GENERAL CHARACTERISTIC FEATURES OF INFLAMMATION OF TISSUES SCHLD IN CHILDREN. ACUTE AND CHRONIC PERIOSTITIS. ACUTE AND CHRONIC OSTEOMYELITIS OF THE FACIAL BONES. CLASSIFICATION, ETIOLOGY, PATHOGENESIS, CLINICAL FORMS OF THE DISEASE. PATTERNS MANIFESTATIONS IN CHILDREN OF ALL AGES. DIAGNOSIS, DIFFERENTIAL DIAGNOSIS, TREATMENT, COMPLICATIONS AND THEIR PREVENTION.INFLAMMATORY ODONTOGENIC CYSTS OF THE JAWS OF TEMPORARY AND PERMANENT TEETH.

Acute inflammatory processes belong to the category of diseases in which mostly shows therapeutic intervention in the early hours of addressing patients for medical care, ie diseases that require immediate surgery.

Such diseases include acute odontogenic inflammatory maxillofacial area: abscess, osteomyelitis, abscesses, cellulitis, and lymphadenitis, which is a consequence of pathological processes that develop in the mouth, and so on. (Table 1).

             Keep in mind that the efficiency of the physician in these diseases is needed quality because often only immediately conducted surgery can prevent serious complications and relieve the patient from suffering.

Given the proximity of the brain, anatomically-topographic features that contribute to the rapid spread of the inflammatory process, as well as massive vascularity, which causes active inflammation and absorption of food intoxication, meaning immediate surgery can not be overemphasized.

It is likely that doctors in any specialty should have a basic knowledge for establishing the correct diagnosis and an immediate intervention for acute purulent diseases of maxillofacial area.

Among the inflammatory diseases of the maxillofacial area and neck most common odontogenic processes.

Acute Periodontitis

Etiology and pathogenesis

Acute periodontitis may be acute primary or secondary, is a consequence of worsening of existing chronic periodontitis.

Periodontitis are infectious and nein-fektsiyni that arise from the chemical (during dental treatment) or mechanical (blow, bruise, fall, etc.). Periodontal injury.
Most emerging infectious periodontitis.

The source of infection matched enters the periodontal is usually numb the tooth pulp. With a root canal tooth germs get into periodontal through apical opening of the root. This contributes to pressure food during chewing: putrid contents of the channel while moving, "utrambovuyetsya" and enters the periodontium. Infection comes from channel Periodontal and during medical manipulations in the treatment of "gangrenous" or pulpitnyh teeth. Because promotion infection top emerging so-called apical (apical) periodontitis.

Recently, there are toxic pulpit as a consequence use photopolymers

kariyesnyh filling cavities and wedge cervical defects of teeth. These "fotopolimerpulpity" later complicated by toxic periodontitis.

The second way of infection in periodontal - gum over the edge, that is the bottom gingival groove, resulting in developing so-called marginal (marginal) periodontitis matched captures the part of the periodontium, which is adjacent to the neck of the tooth.

The third way of infection in Periodontal - hematogenous and lymphogenous (during flu, sore throat, fever and other infectious diseases).

The fourth way - consistent distribution, which happens when hinhivostomatytah, osteomyelitis, inflammation of the maxillary sinus, ne-rykoronitah.

Osteomiyelitychni periodontitis occur simultaneously in several intact teeth (at Odon-tohennomu or neodontohennomu osteomyelitis of the jaws).

Among neinfektsiyyyh periodontitis distinguished:

1) those arising from chemical injury periodontal (there are in treating tooth roots formalin, aqua regia, arsenic trioxide and other toxic and caustic substances);

2) traumatic periodontitis, emerging from both acute (one-stage) or injury-hit during rozkushuvannya nuts, sugar or ankles, use millerivskoyu needle, and with chronic injury (permanent overload tooth prosthesis, peeling seeds, holding nails or other objects between teeth).

Depending on the clinical course, the extent of the prevalence and nature of pathological changes 1. G. Lukomski distinguishes three forms of periodontitis:

I. Acute (exudative) periodontitis:

a) serous (limited and diffuse);

b) septic (limited and diffuse).

II. Chronic (proliferative) periodontitis:

a) fibrous;

b) granulating;

c) granulomatous.

III. Exacerbations of chronic periodontitis.

A. 1. Evdokimov distinguishes among chronic periodontitis these, combined with hipertsemen-tozom.

Hospital acute serous periodontitis

Characteristic blurred spontaneous pain that increases with pressure on the tooth and the use of hot food or water. The patient feels as if a tooth "grown up" or moved from the tooth socket. The pain is not radiating, so the patient can accurately show struck tooth. Although during chewing and pain increases, but if the patient somknite teeth and keep some time locked jaw, the pain gradually subsides almost completely or significantly reduced.

OBJECTIVE: usually no signs of swelling of the mucous membrane of the gums and periosteum is not visible, static tooth is not broken. Regional lymph nodes (pidboridni or submandibular) slightly enlarged and slightly painful. Percussion tooth accompanied by acute pain.

Pathological Anatomy. Redness and thickening of the periodontal tooth root apex (macroscopically): microscopically - redness, swelling and slight leukocytic infiltration apical perytssmentu.

Treatment of serous periodontitis at an early stage of the disease may be conservative (if the tooth is value in functional and cosmetic regard). Unfortunately, the sick, of course, go to the doctor when the stage serous inflammation is gone and there is purulent inflammation of periodontium. Often acute purulent peryudontyt is a consequence not of serous periodontitis, and purulent pulpitis.

