual surfaces of the lower jaw in the area 45-48
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. Multislice 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 bone tissue destruction ranging in size from 2.5 to 9.8 mm are visualized. On the lingual and vestibular surfaces there are linear and fringed periosteal layers, more pronounced in the area of the body of the lower jaw in the projection of 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. Multislice computed tomograms of a 9-year-old child: A- axial section; b- MPR in coronal 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 clearly altered due to the presence of different-sized foci and foci of rarefaction and osteosclerosis, with uneven, unclear contours, practically not demarcated 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 ratios are not changed. In both TMJs, the relationships are not disturbed, the articular heads are swollen, and in some places the integrity of the contours is compromised. In the left maxillary sinus and cells of the ethmoid labyrinth there is soft tissue content 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: lymph node of reduced echogenicity, thickened cortex; V- Ultrasound, Color Doppler mode: enhancement of the vascular pattern in the projection of the hilum of the lymph node
Rice. 1.15. Ultrasound, color flow mode: the lymph node is round in shape, low echogenicity, heterogeneous structure, along the periphery there is a hypoechoic rim (edema zone). Acute lymphadenitis in the periadenitis stage
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 acute respiratory viral infection: A - appearance; b- Ultrasound, B-mode: the echogenicity of the lymph node is reduced, a fluid area is identified in the projection (abscess area); V- Ultrasound, color dispersion mode: in the projection of the lymph node there is an increase in the vascular pattern, the abscess area is avascular
Rice. 1.20. Abscessing lymphadenitis of the right submandibular region with the development of adenophlegmon. Ultrasound, color flow mode: the capsule of the lymph node is intermittent, fluid areas are detected 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 there are liquid areas
Rice. 1.24. Child 14 years old. Abscess of the lower lip: a, b - the child's appearance; V- Ultrasound, B-mode: formation of reduced echogenicity with the presence of a liquid area 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 area 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 boil of the right zygomatic region
Rice. 1.30. Child 6 years old. Exacerbation of chronic parenchymal left-sided parotitis
Rice. 1.31. Child 13 years old. Exacerbation of chronic left-sided parenchymal parotitis
Rice. 1.32. Chronic left-sided parenchymal parotitis, initial clinical and radiological stage. Orthopantomosialogram of a 9-year-old child
Rice. 1.33. Chronic bilateral parenchymal parotitis, initial clinical and radiological stage. Orthopantomosialogram 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. Orthopantomosialogram of a 15 year old child
Rice. 1.36. Chronic bilateral nonspecific parotitis, remission. Ultrasound, color flow mode: the salivary gland is enlarged in size, decreased echogenicity with the presence of small cysts; vascularization is not changed
Rice. 1.37. Chronic bilateral nonspecific parotitis, exacerbation. Ultrasound, color flow 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 an 11-year-old child (axial projection)
Rice. 1.40. Salivary stone disease of the left submandibular salivary gland. Ultrasound, B-mode: the gland duct is dilated, a calculus is detected in its lumen
Rice. 1.41. Salivary stone disease of the right submandibular salivary gland. Sialogram of an 8-year-old child. The dilation of the duct and a stone at the mouth of the duct are determined
Rice. 1.42. Salivary stone disease of the left submandibular salivary gland. Multislice computed tomogram 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 angle, stones measuring 2.5 and 8.5 mm, with clear wavy contours, and a density of 1826 units are visualized. N
Periostitis of the jaw
One of the fairly common complications of inflammatory processes in periodontal tissues is periostitis of the jaw. Periostitis can occur as a result of further spread of the process during acute apical, as well as during exacerbation of chronic apical periodontitis. In some cases, it may be a consequence of marginal periodontitis or infection of the wound after tooth extraction.
Purulent exudate from the periodontium gets under the periosteum of the jaw. Most often, exudate accumulated in the periodontal fissure passes through small holes in the bone tissue (the system of the so-called Haversian and Volkmann tubules) and the cortical plate and reaches the periosteum. It peels off in a certain area. The inflammatory exudate also affects the outer layer of bone tissue, but bone necrosis, as well as other changes characteristic of the osteomyelitic process, do not occur (Fig. 37).
The disease is accompanied by severe (sometimes throbbing) pain, which is a consequence of peeling and stretching of the periosteum by inflammatory exudate. The pain is severe and can radiate to the temple, eye, ear. As a rule, cold alleviates pain, while heat, on the contrary, intensifies it.
Periostitis is accompanied by changes in the surrounding soft tissues. Swelling of the soft tissues of the cheek, chin, and submandibular region appears, depending on the location of the process. As G. A. Vasiliev notes, when periostitis spreads “from the upper canine and upper premolars, collateral edema, located somewhat to the side, covers a large area of the face. Not only the tissues in the cheek and zygomatic region swell strongly, but there is a transition of swelling to the lower, and often and upper eyelid. The process arising from the upper large molars is characterized by swelling reaching posteriorly almost to the auricle."
