1. Sharp and chronic odontogenic sinusitis of upperjawal sinus
Sharp and chronic odontogenic sinusitis of upperjawal sinus. Arthritis and arthrosis of tympano-maxillar joint. Sharp and chronic syaloadenitis.

2. Osteomyelitis - is the simultaneous ignition of all components of the bone: the jaw bone marrow, compact and spongy bone substance and around soft tissue allergic infectious origin.

3. By etiology osteomyelitis is divided into: - Infectious      a) nonspecific (caused by pus germs)      b) specific (tuberculosis, syphilitic, etc.). - Non-contagious

4. Depending how infection penetrate inside the bone : - Odontogenic osteomyelitis - Not odontogenic osteomyelitis      a) hematogenous osteomyelitis      b) post-traumatic osteomyelitis     c ) gunshot osteomyelitis      d) contact osteomyelitis

5. THEORY OF osteomyelitis 1. Vascular theory of Bobrov (1888)
THEORY OF osteomyelitis   1. Vascular theory of Bobrov (1888). Bobrov considered the main factor that determines the possibility of the formation of infections in the bone, it is specific blood system and slow blood flow in the capillaries.

6. Thromboembolic theory of Leksera (1894)
Thromboembolic theory of Leksera (1894). The basis of this theory is the situation when the small blood vessels are block by the embolus, which is presented ,as believed Lekser, by staphylococcal crumple.      Vilnius (1934), based on the concept of Leksera tried to better illuminate the pathogenesis of osteomyelitis, Further thrombosis distributed in the vascular system. This process he called progressive thrombosis. As a result, it appears violations of blood circulation, and further some point of necrosis.      

7. Hypersensitivity theory ZM Deryzhanova (1937 - 1940 years)
Hypersensitivity theory ZM Deryzhanova ( years).    The basis of this theory was put by factors of sensitization of the organism. Deryzhanov think that in the pathogenesis of osteomyelitis : factors of vascular thrombosis and embolism of bone don’t play role . Acute infective osteomyelitis develops only in the sensitized organism. great importance to this organism is present of dormant infection and non-specific stimulus (injury, hypothermia, etc.).. The form of osteomyelitis depends not only from the nature of the causative agent. But big role play the reactivity of the organism.

8. Neurological theory.        Leading position in this theory is the vascular spasm. In result we have violations of the normal blood circulation and trophic tissue. Specified spasm it is resulting from the action on the body excessively strong stimuli,(trauma, hypothermia, etc..).    Pathogenesis of acute hematogenous osteomyelitis it is very complicated. This process can be seen only in a complex of many factors. these theories complement each other

9. Hematogenous osteomyelitis

10. Hematogenous osteomyelitis usually occurs in children and adolescent males, 90%.It is Result from the ingress of infection from other plays of body. From the primary focus of infections (furuncles, carbuncles, phlegmons, abscess, carious teeth, erysipelas, infected wounds, tonsillitis, chronic inflammation of the nasal sinus and ears, etc..) Bacterial embolus fall in bone marrow and cause inflammation. Typically it is caused by staphylococcal flora (60-80%) in second place streptococcal (5-30%), Gram-negative bacteria ,anaerobes, mixed flora (10-15%). The course of osteomyelitis depends on several factors: the localization of process, the virulence of the microorganism, immunological properties of the body. From Clinical course , osteomyelitis divide on the next form toxic sepsis local The disease usually begins with acute fever, deterioration of general condition. Severe complication of infection is metastasis to other bones, organs, development of sepsis. X-ray signs of osteomyelitis demonstrated on th day after beginning of inflammation

11. Acute hematogenous osteomyelitis: In the first 1-2 days the patient emphasizes the general malaise ,muscle pain, headaches. Then there fever with persistent rise in temperature to 39 ° C and above, weakness, sometimes vomiting. Overall condition is difficult, clouded consciousness, there is delirium, symptoms of irritation of brain membranes, and sometimes seizures. Appetite disappears, furred tongue, dry. Face becomes pale, the eyes sink, lips and mucous membranes change in color, dry skin,. Arterial pressure decreased, heart tone deaf, frequent pulse, weak content, and usually corresponds to the temperature. Breathing rapid, shallow. In the lungs sometimes showing symptoms of pneumonia. Liver and spleen enlarged, painful to palpation. Sometimes the painful region of the kidneys, urine little protein in the urine and cylinders. In 1-2 days the disease appears strictly localized pain in the affected bone. pain is sharp, boring . Due to the deep location of the fire are important methodical palpation.

12. Hematogenous osteomyelitis

13. Post traumatic osteomyelitis (acute stage )

14. Post traumatic osteomyelitis (chronic stage )

15. Osteomyelitis after treatment

16. Chronic hematogenous osteomyelitis: The reason for conversion of acute osteomyelitis in chronic, it is necrosis of the infected area of spongy or compact part of the bone . Sequestration, which formed , it is one of the main substrate , what supporting reactive inflammation of the surrounding bone tissue. (injury, hypothermia, general illness, etc.)..

17. treatment is antibacterial, detoxification, desensitizing, and correction of metabolic disorders   From detoxification to be appointed 10% glucose with insulin ,hemodez, to desensitizing- preparations calcium Dimedrol, suprastyn, pipolfen, to enhance specific immunity - staphylococcal plasma, After calming down of the acute process is active staphylococcal toxoid immunization. Often assigned a direct blood transfusion. Antibacterial therapy is the complete normalization temperature curve of blood and elimination of local

18. Contact osteomyelitis occurs as a result of direct contact between infectious fireplace and bone occurs close contact. For example, furuncles, carbuncles, prolonged inflammation of the gums, extensive purulent wounds scalp and others. The disease is characterized by relatively long-term existence of purulent process. Total body temperature of patients often remains normal. Leucocytosis and raised ESR occur in some patients. Radiographic changes are similar to those in chronic hematogenous osteomyelitis.

19. The clinical course of gunshot osteomyelitis of the jaws diversity differs and depends on patient age, localization and stage of the process of morphological changes in bone tissue and other reasons. The course of gunshot osteomyelitis of the maxilla are more benign than the bottom (due to the anatomical structure of the jaws). In acute osteomyelitis of firearms in blood marked

20. Gun shot osteomyelitis

21. Treatment of gunshot osteomyelitis of the jaws depends on the stage of the process and is surgical intervention (abscess or sekvestrektomiya sections, depending on the timing of its implementation, carefully remove the altered tissue, etc.), antibacterial therapy (depending on the sensitivity of the causative agent), naychastishesche cephalosporin use II-III generation, gentamicin, amikacin, metrohil, at least - vancomycin, tienam, detoxification and general health treatment, immuno-and physiotherapy. Patients spend correction fluid and electrolyte balance and acid-base status, heparin, vitamins and oksyhenobaroterapiyu, entered reparanty.  The best time for surgical intervention in osteomyelitis of firearms is a period in the course of wound process in which gunshot wound in one hand, there is the awakening of the maximum regenerative ability of tissues, and another - is more or less clear separation sequestration. This period typically corresponds to 6-8 weeks after injury, these terms are most suitable for holding sekvestrektomiyi.

22. Complication of osteomyelitis