Hospital acute suppurative periodontitis

Complaints of patients with sharp constant pain that radiates to the ear, temple, eye - over the course of the branches of the trigeminal nerve, patients say that the pain slightly reduced from the effects of cold and aggravated by heat. Serried teeth impossible for tooth sharply reacts to the slightest touch antagonist and even the tongue. Lips are not fully merge. The patient can not sleep because supine pain intensified.

OBJECTIVE: countenance distressing, restless (fear to touch the tooth). Around the patient's tooth gums swollen and slightly hyperemic alveolar increase smoothed, navkoloshelepni tissue normal or slightly swollen.

Regional lymph nodes are enlarged and painful on palpation. Vertical percussion of the tooth, which make it very gently, causing excruciating pain. Horizontal percussion also causes sharp pain reaction. Causal tooth usually "gangrenous" loose and lively.

In the blood, sometimes there is a slight leukocytosis with an increase in the number of segment-nuclear and young neutrophils, erythrocyte sedimentation rate accelerated slightly (up to 20-30 mm in 1 h). Maximum resistance of erythrocytes increased and the minimum - remains the norm (0.36).

Body temperature is usually not increased, but sometimes there are low-grade. The degree of changes in body temperature and blood depends on the individual condition of the patient reactivity.

In primary acute periodontitis significant changes on radiographs is not observed. In the case of the development of acute process (due to exacerbation of chronic periodontitis) shows similar to flame or rounded thinning of bone tissue.

Pathological Anatomy. In periodontal leukocyte infiltration, mainly due to the large kilkosh. lymphocytes, there are small pockets of pus, which gradually merge, destroying and vidsharovuyuchy perytsement from the root. In bone hole-reactive dystrophic changes. In the walls of the hole, preferably I Lyantse its bottom, bone reconstructed: resolves it appears a number of gaps filled osteoclast, we, expanding holes in the bone, through which the Paris-DonNTU combined with bone marrow, bone marrow is pulling some holes * Normally separated from periodontal bone. In the bone marrow - swelling and infiltration leykotsytamh sometimes diffuse purulent infiltration of certain bone marrow spaces.

It should be noted that necrosis Bone "Mr. Brain" tissue not ^ vschouyshltish: Because purulent infiltration of cells in the absence of bone, can not be regarded as a "classic" manifestation osteomiyelitychnoho process (by G. Vasilyev, 1956).

Thus, clinical and histological data provide a basis for the acute purulent peri-dontyt a separate nosological form and do not consider it an initial phase of osteomyelitis.

Microflora in Periodontitis usually mixed, characterized by content Root canal tooth - purulent and putrefactive microbes. However, according to FI Ishanhodzhayevoyi (1965), possible dominance monomikrobnoyi flora, including streptococci.

Treatment

The task of the doctor is to first reduce and then eliminate pain, eliminate inflammation, prevent the spread of purulent process in the adjacent tissue. All therapeutic measures are divided into local and general. To address these three tasks should provide vidtikannya purulent exudate from periodontal. This should first resolve the issue of functional value "causal" tooth (which is usually a large defect) and the feasibility of its preservation.

There are several ways through which you can provide with periodontal vidtikannya manure. If the tooth is not destroyed and saving it is desirable and necessary, open the pulp chamber, clean and extend the root canal, after which the cavity drop out manure. This pain immediately begins to subside, reduced severity of inflammatory process. If the tooth is sealed to ensure vidtikannya manure a little harder, but possible good anesthesia. The doctor must firmly hold tooth fingers that it will not move during manipulation.

Ineffectiveness of conservative therapy may be caused by obstruction of channels (their obliteration), the presence of channel-pulpoekst raktora or boron, curved roots, as well as a decrease in protective immunological properties of the organism. In the absence of a vidtikannya purulent exudate through the canal and pulp chamber doctor has to find another way for drainage periodontium. In such cases, or when. Despite the ongoing drainage canal, acute effects are increasing, making the cut in the transitional crease roztynayuchy mucosa and periosteum, in 1-2 days you can try again to create a channel patency. Sometimes combined vidtikannya pus through the tooth and root canal through an incision in the crease of the transition.

If the tooth is significantly damaged and is not an anatomical and functional value for the prosthesis, and attempts to save him were unsuccessful, the tooth is removed, then the hole for 24-28 minutes drain narrow rubber or gauze strip.

Questions about tooth extraction in acute inflammation of the periodontium and jaws long comprehensively discussed in domestic and foreign literature. The fact that an isolated tooth is not always quickly leads to the elimination of inflammation. Moreover, sometimes when the patient agrees to remove long tooth (or his doctor does not offer this operation), and then still removes tooth, then, in spite of this, the inflammatory process may progress: vidtikannya provided as inflammation increases, because the body already unable to cope with infection and intoxication.

In this situation, patients tend to associate the deterioration of his condition with the removal of the tooth.

As the observations of several authors, the earlier the beginning of acute periodontitis tooth is removed, the terms are shorter elimination of inflammation and the easier it is to prevent the spread of acute suppurative process in adjacent bone and soft tissue. Hence the conclusion: if the doctor is no certainty in the possibility and necessity of conservative therapy must remove tooth earliest.