Exudate during periostitis can penetrate not only into the vestibular side, but also towards the oral cavity - causing the formation of an abscess (abscess) in the palate or in the area of the bottom of the mouth, and also with an inflammatory process in the upper jaw, it can enter the maxillary cavity and cause sinusitis.
The mucous membrane in the area of the causative tooth is always hyperemic and swollen. The transition fold is smoothed. Palpation of the affected area is painful. Percussion of the tooth causes less pain than with acute periodontitis. With further progression of the process, a fluctuation is noted in the area of edema, then the formation of a fistulous tract in the vestibule or the oral cavity itself. In the worst case, pus penetrates into the soft tissues surrounding the jaw.
The general condition of patients with periostitis worsens. The response to inflammation depends on the prevalence and severity of the process, as well as on the reactivity of the patient’s body. The temperature rises to an average of 37.7-38.2°C. General weakness, insomnia, and loss of appetite appear.
Experience shows that treatment for acute periostitis should be radical and surgical. It is necessary to perform a wide opening of the inflammatory focus and create sufficiently good conditions for the free outflow of exudate. To do this, soft tissues and periosteum are dissected from the side of the oral cavity in the area where the greatest accumulation of pus is observed. As a rule, the intervention is performed under local anesthesia. To prevent the edges of the wound from sticking together and interfering with the outflow of pus, a rubber strip or a strip of iodoform gauze is inserted into the wound.
Patients are prescribed rinsing the mouth with a weak solution of potassium permanganate or soda solution, sulfonamide drugs 1.0 g 4-6 times a day, analgesics for pain, calcium chloride 10% 1 tablespoon 3 times a day. In some cases, it is necessary to resort to intramuscular injections of antibiotics.
In the initial stage of periostitis of the jaw, if the patient’s condition is satisfactory and there is no fluctuation, resorption of the infiltrate can occur without surgical intervention. In these cases, you can resort to physiotherapeutic treatment methods (UHF, Solux, blue light lamp), recommend that patients rinse the mouth with warm disinfectant solutions and prescribe sulfa drugs. Some note a good effect when using a warming ointment dressing according to Dubrovin (4% yellow mercury ointment). If there is no improvement within several days, it is necessary to move on to radical treatment.
During treatment, it is necessary to immediately assess the feasibility of preserving the causative tooth. If a tooth is of no value for chewing function (the crown is destroyed, the root is exposed, tooth mobility is pronounced, etc.), it must be removed. In some cases, timely removal of the causative tooth provides a good drainage of exudate and allows the inflammatory process to be eliminated without additional surgical interventions.
Correctly administered treatment makes it possible to restore the patient's ability to work within 2-4 days. If treatment is carried out incorrectly, the process can spread to the jaw bone, resulting in odontogenic (dental origin) osteomyelitis.
Osteomyelitis of the jaw
This is a disease of the jaw bones, resulting from the penetration of infection from the periodontal lesion into the thickness of the jaw bones. Odontogenic osteomyelitis is a fairly common disease. Approximately 35-55% of all osteomyelitis is osteomyelitis of the jaws, among which odontogenic osteomyelitis takes the main place. With this form of the inflammatory process, the penetration of infection into the bone tissue is associated with dental diseases. Topographically, there is a very close connection between the periodontium and the medullary substance of the jaw. Very often, infection from the apical and, less commonly, from the marginal periodontium penetrates into the bone tissue. Odontogenic osteomyelitis can also occur when the wound becomes infected after tooth extraction. The most common localization of the inflammatory process is the lower jaw, according to M. G. Lukomsky - in 89.6% of cases, and the area of the lower molars is affected in 70%, while the upper jaw accounts for only 10.4% of single-gene osteomyelitis.
As already mentioned, the cause of the development of odontogenic osteomyelitis of the jaw is most often apical periodontitis of the tooth. Patients note that at first one specific tooth hurt, and then the pain becomes widespread and affects a group of teeth in a given jaw. Swelling of the soft tissues of the face appears, and pus, breaking through the bone canaliculi, can cause inflammation of the soft tissues - an abscess or phlegmon.
When examining the oral cavity, there is hyperemia and swelling of the mucous membrane on both sides of the alveolar process in the affected area, which includes the area of several teeth. The teeth are mobile, their percussion is painful. Palpation of the affected area also causes pain, and some thickening of the jaw body is noted. Regional lymph nodes are enlarged and painful.
When inflammation is localized in the area of the molars, especially the lower ones, mouth opening is limited due to the involvement of the masticatory muscles in the process. The general condition of the patients is serious. The temperature rises to 39-39.5°C. Patients complain of headache, insomnia, loss of appetite, and general weakness. Phenomena of general intoxication of the body are noted. The skin and mucous membranes are pale, the pulse is rapid. Eating is difficult due to poor mouth opening and the presence of an inflammatory process. Saliva is viscous. Putrid odor from the mouth. The functioning of the gastrointestinal tract is disrupted.
