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

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Sharp and chronic odontogenic sinusitis of
upperjawal sinus. Arthritis and arthrosis of
tympano-maxillar joint. Sharp and chronic
syaloadenitis.
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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.
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By etiology osteomyelitis is divided into-
Infectious     a) nonspecific (caused by pus
germs)     b) specific (tuberculosis,
syphilitic, etc.).- Non-contagious
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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
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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.
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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.      
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Hypersensitivity theory ZM Deryzhanova (1937 -
1940 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 dont
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.
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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
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Hematogenous osteomyelitis
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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
formtoxicsepsislocal 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 10-12-th day after beginning of
inflammation
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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.
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Hematogenous osteomyelitis
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Post traumatic osteomyelitis (acute stage )
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Post traumatic osteomyelitis (chronic stage )
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Osteomyelitis after treatment
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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.)..
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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
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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.
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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
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Gun shot osteomyelitis
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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.
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Complication of osteomyelitis