However, one should bear in mind that even early (in the 1-day illness) tooth is not always prevents inflammation in the periosteum, bone, soft tissue around them, especially in those patients who have periodontitis often exacerbated and contributed to the development of in the body of sensitization and training ground for hyperergic course of inflammation.

For this reason it is desirable in the scheme sedation before removing a tooth or before the opening of the crease in the transition include gums, sybilizuvalni drugs can reduce the degree hyperergic response to injury, which has a doctor. This intervention should be to give the patient any antihistamine (pipolfen, suprastin, diphenhydramine, diazolin etc.).

If the tooth has a functional value that is anatomically quite full, you can delete it, and then, after subsiding acute effects of inflammation, replantuvaty.

In case of refusal of tooth extraction should invite him to make the cut in the transitional crease and hold general therapeutic measures (antibiotics, sulfanilamide

drugs, etc.), assign UHF-therapy sessions 10.18), electrophoresis of potassium iodide to the area of inflammation.

General therapeutic measures after tooth extraction or cut on the crease transition are as follows: after securing vidtikannya manure prescribed bacteriostatic drugs, sulfonamides (sulhin, streptotsid 0,5-1 g 3-4 times a day), combining them with antibiotics. Simultaneously used analgesics-Amidopyrine, fenatsytyn, acetylsalicylic acid (in 0,25-0 ^ 5 g 3 times a day), combining these tools with caffeine (0.3 g) *. 2-3 days after cutting the boil to apply heat (blue light, sollux - 15 minutes every 2-3 hours), diadynamic (currents Bernard), UHF and others.

Results and complications

If treatment was correct and timely, comes complete elimination of inflammation, but if the treatment is not performed, purulent exudate, without affecting significantly the bone, periodontal penetrate directly into the periosteum (via lymphatic vessels and advanced breakthrough and haver-Owl channels), causing acute purulent periostitis of the jaw.

Purulent exudate, hitting a bone, can cause limited or diffuse osteomyelitis, and in adjacent navkolosche-lepnyh soft tissues and lymph nodes, cellulitis, abscesses, lymphadenitis. However, most manure flowing through the gingival pocket or fistula, and then acute periodontitis becomes chronic, combined with chronic lymphadenitis. If the treatment is carried out correctly or are ineffective, they can develop the same complications (abscess or osteomyelitis of the jaw, abscess, lymphadenitis, chronic periodontitis). Perhaps a combination of all or some of these processes, the transition to another one complications.
Chronic periodontitis

Etiology and pathogenesis

Certainly chronic periodontitis due to continuous and prolonged infection periodontal microflora of the root canal tooth. Sometimes chronic periodontitis is the result of acute periodontitis. Pathogens are streptococci, staphylococci, sometimes - Various mixed flora.

Lethargy, gradual increase of chronic periodontitis due to the presence of local mesenchymal protective mechanisms in periodontal and mobilization of all protective devices against micro organism, which gradually penetrates into it.

The clinical course and nature of pathological changes in lohoanatomichnyh navkoloverhivkovyh tissues of chronic periodontitis may be divided into stable (fibrotic, granulomatosis-tion) and the active flow (granulating, pointed granulomatous) forms. Thus, the presence of chronic inflammation of complete cells indicates a stabilization process, and their disappearance - his aggravation.

Chronic fibrotic periodontitis may occur as a result of feedback granulating or granulomatous (mostly), periodontitis or as the first form of chronic periodontitis.

Clinic

Certainly no complaints, only in case of aggravation, pain during chewing and percussion (in the vertical direction).

X-ray determined advanced periodontal gap, especially in the apical part; outlines perytsementu - unequal matched tumor caused by cement (so-called hipertsementozom). Bone wall peri-dontalnoyi slit thickened, sklerozovana and gives denser and wider than normal, shadow.

Pathological Anatomy. Macroscopically perytse-ment thickened or navkoloverhivkoviy part or the entire length of the color thickened parts - white, microscopically - bundles grubovoloknistye connective tissue between the beams sometimes placed kruhloklitynnyh cell infiltrates.

Treatment

If the tooth is not treated conservatively and does not represent value for the prosthesis, it is removed and the hole carefully vyshkribayut kyuretazhnoyu small spoon. If the tooth is not destroyed, but can not be treated conservatively, it replantuyut acc known procedures.

Chronic granulating periodontitis

The most active form of chronic periodok-Titus.

Clinic

Complaints of patients: pain during pryymank * solid or hot food on the gums is usually a fistula (long), which is periodically opened and closed **-vayetsya. Before vidkrytttyam fistula pain exacerbated deteriorating health. However: the presence of the fistula is not required. Sometimes zovesh no complaints of pain. The patient only Note ^ ': weak redness (hyperemia) gums and their Dialled

Chronic periodontitis

Etiology and pathogenesis

Certainly chronic periodontitis due to continuous and prolonged infection periodontal microflora of the root canal tooth. Sometimes chronic periodontitis is the result of acute periodontitis. Pathogens are streptococci, staphylococci, sometimes - Various mixed flora.

Lethargy, gradual increase of chronic periodontitis due to the presence of local mesenchymal protective mechanisms in periodontal and mobilization of all protective devices against micro organism, which gradually penetrates into it.

The clinical course "and the nature of the pathological changes in lohoanatomichnyh navkoloverhivkovyi tissues of chronic periodontitis may be divided into stable (fibrotic, granulomatosis-tion) and the active flow (granulating, pointed granulomatous) forms. Thus, the presence of chronic inflammation of complete cells indicates stabilization process, and their disappearance - his aggravation.