Red blood cells fall, and the number of leukocytes reaches 2x10³ with a decrease in the number of lymphocytes. ESR reaches high numbers. The specific gravity of urine is high and protein appears in it. The general condition of patients requires their hospitalization and treatment by a dentist, and in his absence, by a surgeon.
A radiograph can help in making a diagnosis no earlier than 2 weeks after the disease.
During this period, disturbances in the bone structure of the jaw and thickening of the periosteum can be noted.
2-3 weeks after the onset of the disease, acute symptoms subside and the process can become chronic. At the same time, the general condition of the patients improves. Painful sensations gradually decrease or disappear completely. The teeth in the affected area continue to remain somewhat mobile, but they may not be painful upon percussion. Hyperemia of the mucous membrane disappears, swelling of the soft tissues of the oral cavity decreases. The discharge of pus continues through the fistulous tract or incision line for a long time. The temperature of patients drops to subfebrile. The phenomena of intoxication of the body are reduced, sleep, appetite, and the functioning of the gastrointestinal tract are restored. Laboratory test data are approaching normal.
The most characteristic feature of the stage of chronic osteomyelitis is the separation of dead areas of bone tissue - sequestration. Depending on the volume and degree of the inflammatory process, both small areas of bone tissue and very large areas of bone can be subject to sequestration.
In some cases of osteomyelitis, rejection of the alveolar process, zygomatic bone, and even a portion of the body of the jaw may occur in the upper jaw. The sequestration process is clearly visible on an x-ray (Fig. 38).
Treatment acute osteomyelitis should be complex and include surgical, drug and physiotherapeutic methods.
In the initial stage, removal of the causative tooth is indicated. This ensures a good outflow of purulent exudate and in most cases eliminates the process. With diffuse osteomyelitis, you cannot limit yourself to tooth extraction. It is necessary to eliminate the main purulent focus in the soft tissues (abscess or phlegmon). Depending on its location, an intraoral or extraoral incision is made. The incision should be wide enough to allow good drainage of pus. To do this, the wound is drained with a rubber strip or a strip of iodoform gauze. The use of iodoform gauze in such cases is not always effective, since it swells, becomes saturated with exudate, and closes the lumen of the wound; at the same time, the outflow of pus stops.
Good results are obtained by applying a wet bandage to the wound with a hypertonic solution of magnesium sulfate or an antiseptic solution. Patients are prescribed sulfonamide drugs up to 1 g every 4 hours intramuscularly, antibiotic injections 4 times a day, autohemotherapy, desensitizing agents, and vitamins. To reduce severe pain, amidopyrine, phenacetin and other painkillers are prescribed orally with the addition of aspirin, caffeine or luminal.
Rp.: Phenacetini
Ac. acetylsalicylici aa.......... 0.25
M. f. pulv. D.t. d. No. 12
S. One powder 3-4 times a day
Rp. Phenobarbitali............. 0.05
Amydopirini............... 0.3
Phenacetini............... 0.25
Coffeini natrio-benzoici........ 0.05
M. f. pulv D. t. d. No. 12
S. 1 powder 1-2 times a day
It is necessary to monitor the condition of the cardiovascular system.
Good nutrition is of great importance. But most patients cannot eat normally due to the inflammatory process in the maxillofacial area. Therefore, food should be high-calorie, fortified and crushed. If necessary (for example, when the jaws are brought together), it can be administered using a special sippy cup.
In the chronic course of the osteomyelitic process, the main point of treatment is the removal of the separated bone sequester. This operation is called sequestrectomy. It is performed when the sequester has completely separated from the surrounding bone tissue, which usually happens 4-5 weeks after the onset of the disease. After removal of the sequester, the wound is sutured, leaving drainage, or tamponed with iodoform gauze, which is changed after 4-5 days. Patients are recommended to be given sulfonamide drugs. To speed up the restoration of bone structure, calcium supplements are prescribed, as well as vitamins C and D. Physiotherapeutic procedures can be recommended: irradiation with a quartz lamp, UHF.
If the causative tooth (or teeth) was not removed in the acute period, then it is advisable to preserve it. In case of chronic osteomyelitis, if there is no mobility of the teeth, you should refrain from removing them. If the pulp of such teeth is dead, then it is necessary to trepan them and fill them, which preserves the teeth for a long time.
Pericoronitis
Inflammatory processes of the jaws also include cases of difficult eruption of wisdom teeth, accompanied by damage to surrounding tissues.
The eruption of both primary and permanent teeth normally proceeds without any complications. The exception is the eruption of wisdom teeth, which in some cases can be difficult. This is most often observed during the eruption of wisdom teeth in the lower jaw and very rarely in the upper jaw.
Difficult eruption of third molars is usually associated with a lack of space in the alveolar process, incorrect position of the tooth, or the presence of a dense mucous membrane that completely or partially covers the crown of the tooth. In these cases, most often the eruption of one or two cusps of the wisdom tooth occurs, after which the position of the tooth no longer changes (Fig. 39). Part of the chewing surface remains covered with a mucous membrane - the so-called hood. Mucus accumulates under the latter, food debris gets in, and oral microbes are introduced. In addition, the mucous membrane covering part of the chewing surface is subject to injury by antagonist teeth when chewing. All these points lead to the occurrence of an inflammatory process that gradually progresses. The edges of the mucosal hood may ulcerate. A chronic, sluggish inflammatory process gradually causes changes in the surrounding tissues. First of all, cicatricial changes in the hood occur, expansion of the periodontal fissure, etc. This leads to the spread of the inflammatory process - pericoronitis, which is accompanied by pronounced clinical symptoms. Patients complain of pain in the area of the causative tooth, often radiating to the ear, and pain when swallowing. Due to inflammatory edema covering the attachment areas of the masticatory muscles, mouth opening is limited. Eating is difficult. Swelling of the soft tissues appears in the area of the angle of the jaw on the corresponding side. The temperature rises to 37.3-38°C.
The mucous membrane in the area of the causative tooth is hyperemic and swollen. Abscesses may occur on the lingual or buccal side. There is pus coming out from under the hood. The slightest pressure on it causes severe pain and increases the release of exudate. Regional lymph nodes are enlarged and painful on palpation.
With further progression of the process, mouth opening is further limited until it is completely impossible to eat solid food. Pain when swallowing increases. Lymphadenitis is increasing. The process can be complicated by phlegmon or spread to bone tissue - osteomyelitis occurs. In cases of pericoronitis, treatment should be radical, although it does not always require surgical intervention.
Depending on the severity of the process and the general condition of the patient, various treatment methods are recommended. For jaw reduction and inflammatory edema, we currently widely use the trigeminsympathetic blockade proposed by M.P. Zhakov, which has proven to be very effective.
After removing acute inflammatory phenomena, it is advisable to determine the position of the tooth using radiography. If the wisdom tooth is in a position that prevents its eruption, it should be removed (Fig. 40). In other cases, it is necessary to rinse the pocket under the hood with a weak solution of chloramine, ethacridine lactate (rivanol) or potassium permanganate. Then a strip of iodoform gauze is carefully inserted under the hood to slightly squeeze it out and release the chewing surface of the crown. Iodoform gauze is changed every other day. Warm disinfectant rinses and sulfonamide preparations 1 g 4-6 times a day are prescribed to the patient at home.
If this treatment does not help, it is necessary to excise the hood covering the chewing surface of the wisdom tooth. It is performed under local infiltration anesthesia. The edges of the wound after excision of the hood can be coagulated. Removal of a wisdom tooth that cannot erupt or is the cause of relapses of pericoronitis is carried out after the acute inflammatory phenomena have subsided. It is carried out using an elevator or you have to resort to gouging with a chisel and hammer, after which the wound is carefully treated. It is advisable to apply stitches.
Abscesses and cellulitis
These inflammatory processes in the maxillofacial area most often accompany osteomyelitis of the jaws and other bones of the facial skeleton, and can also be a complication in the purulent-dystrophic form of periodontal disease, gingivostomatitis, jaw fractures and some other diseases. These are serious and extremely dangerous diseases.
Among the microbial pathogens, various coccal groups were identified (staphylococcus, streptococcus, pneumococcus, diplococcus), fusiform and Escherichia coli, as well as anaerobic forms.
Abscesses and phlegmons have a wide variety of clinical manifestations, which depends both on the general condition of the body, the virulence of the infection, and on the localization of the inflammatory process. The latter usually develops in the subcutaneous, intermuscular and interfascial loose tissue, and can also affect the lymph nodes.
Due to the resulting inflammatory infiltrate and concomitant collateral edema of surrounding tissues, facial asymmetry usually occurs. The natural folds of the face are smoothed out. The skin is tense. With superficially located phlegmon, skin hyperemia is expressed. The mucous membranes of the lips and oral cavity are dry, pale, the tongue is coated. Depending on the nature and clinical course of the inflammatory process, as well as the onset of intoxication of the body, general disorders usually develop to one degree or another. They are expressed in malaise, insomnia, loss of appetite. Patients complain of headaches and frequent chills. The temperature can range from subfebrile to 39-40°C. Pulse and breathing are increased. Externally, the patient's face becomes pale and haggard.
Among local disorders, the most common are chewing disorders associated with inflammatory contracture, pain when swallowing, in some cases speech and breathing disorders, and copious secretion of viscous saliva.
The most severe cases of phlegmon are those caused by anaerobic forms of microbes. With a weak local tissue reaction and reduced body resistance, the prognosis may be questionable.
The blood picture is characteristic of inflammatory processes: the number of red blood cells and hemoglobin decreases, a shift in the leukocyte formula to the left is noted, ESR is increased, in some cases reaching 40 mm per hour.
As A.I. Evdokimov emphasizes, “at the height of the inflammatory process, protein is detected in the urine (a sign of toxic nephritis), therefore a systematic examination of urine is mandatory.”