Chronic fibrotic periodontitis may occur as a result of feedback granulating or granulomatous (often periodontitis or as the first form hronichnoh: periodontitis.

Clinic

Certainly no complaints, only in case of aggravation, pain during chewing and pr * percussion (in the vertical direction).

X-ray defined extensions periodontal gap, especially at the top;-hand side; perytsementu shape - rough, Sw due to tumor cement (so-zvyi him hipertsementozom). Bone wall perk-dontalnoyi slit thickened, sklerozovan enables denser and wider than normal, shadow.

Pathological Anatomy. Macroscopically featherbeds cop thickened or navkoloverhivkoviy his chi sity matrix, or the entire length of the color thickened h sity matrix - white, microscopically - bundles hrubovolok stand connective tissue between the beams sometimes pc> mishuyutsya kruhloklitynnyh cell infiltrate. "

Treatment

If the tooth is not treated conservatively and does not represent value for protezuye ^-tion, it is removed and the hole carefully vyshkry-bayut kyuretazhnoyu small spoon. I have a tooth that is not destroyed, but can not be treated conservatively, it replantuyut also known procedures.

Chronic granulating periodontitis

The most active form of chronic period Titus.

Clinic

Complaints of patients: pain during adoptee "solid or hot food on the gums is usually a fistula (long), which periodically opens and closes. Before vidkrytttyam fistula pain exacerbated deteriorating health. Av fistula presence is not required. Sometimes zova no complaints of pain. Patient notes only faint redness (hyperemia) and gum swelling.

OBJECTIVE: usually broken tooth, "gangrenous" percussion has a weak pain hipereminovani gums, swollen, pressing tool is long depression (dimple). Often seen on the gums fistula with protrusion of granulation, it can be localized and the face, chin, near the edge of the mandible or the inner corner of the eye, in the zygomatic region, the neck.

Root canal moist, with traces of blood due to germination had granulation.

The X-ray visible nekonturovana, uneven strip thinning of bone around the tooth.
Pathological Anatomy. Evidently overgrowth of granulation outside periodontium, this caused lobular, polum'yapodibna resorption cortical substance wall socket tooth that appears on the radiograph. Among granulation - accumulation of leukocytes and histiocytes, a small number of plasma cells, resorption of cement and dentin of the root, along with proliferative phenomena is clearly identified and exudation, especially during exacerbations that are associated with closing the fistula or weakening immunity (due with a history of flu, sore throat, general cooling, overwork or nutrition, injury, etc.).

Pathological, microbiologically and clinically granulating periodontitis should be regarded as most typical and most formidable cell odontogenic infection. In this cell in the body receives food poisoning, causing him sensitization.
Residual granuloma of filling material in the area of the removed tooth 46.
Treatment

Conservative treatment is successful only good patency of roots and their possible obturation filling material, then comes fybrotyzatsyya, scarring, ie clinical recovery.

Surgical treatment is indicated in case of obliteration of the roots, and after ineffective conservative treatment. One of the following surgical treatment:

1) tooth extraction and curettage of granulation with small holes kyuretazhnoyu spoon;

2) if the tooth is sufficiently complete, until Zana replantation (see below);

3) if granulation formed in migratory subcutaneous granuloma, you should remove it; transition to the crease to cut cord, and the "causal" tooth remove or hold it replantation.

Chronic granulomatous periodontitis

If chronic granulating periodontitis can not be cured completely, it can become hidden, torpid and asymptomatic pe-

Chronic granulomatous periodontitis
If chronic granulating periodontitis can not be cured completely, it can become hidden, torpid and asymptomatic. Around the diseased granulations gradually grows fibrous, connective tissue capsule. This process of gradual coverage, a kind of "taming", "blocking" granulation IG Lukomski called granulomatous process that eventually ends basal formation of dental granulomas.

Clinic

Complaints usually does not happen, because the phenomenon of exudation hardly expressed.

The X-ray shows roundish shape dilution with equal, sharp edges, size - from millet seed to a small pea.

Pathological Anatomy

Macroscopically: on top of the removed tooth root "hanging" round growths, the color of it - from light yellow to dark red, it is - granuloma closely associated with the root and is therefore usually removed with it.

Microscopically 1.1. Davydenko (1966) distinguishes between three types of granules:
1. Simple granuloma:
a) simple cell;
b) simple fibrotyzyvni;
c) simple cystic.
2. Epithelial granuloma:
a) epithelial cell;

b) epithelial fibrotyzyvni.

3. Epithelial cystic granuloma:

a) nefibrotyzyvni;

b) fibrotyzyvni.

Epithelial cavity in granuloma subsequently merged, filled with inflammatory exudate and fatty detritus, forming first kistohranulomu, and then - cyst. Increasing in size, granuloma leads to atrophy and bone deformities gums. It can be localized not only in the thickness of bone (spongy), but also under the periosteum, under the mucous membrane of the gums and under the skin (A. X. Asiyatylov, 1969).