Treatment. Early opening of the focus of the inflammatory process (phlegmon or abscess) is the main therapeutic surgical measure. It is indicated in the presence of infiltration and elevated temperature. Even in cases where pus is not released, tissue tension is reduced and conditions are created for the outflow of exudate. Surgical intervention should be performed by a dentist or general surgeon, based on the anatomical and topographical features of the affected area. The introduction of antibiotics, especially broad-spectrum antibiotics, as well as sulfonamides, has become widespread. In this case, it is necessary to take into account the resistance of bacteria and their sensitivity to a particular drug.
To reduce pain it is necessary to prescribe painkillers. In case of sluggish inflammation, as well as at the onset of the disease, it is recommended to take UHF therapy, dry heat, and an ointment dressing according to Dubrovin.
It is necessary to pay great attention to the activity of the cardiovascular system. For this purpose, tinctures of valerian, cordiamine, camphor and some other remedies are recommended. Bed rest is mandatory in the acute period of the disease, and patients should be in a semi-sitting position in order to prevent aspiration pneumonia. A dairy-vegetable diet, plenty of fluids, and vitamins are recommended, primarily ascorbic acid and vitamin B1
Surgery is most often performed under local anesthesia, although the use of anesthesia is also possible. The incisions are made wide, up to 8-10 cm long, depending on the localization of the process, to the entire depth of the tissue. In this case, the location of large vessels and nerve branches must be taken into account so as not to damage them. To do this, it is necessary to adhere to the anatomical and topographical requirements for incisions in the maxillofacial area.
If pus is released upon opening, the wound is usually drained with a rubber strip or rubber tube.
In case of putrefactive-necrotic tissue decay, irrigate the wound abundantly with a 3% solution of hydrogen peroxide, a weak solution of potassium permanganate, etc.
For dry tissues, to increase their vital activity and reduce the absorption of toxins, wet gauze dressings moistened with a hypertopic solution of table salt or magnesium sulfate are applied to the wound surface.
In cases where the cause of the inflammatory process in the maxillofacial area is one or another tooth, if access to it is difficult (due to swelling, contracture, etc.), removal can be postponed until the acute phenomena are eliminated. In all other cases, removal of the causative tooth should be carried out simultaneously with the opening of the phlegmon.
Specific inflammatory processes require pathogenetic therapy.
In odontogenic inflammatory diseases, due to the close anatomical connection of the tooth with the jaw, a spread of the infectious-inflammatory process to the bone tissue is always observed to one degree or another. If the area of distribution of this process is limited to the periodontal tissues of one tooth, it is considered as periodontitis. The spread of the infectious-inflammatory process in the jaw beyond the periodontium of one tooth with the involvement of adjacent bone structures leads to the emergence of a qualitatively new condition of osteomyelitis. Although the term “osteomyelitis” is literally translated as inflammation of the bone marrow, in the clinic it is used to refer to an inflammatory process that extends to all elements of the bone as an organ: bone marrow, the main substance of the bone with the contents of the nutrient channels and channels of the osteon system, the periosteum (periosteum).
The infectious-inflammatory process in the perimaxillary tissues can occur as a diffuse purulent inflammation (phlegmon) or as a limited purulent process (abscesses). Cellulitis and abscesses, the development of which is associated with an infectious-inflammatory process in the periodontium of the tooth, are interpreted as odontogenic.
Thus, depending on the extent of bone tissue damage and the prevalence of the infectious-inflammatory process in the perimaxillary soft tissues, the following main forms of odontogenic inflammatory diseases are distinguished:
1) periodontitis;
2) odontogenic osteomyelitis;
3) odontogenic periostitis;
4) odontogenic abscesses and phlegmons;
5) odontogenic lymphadenitis.
Pathogenesis
The term “odontogenic inflammatory diseases” is a collective term. It includes a number of quite clearly clinically defined forms of diseases (periodontitis, periostitis, osteomyelitis, abscess and phlegmon, lymphadenitis, odontogenic sinusitis), which at the same time can be considered as various manifestations of a dynamically occurring odontogenic infectious process.
Attempts to understand the causes and patterns of development of this process and to study the connection between these clinical manifestations have been undertaken for a long time. Much is being done in this direction today.
However, in order to construct a fairly complete and universal theory of the pathogenesis of odontogenic inflammatory diseases, it is necessary to first answer a number of specific questions, the main of which can be formulated as follows:
1. how do weakly pathogenic and non-pathogenic microorganisms, penetrating from the oral cavity into the periodontium and bone tissue, cause the development of a violent infectious-inflammatory process there?
2. what are the mechanisms of exacerbation of chronic odontogenic infection?
3. what are the mechanisms of spread of the odontogenic infectious process?
4.What factors determine the extent of bone tissue damage in odontogenic osteomyelitis?
Mechanisms of allergy in the pathogenesis of odontogenic inflammatory diseases.
Essentially, the answer to the question of how weakly pathogenic and non-pathogenic microorganisms, penetrating from the oral cavity into periodontal tissue and bone tissue, cause a violent infectious-inflammatory process there, was given at the beginning of the 20th century by M. Arthus and G.P. Sakharov. They found that after 4-5 subcutaneous injections of horse serum into rabbits, a violent inflammatory reaction with pronounced alteration occurs at the site of the allowing intradermal injection of the serum. Since the animals were injected with identical serum throughout the experiment, it was concluded that the mechanism of the observed phenomenon was associated with a change in the rabbit’s body’s ability to respond to repeated administration of a foreign protein. Later, this phenomenon was used to reproduce osteomyelitis of long tubular bones in an experiment (Derizhanov S. M.) and osteomyelitis of the lower jaw (Snezhko Ya. M., Vasiliev G. A.).
Currently, the mechanism of the Arthus-Sakharov phenomenon has been studied quite well. According to the classification, it belongs to type III immunopathological reactions. Its essence boils down to the following. Under the influence of whey protein entering the body, which has antigenic properties, antibodies are produced, and this is the basis for sensitization of the body. Against this background, local administration of a resolving dose of antigen is accompanied by the penetration of the latter into the vascular bed, where an antigen-antibody complex is formed. This complex is fixed on the membranes of vascular endothelial cells, thereby turning them into target cells. Neutrophil leukocytes, phagocytosing immune complexes, simultaneously damage the cell membrane, which leads to the release of lysosomal enzymes, mediators of inflammation. This is accompanied by activation of platelet factor 3 and may cause intravascular coagulation, leading to impaired microcirculation and tissue necrosis.
There is reason to believe that the described immunopathological reaction also occurs in the pathogenesis of odontogenic infection. True, in odontogenic inflammatory diseases, antigens of a different nature act than in the experiments of Artus-Sakharov, S. M. Derizhanov and others. The role of antigen in them is the waste products of microbes, the structural elements of the microbial cell, released after its death. This interpretation of one of the links in the pathogenesis of odontogenic infection allows us to understand the reason why in many patients non-pathogenic microbes turn out to be the causative agent of the disease. Apparently, in a sensitized organism, their damaging effect is mediated through the mechanisms of the immunopathological reaction just described (Fig. 1).
As for the sensitization of the macroorganism to staphylococci and streptococci as the most likely causative agents of odontogenic inflammatory diseases, it may precede the occurrence of an odontogenic infectious process, i.e. sensitization occurs under the influence of the same type of microflora of the infectious focus of any other localization.
Rice. 1. Some mechanisms of tissue damage during the development of an odontogenic infectious-inflammatory process.
With the penetration of microbes through a defect in the hard tissues of the tooth into the pulp and especially periodontal tissue, the sensitization of the body increases.
However, it would be wrong to consider the fact of the development of infectious-allergic inflammation at the site of the introduction of microbes into the periodontium as a phenomenon absolutely harmful to the macroorganism. The biological meaning of this reaction is to quickly activate immune mechanisms to localize the infectious focus, prevent the generalization of infection and thereby maintain the constancy of the internal environment of the macroorganism.
A peculiar feature of odontogenic infection is that the patient’s body cannot independently, without appropriate therapeutic measures, stop the entry of microorganisms into the periodontium through the tooth root canal. This means that one cannot count on self-healing and complete elimination of the infectious-inflammatory focus in the periodontium. In the best case, the process stabilizes, resulting in the formation of a chronic focus of odontogenic infection, which is in a state of dynamic equilibrium with the patient’s body.
To introduce the main nosologies of specific diseases (actinomycosis, tuberculosis, syphilis, AIDS (HIV infection)), their clinical manifestations in the maxillofacial region, and to outline the nature and features of the course of specific diseases of the maxillofacial region. PURPOSE OF THE LECTURE:
OBJECTIVES OF THE LECTURE: 1. To introduce the etiology and clinical picture of specific diseases (actinomycosis, tuberculosis, syphilis, AIDS (HIV infection)). 2. To familiarize with the principles of emergency hospitalization of patients with specific diseases (actinomycosis, tuberculosis, syphilis, AIDS (HIV infection)) of the maxillofacial area.
Lecture outline: 1. Etiology and pathogenesis of specific inflammatory diseases of the maxillofacial area. 2. Features of clinical manifestations and modern principles of diagnosis of actinomycosis. 3. Features of clinical manifestations and modern principles of diagnosing tuberculosis. 4. Features of clinical manifestations and modern principles of diagnosing syphilis. 5. Features of clinical manifestations and modern principles of diagnosing AIDS. 6. Principles of medical and surgical methods of treatment of specific inflammatory diseases of the maxillofacial area.