In electron microscopic examination (GP Bernadska, LO Stenchenko, T. Andrienko, 1991) plot odontogenic granulomas found that they are characterized by the formation of monocytic infiltration and proliferation of connective tissue elements. The cellular composition of granulomas characterized by containing cellular elements: some in the cell game nulematoznoho inflammation dominated by mature epithelial oyidni cells, along with other epitelioidnymy cells multinucleated giant cells are present. Ultrastructural organization of cells shows a different degree of their maturity and functional activity. Thus, mononuclear phagocytes are represented mainly by monocytes and their more mature forms - macrophages. Monocytes - small cells with a smooth surface, in the nucleus is diffuse chromatin, cytoplasm - moderate electron density with developed endoplasmic grid, Golgi apparatus, mitochondria, and a large number of small-sized dense bodies. Macrophages are more diverse in structure and polymorphic form. Number of inclusions and vacuoles varies in different cells, consider the criterion intensity of their metabolism and phagocytosis. Mature macrophages have on their surface thin finger spines. In their cytoplasm many phagocytic vacuole, primary and secondary lysosomes, multyvezykulyarnyh cells, the remaining cells of different types, fragments of red blood cells and neutrophils. In macrophages degraded organelles undergo degradation in the cytoplasm appear great autofahosomy, sehresomy and lamellar bodies.

Epitelioschni cells are characterized by flattened with numerous folds on the cell surface. Typically, these cells form aggregation hatsiyni clusters are closely intertwined with their shoots on the type of connection "zip". In epithelioid cells developed as energy and synthetic machinery, as evidenced by the presence of well-developed granular endoplasmic ungrainy and nets, numerous mitochondria. About secretory function epitelioidnyh cells indicates the presence in their cytoplasm elektronnoschilnyh granules restriction membranes. In some granules, their central part is elektronnoprozoroyu.

Some patients in the cell granulomas are multinucleated giant cells, which is inherent polymorphism. Often they contain from 5 to 10 nuclei, which are characterized by diffuse chromatin deployment, intussusception keriolemy, presence of nucleoli. The cytoplasm of giant cells rich in cell organelles. Well-developed endoplasmic mesh elements, there are many mitochondria roundish shape and small size. External and internal rishnomitohondrialna membrane characterized by distinct tortuosity. As epitelioschni cells, giant cells containing dark osmiofilni pellets, which are predominantly elongated shape. Moreover, in the cytoplasm of giant cells are lamellar osmiofilni cells, which may indicate an intensification peroksndnoho lipid in the cell.

In addition to the aforementioned cellular elements in the focus of granulomatous inflammation are sometimes aggregation of neutrophils, lymphocytes, fibroblasts, plasma cells. The latter have different functional activity. Tanks endoplasmic mesh in some of them considerably expanded. Can vybuvatysya separation tanks filled secret in the intercellular space containing collagen fibers of varying degrees of maturity, elastic fibers, yarns and conglomerates of fibrin.

Blood microvessels in the focus of granulomatous inflammation characterized not only by changes in the structural organization of the vascular wall, but blood rheological disorders. Red blood cells are often deformed shape with pronounced psevdopodiyamn, marked adhesion of erythrocytes and leukocyte and elements to the vascular wall, diapedesis of blood cells. In such microvascular endothelial for aqueous lining pathologically characterized by alternating light and dark endoteliopytiv.

Endothelial cells of capillaries most swollen, their nuclei are characterized by leaching chromatin maybe mikroplazmatozu phenomenon in the cytoplasm appear mikrofibrylyarni structure. Basement membrane of capillaries extended a fibrous structure. There tumor capillaries.

So electronmicroscopic study area granulomatous inflammation gives grounds to conclude preferential development in patients with epithelioid granulomas, the hallmark of which is the aggregation of epithelioid cells and giant cell formation.

Ultrastructural study of odonto-genic areas radykulyarishh cysts indicate their formation in cell chronic inflammatory periodontitis. This is confirmed by the presence of cellular infiltration, mainly of macrophages, plasma cells and cellular elements of the blood. Notably prevalence of degenerative and destructive processes in cells infiltrate up to their necrosis. Characteristic is the formation of giant vacuoles elektronnoprozoryh. They compress adjacent tissue, cause deformation and destruction of their components. The structure of the walls of cystic formations represented mainly by fibroblasts, remnants of proliferating cell structures and elements of connective tissue composed of collagen fibers of varying degrees of maturity, and conglomerates of fibrin strands.

Thus, a possible source of odoptohennyh cysts of the jaws with odoiitoheyishi granulomas. Since the presence of chronic inflammation may be the only source kistoutvorennya but constitute peredpuhlytshy state should take measures to prevent the development of granulomas in jaw bones.

Treatment

May be conservative or surgical. If the size of granulomas small (up to 0.5-0.8 cm), conservative treatment leads to regression of granulomas with its epithelial elements.

If conservative treatment is not indicated or proved ineffective, use one of the surgical methods: 1) tooth (root) followed by curettage hole or spoon excavator: 2) root apex resection with simultaneous removal of granulomas, 3) removal of granulomas (without resection root apex), 4) tooth replantation, 5) gen-misektsiya, 6) koronaroradykulyarna separation.

Anikotomiya, resection (amputation) root apex

Indications apikotomiyi:

1) the presence of large granulomas;

2) random polamannya pulpoekstraktora or boron in the apical part of the root:

3) traumatic fracture or perforation of the root of its forest area in the top, removing bone sequestration in the treatment of chronic osteomyelitis;

4) nedoplombuvannya and failed pereplombu-ing roots;

5) curved root.

Contraindications: 1) extensive destruction crown and no prospect of use for tooth prosthesis, 2) significant mobility of root and 3) lateral placement granulomas, 4) poor general condition of the patient, which does not allow an operation-apikotomiyu.