1. deep or muscular form, localized in the thickness of the muscles and intermuscular tissue; 2. subcutaneous form - localized in the subcutaneous base; 3. cutaneous form - involves only the skin. ACTINOMYCOSIS OF THE HEAD AND NECK IS DIVIDED INTO THREE GROUPS DEPENDING ON THE DEPTH OF THE LESION:
1) cutaneous form; 2) musculocutaneous form; 3) musculoskeletal form: a) destructive; b) neoplastic; 4) generalized form, involving the skin, muscles, bone, mucous membrane of the oral cavity K.I. BERDYGAN (1958) CLASSIFIED ACTINAMICOSIS OF THE MAXILLOFACIAL AND CERVICAL AREAS AS FOLLOWS:
CLASSIFICATION, T.G. ROBUSTOVA (1992) Face, Neck, Jaws and oral cavity: Skin; Subcutaneous; Submucosal; Mucous; Odontogenic actinomycosis granuloma; Subcutaneous intermuscular (deep); Actinomycosis of lymph nodes; Actinomycosis of the jaw periosteum; Actinomycosis of the jaws Actinomycosis of the oral cavity organs - tongue, tonsils, salivary glands, maxillary sinus.
Differential diagnosis To learn to distinguish actinomycosis from banal (nonspecific) inflammatory processes - Retromolar periostitis due to difficult eruption of the lower wisdom tooth, Acute and chronic odontogenic osteomyelitis, Odontogenic subcutaneous migrating granuloma, Tuberculosis of the jaw, tongue, lymph nodes, maxillary sinuses, etc.
The following symptoms are characteristic of chronic osteomyelitis of the jaw: Single fistula, the presence of osteoporosis and sequestration or granulations protruding from the fistula; the skin does not have a bluish tint, and the infiltrate does not have a woody density and many fistulas. Sequestrectomy and curettage lead to recovery.
THERAPY FOR ACTINOMYCOSIS OF THE MAXILLOFACIAL AREA AND NECK SHOULD BE COMPREHENSIVE AND INCLUDE: Surgical treatment methods with local effects on the wound process; Impact on specific immunity; Increased overall reactivity of the body; Impact on concomitant purulent infection; Anti-inflammatory, desensitizing, symptomatic therapy, treatment of common concomitant diseases; Physical methods of treatment and exercise therapy.
The tuberculosis bacillus can enter the jaw bones in the following ways: Hematogenous - through blood vessels; Lymphogenic - through lymphatic vessels: Through intracanalicular pathways - through the respiratory and digestive tubes; Continuing - from the mucous membrane of the gums and tongue.
PATHOGENESIS 1. Infection with syphilis occurs sexually: Treponema pallidum enters the mucous membrane or skin, often when their integrity is damaged. 2. Infection can also occur through extrasexual contact: (domestic syphilis) in utero from a mother with syphilis (congenital syphilis).
At the site of penetration, a hard chancre (ulcus durum)-sypholoma is formed: The surface is smooth, the color of raw meat is covered with a serous coating in the center, a grayish-yellow coating is painless on palpation; regional lymphadenitis is noted in the primary period (siphelis primary)
Secondary period – syphilis secundaria. There are various spotted papular or less commonly pustular rashes: (secondary syphilides). Syphilitic tonsillitis is observed. Round-oval papules are observed on the oral mucosa, sometimes with an erosive surface. They can be on any areas: palatine arch, palate, lip, tongue. Regardless of localization. There are specific signs: a) a peculiar pale reddish color, b) lack of inclination to merge (focus); c) absence of subjective sensations; d) polymorphism - true and evolutionary is accompanied by polyadenitis.
Differential diagnosis. 1. Ulcerative form of primary syphiloma on the lip. 2. With gummous lesions in the tertiary period of syphilis, the gums of the oral mucosa have common symptoms with ulcers formed as a result of injury. 3. Gummy glossitis must be differentiated from ulcers on the tongue in tuberculosis, especially milliary tuberculosis. 4. Syphilitic lesions of the periosteum and bone tissue of the jaws should be distinguished from nonspecific and specific lesions of these tissues.
TREATMENT Treatment of syphilis is carried out in a specialized venereology hospital or dispensary.
After HIV infection, AIDS develops in the first 5 years: in 20% of infected persons, within 10 years in approximately 50%. In people infected with HIV, the pathogen is found in various biological fluids: blood, sperm, vaginal secretions, breast milk, saliva, tear fluid, sweat, AIDS
1. Various clinical forms of candidiasis. 2. Viral infections. 3. Hairy (villous) leukoplakia. 4. Ulcerative necrotizing gingivostomatitis. 5. Progressive form of periodontitis (HIV periodontitis). 6. Kaposi's sarcoma. Diseases of the oral mucosa associated with HIV infection include:
Symptoms of HIV infection in the oral cavity (London, 1992) Group 1 - lesions clearly associated with HIV infection. This group includes the following nosological forms: - candidiasis (erythematous, pseudomembranous, hyperplastic); - hairy leukoplakia; - marginal gingivitis; - ulcerative necrotizing gingivitis; - destructive periodontitis; - Kaposi's sarcoma; - Non-Hodgkin's lymphoma. Group 2 - lesions less clearly associated with HIV infection: - bacterial infections; - diseases of the salivary glands; - viral infections; - thrombocytopenic purpura. Group 3 - lesions that may occur with HIV infection, but are not associated with it.