Preparing for surgery is that the morning of the operation complete treatment fastening their roots.

Method of operation

Perform local anesthesia, making trapezoidal or oval cut gum mucous membrane and periosteum. Basis flap should be returned to the transitional folds. Flap size should be larger than the estimated bone defect at the site of granuloma. Detach the flap rugine, trepanuyut bone, transmitting amputation root apex (better not chisel and fisurnnm boron) and extracted granuloma. Smooths out of the stump, acting, ie the root of the tooth. Cavity in the bone vyshkribayut and washed with antiseptic solution or antibiotics. Flap puts in its place and fixes 3.4 kethutovymy knotted sutures or polyamide fishing line. Sutures are removed on the 5-6th day.

Retrograde amalgam filling upper root canal during resection of the root apex:

and vidpylyuvannya root apex boron fisurnnm b treatment stump root cutter: in amalgam fillings root canal extended areas: the upper section of root canal sealed: the muco-oxide flap imposed seams (with G. Vasilyev).

During surgery should pay attention to obturation canal cement. If not, consider making retrograde amalgam fillings.

Stages transaction root apex resection with retrograde filling of.
Operation removal granulomas and cysts, granulomas, some authors (MA Bildyukevych and VP Kamashyna, 1964) performed without resection of the root apex of the tooth. This allows the teeth to provide a more reliable stability in the alveolar process.

One of the surgical treatments for chronic and exacerbations of chronic periodontitis tooth replantation is proposed by Ambroise Pare in 1594 Now it is used more and more by the significant research aimed at substantiating nayratsio-nalnishoyi operation technique. For example, only one issue "stomatology» (№ 5, 1995, p. 77-85) published 24 articles on the experience of using the method of replantation and transplantation of teeth (LA Cor-shunovoyu - in 80 patients; V. S. Vorobyov et al, - 284; A. Akhmedov - 86, VP-Chun Cove - 25, I. Engelmann - 202, VP Dana-hatch - 141; A. Trushnykovym - 305, AV Yarovykovoyu et al. - 141, EN Buch-man - 188; A. Afanasyev - 476, etc.).

The operation is as follows: after careful tooth removal (not to damage the root and the wall socket) vyshkribayut hole, sealed channels and cavity of the tooth, saw off the top of the roots are removed from the wells blood clots and washed with a solution of antibiotics. Then introduce a tooth in his hole and ukriplyayut Kapova apparatus with bus rapid kotverdnuchoyi plastic or wire. Prescribe antibiotics (intramuscular). After 1.5-2 months tooth survives and can function long (5.2.10 and older).

Engraftment replantovanoho tooth is one of three types: 1) periodontal-him (with the full preservation of the periosteum alveoli and residual periodontal replantata on the vine), 2) periodontitis-fibrous (when they are partially preserved), 3) osteoid (when they are completely absent) .

In acute odontogenic inflammatory processes (exacerbations of chronic and acute periodon-tytah and acute osteomyelitis) is sometimes also used method of tooth replantation. Engineering operations in this case differs from the above in that it is conducted in two stages. The first stage is to remove a tooth and filling the hole swab dipped in a solution of a mixture of antibiotics. The patient was released home, making the appropriate destination to eliminate acute inflammation i. After 5-20 days. ie after missing signs of acute inflammation, tooth that is stored in antibiotic solution at 4 ° C, sealed and replsshtuyut the usual method of removing pre wells swab and granulation. So tooth replantation performed on the second stage, after the elimination of acute inflammation (periodontitis, osteomyelitis or periostitis).

There are reports of successful use of one-stage replantation of permanent teeth and acute exacerbations of chronic peri-dontytah, abscess and osteomyelitis, even with tight jaws (BS Cherkassky, 1967 VI Serdyukov, M. Mitkov, 1989).

In this one-stage replantation (both single-rooted and permanent teeth) should not only carefully pull the tooth, but also make the cut along the crease of the transition following its drainage rubber strip and within 6-7 days to deliberate the total en-tybiotykoterapiyu.

Before replantation tooth (pre-sealed) the hole vyshkribayut granulation. This should keep cement replantovanoho tooth resection do its apex, but Periodontal contrary, be removed because he in'yektovanyy leukocytes, and in the top section - just melted. Replantation is unsuccessful in applying it at the sharp granulating periodontitis.

Some authors recommend not to hold any special fixing replantovanoho tooth because it may give teeth unnatural position.

Forecast

Replantovanyy acute inflammation of the tooth is strengthened and can operate over 30-45 days. According to VA Kozlov (1974), which summarized a great personal experience replantation 2249 teeth and literature data on long-term effects of teeth replantation is 4313 (from 2 to 11 years) conservation replantovanyh teeth observed on average 82.9%.

The reasons for the forced removal or loss of self replantovanyh teeth are often gradual resorption of roots, at least - incorrect technique immediate replantation of acute and chronic inflammatory diseases of the genital periodontium and jaw bones.

Thus, contributes to tooth replantation as chronic and acute odontohennph processes in periodontal and surrounding tissues, if you follow the technique of this operation.

It should be noted that in recent years some authors have often used such methods and treatment of chronic leriodontytiv as transplantation of teeth from the corpse, hemisektsiya ^ removal of one of the roots and the preservation of the other to be used as a support dental bridges) and koronaroradykulyarna separation.

Hemisektsiya

Indications for this surgery: the presence of deep bone pockets in the area of one of the roots of the premolars or molars, fracture of one of the roots of the tooth mizhko-radicands granuloma pulp chamber floor perforation in the treatment of the tooth, resulting in thinning top interalveolar septum after thinning of bone tissue near one of its roots, and the inability of the resected root apex of the tooth.

By contraindications include: significant defect bone tissues hole where a tooth has no cosmetic or functional value, the increased presence of roots, acute inflammation of the oral mucosa, impassable canals tooth root, the mobility of his general condition, which does not allow the operation.

This operation can be done in two ways - with detachment muco-oxide layer without delamination. Next fisurnym boron or separation disc cut the crown of the tooth and bifurcation and remove the broken part of the tooth. It should be remembered that complications may be the same as when removing a tooth.

The literature (VP Poltava, 1976, VP Pochyvalin, 1984, etc.). Indicate high efficiency (90-100%) of these surgical interventions in patients with chronic periodontitis.

During koronaroradykulyarnoyu separation must be understood dissection tooth into two parts (used in the treatment of periodontitis at the mandibular molars) in the area of bifurcation followed carefully smoothing overhanging edges, carrying plot curettage mizhkorenevoyi pathological pocket and covering every segment of the root crown.

Displayed: mizhkorenevoyi presence of granulomas small, perforated bottom tooth watering top mizhkorenevoyi partitions.

Operation is contraindicated in pathological processes in the field mizhkorenevoyi partitions (liquidation of which can lead to exposure of more than 1/3 the length of the root), fused roots, low-hosted bifurcation mobility

5uba, pathological bone deep pockets, an inflammatory condition, sho does not allow the operation. Where not Realize-gi or that surgery, surgeon WMD-tions do surgery tooth extraction.
Operation is contraindicated in pathological processes in the field mizhkorenevoyi partitions (liquidation of which can lead to exposure of more than 1/3 the length of the root), fused roots, low-hosted bifurcation mobility

5uba, pathological bone deep pockets, an inflammatory condition, sho does not allow the operation. Where not Realize-gi or that surgery, surgeon WMD-tions do surgery tooth extraction.

Accumulation of experience in applying these methods in the future will tell how effective they are (in the case of a positive long-term results).

Prevention of acute and chronic apical and marginal periodontitis

Given that periodontal infection is untreated or poorly sealed teeth causes "occupation" approximately 30-50% bed vrho fund Maxillofacial branches (CIS) patients with acute inflammation of the face and neck, and the number of outpatient and hospitalized patients tends to decrease (AG Shargorodsky et al., 1990), requires that prevention of acute and inflammatory odontogenic periodontitis conducted in the following areas:

1) persistent state multifaceted prevention of dental caries;

2) systematic, convincing that comes to people's minds, health and educational work through the media about zhubnosti untimely treatment of teeth and gums (the demonstration of television movies and featuring in newspapers fizionomiy patients affected by acute abscess, osteomyelitis, cellulitis, mediastinitis , sepsis, thrombophlebitis, and others., experience shows that the sanitary-educational work without such impressive demonstrations, usually does not cause listeners or readers desire to quickly get rid of the "hole in the tooth" or the rotten roots;

3) providing low-income individuals free dental care;

4) establishing strict systematic control over the quality of treatment and sealing

canals, especially multi (found that only 15.2% of their channels obturuyutsya on the length), using all modern medication and physical means (laser, ultrasound, iontophoresis, etc..) in the treatment of acute and sharp periodontitis;

5) abolish the practice of conservative treatment of chronic periodontitis when there are contraindications (such as distortion or permeability of root canals), while managed tysya to surgical treatment method (APiK-volume, hemisektsiya etc.);

6) establish a rigorous outpatient Choco terihannya every conservatively treated periodontytnym tooth within 12-24 months, and in the case of apparent lack of normalization in the periapical area - remove the tooth (to avoid aggravation periodontytuta developing more severe complications, including severe osteoflehmony) or use a surgical technique treatment of the tooth;

7) in all public and private dental clinics provide patients with the necessary tools and techniques painless treatment of caries, pulpitnyh and periodon-tytnyh teeth to dental chair and drilling machine ceased to be intimidating (since childhood) attributes of medical care;

8) to improve the quality of treatment of chronic marginal periodontitis періодонтитів.Профілактика and other surgical inflammation in zuboscheleppiy system is to prevent disease steam DonNTU, including dental caries, gingivitis, pulpitis, periodontitis, on the basis of total nozmitsnyuvalnoyi prevention of all diseases in humans: a rational food, a combination of work and rest, oral hygiene, prevention and hypokinesia hypofunction of masticatory system is "coronary heart disease in the maxillofacial area" (AA Skaher, 1985 NK Loginova, 1993, 1995).



Clinical migrating subcutaneous granuloma.

Osteomielitis of the jaws: etiology, pathogenesis, classification, clinical course, diagnostics, treatment, complications, prophylaxis.

Osteomyelitis Jaw

Osteomyelitis is an infection of the bone. It can be caused by a variety of microbial agents (most common in staphylococcus aureus) and situations, including:

• An open injury to the bone, such as an open fracture with the bone ends piercing the skin.
• An infection from elsewhere in the body, such as pneumonia or a urinary tract infection that has spread to the bone through the blood (bacteremia, sepsis).
• A minor trauma, which can lead to a blood clot around the bone and then a secondary infection from seeding of bacteria.
• Bacteria in the bloodstream bacteremia (poor dentition), which is deposited in a focal (localized) area of the bone. This bacterial site in the bone then grows, resulting in destruction of the bone. However, new bone often forms around the site.
• A chronic open wound or soft tissue infection can eventually extend down to the bone surface, leading to a secondary bone infection.