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Inflammatory diseases of the maxillofacial region, and in particular, severe forms of odontogenic inflammatory processes are periodontitis, periostitis, osteomyelitis of the jaws and phlegmon of the surrounding soft tissues. For questions of their etiology and pathogenesis, see the textbook: Therapeutic Dentistry. Ed. E.V. Borovsky. – M.: Medicine, 1989 and Surgical dentistry. Ed. T.G.Robustova. – M.: Medicine, 1990.
Features of the occurrence and course of inflammatory reactions in the tissues of the oral cavity:
Inflammatory processes in the maxillofacial region are characterized by granulomatous inflammation, which is characterized by a limited focus of productive, productive-exudative inflammation, and the formation of limited infiltrates. This inflammation is based on primary growths of granulation tissue infiltrated with polynuclear cells, lymphocytes, and plasma cells in various proportions. An example of such inflammation is dental granuloma - a tumor-like formation near the apex of the tooth made of granulation tissue, surrounded by a fibrous capsule, resulting from chronic inflammation during infection of the periodontium from the tooth canal. In cases of development of inflammatory processes in the maxillofacial area, it is necessary to remember the characteristics of the venous system. The absence of a valve system in the veins of the face makes it possible for a thrombus to rapidly migrate in an ascending direction and cause thrombosis of the peritoneal sinus with an extremely life-threatening prognosis for patients.
Features of changes in the white blood system and hemostasis disorders during inflammatory processes in the tissues of the oral cavity.
Comparative studies of capillary blood of the gums and fingers in people suffering from inflammatory processes in the maxillofacial area (gingivitis, periodontal disease, etc.) revealed statistically significant changes in the composition of leukocytes. These changes concern the absolute number of eosinophils, neutrophils, lymphocytes and monocytes, as well as the total number of leukocytes. In the capillary blood of the gums, the number of phagocytes (eosinophils, neutrophils and monocytes) is significantly lower and the number of immunocompetent cells (lymphocytes) increases. A decrease in the phagocytic activity of neutrophils was revealed (especially in periodontal disease). Since phagocytes are one of the main factors of nonspecific immunity, a decrease in their total number in the gums during inflammatory processes of the oral cavity suggests that these processes develop against the background of a decrease in the body’s nonspecific immune response.
Features of hemostasis in pathology of the oral cavity are determined by the presence in the saliva of the oral fluid of plasma components of the coagulation, fibrinolytic and kallikrein-kinin systems, their various quantitative and qualitative disorders, and changes in their combination.
In chronic inflammatory processes of the oral cavity, with periodontal disease, the content of proteinase inhibitors in the oral fluid decreases, the activity of the proteolytic enzyme system increases, which leads to an increase in the activity of plasmin, thrombin, kallikrein, blood coagulation factors and is manifested by activation of the coagulation, fibrinolytic and kallikreinin systems. Such hemostasis disorders serve as the basis for pathological processes that clinically manifest themselves in the form of blood vessel thrombosis. The absence of a valve system in the veins of the face makes it possible for a blood clot to migrate rapidly in an upward direction. The intimate connection of the venous formations of the maxillofacial region with the pterygoid plexus, and the latter through the middle veins of the dura mater with the cavernous sinus of the dura mater, with the development of thrombosis, can cause a severe complication in the form of thrombosis of the cavernous sinus with an extremely life-threatening prognosis. Therefore, these features of hemostasis in oral pathology must be taken into account when analyzing the patient’s condition and developing doctor’s tactics in cases of the development of inflammatory and other processes in the maxillofacial area.
The role of local hypoxia in the pathogenesis of inflammatory and dystrophic lesions of tissues of the maxillofacial region.
In the development of inflammatory and dystrophic lesions of the tissues of the maxillofacial area (gingivitis, inflammatory-dystrophic form of periodontal disease, etc.), the most pronounced changes occur in the capillary, precapillary and arterial parts of the microcirculatory bed, which leads to hypoxia, metabolic disorders and dystrophic changes in the pulp and periodontium. Against the background of dystrophic tissue damage (periodontal tissue) during chronic hypoxia, regenerative processes sharply decrease. Inhibition of proliferative processes is caused by insufficient energy supply to tissues and is associated with excessive formation of glucocorticoids, which suppress proliferation processes and lengthen all phases of the cell cycle.
In clinical and, in particular, dental practice, for diseases of the oral mucosa and periodontal disease, treatment with oxygen under high pressure is recommended - 3 atm. (hyperbaric oxygenation). The therapeutic effect of hyperbaric oxygenation is based on an increase in the partial pressure of oxygen in body fluids (plasma, lymph, interstitial fluid). This leads to a corresponding increase in their oxygen capacity (by 6.5%) and is accompanied by an increase in the diffusion of oxygen in the hypoxic area of tissues, which helps to normalize the arteriovenous difference in oxygen, i.e. oxygen consumption by the body at rest.
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