Osteomyelitis affects about two out of every 10,000 people. If left untreated, the infection can become chronic and cause a loss of blood supply to the affected bone. When this happens, it can lead to the eventual death of the bone tissue.

Osteomyelitis can affect both adults and children. The bacteria or fungus that can cause osteomyelitis, however, differs among age groups. In adults, osteomyelitis often affects the vertebrae and the pelvis. In children, osteomyelitis usually affects the adjacent ends of long bones. Long bones (bones of the limbs) are large, dense bones that provide strength, structure, and mobility. They include the femur and tibia in the legs and the humerus and radius in the arms.

Osteomyelitis does not occur more commonly in a particular race or gender. However, some people are more at risk for developing the disease, including:

• People with diabetes
• Patients receiving hemodialysis
• People with weakened immune systems
• People with sickle cell disease
• Intravenous drug abusers
• The elderly

Symptoms of osteomyelitis

The symptoms of osteomyelitis can include:

• Pain and/or tenderness in the infected area
• Swelling and warmth in the infected area
• Fever
• Nausea, secondarily from being ill with infection
• General discomfort, uneasiness, or ill feeling
• Drainage of pus through the skin

Additional symptoms that may be associated with this disease include:

• Excessive sweating
• Chills
• Lower back pain (if the spine is involved)
• Swelling of the ankles, feet, and legs
• Changes in gait (walking pattern that is a painful, yielding a limp)

Diagnosing osteomyelitis

To diagnose osteomyelitis, the doctor will first perform a history, review of systems, and a complete physical examination. In doing so, the physician will look for signs or symptoms of soft tissue and bone tenderness and possibly swelling and redness. The doctor will also ask you to describe your symptoms and will evaluate your personal and family medical history. The doctor can then order any of the following tests to assist in confirming the diagnosis:

• Blood tests: When testing the blood, measurements are taken to confirm an infection: a CBC (complete blood count), which will show if there is an increased white blood cell count; an ESR (erythrocyte sedimentation rate); and/or CRP (C-reactive protein) in the bloodstream, which detects and measures inflammation in the body.
• Blood culture: A blood culture is a test used to detect bacteria. A sample of blood is taken and then placed into an environment that will support the growth of bacteria. By allowing the bacteria to grow, the infectious agent can then be identified and tested against different antibiotics in hopes of finding the most effective treatment.
• Needle aspiration: During this test, a needle is used to remove a sample of fluid and cells from the vertebral space, or bony area. It is then sent to the lab to be evaluated by allowing the infectious agent to grow on media.
• Biopsy: A biopsy (tissue sample) of the infected bone may be taken and tested for signs of an invading organism.
• Bone scan: During this test, a small amount of Technetium-99 pyrophosphate, a radioactive material, is injected intravenously into the body. If the bone tissue is healthy, the material will spread in a uniform fashion. However, a tumor or infection in the bone will absorb the material and show an increased concentration of the radioactive material, which can be seen with a special camera that produces the images on a computer screen. The scan can help your doctor detect these abnormalities in their early stages, when X-ray findings may only show normal findings.

Treating and managing osteomyelitis

The objective of treating osteomyelitis is to eliminate the infection and prevent the development of chronic infection. Chronic osteomyelitis can lead to permanent deformity, possible fracture, and chronic problems, so it is important to treat the disease as soon as possible.

Drainage: If there is an open wound or abscess, it may be drained through a procedure called needle aspiration. In this procedure, a needle is inserted into the infected area and the fluid is withdrawn. For culturing to identify the bacteria, deep aspiration is preferred over often-unreliable surface swabs. Most pockets of infected fluid collections (pus pocket or abscess) are drained by open surgical procedures.

Medications: Prescribing antibiotics is the first step in treating osteomyelitis. Antibiotics help the body get rid of bacteria in the bloodstream that may otherwise re-infect the bone. The dosage and type of antibiotic prescribed depends on the type of bacteria present and the extent of infection. While antibiotics are often given intravenously, some are also very effective when given in an oral dosage. It is important to first identify the offending organism through blood cultures, aspiration, and biopsy so that the organism is not masked by an initial inappropriate dose of antibiotics. The preference is to first make attempts to do procedures (aspiration or bone biopsy) to identify the organisms prior to starting antibiotics.

Splinting or cast immobilization: This may be necessary to immobilize the affected bone and nearby joints in order to avoid further trauma and to help the area heal adequately and as quickly as possible. Splinting and cast immobilization are frequently done in children, although motion of joints after initial control is important to prevent stiffness and atrophy.

Surgery: Most well-established bone infections are managed through open surgical procedures during which the destroyed bone is scraped out. In the case of spinal abscesses, surgery is not performed unless there is compression of the spinal cord or nerve roots. Instead, patients with spinal osteomyelitis are given intravenous antibiotics. After surgery, antibiotics against the specific bacteria involved in the infection are then intensively administered during the hospital stay and for many weeks afterward.

With proper treatment, the outcome is usually good for osteomyelitis, although results tend to be worse for chronic osteomyelitis, even with surgery. Some cases of chronic osteomyelitis can be so resistant to treatment that amputation may be required; however, this is rare. Also, over many years, chronic infectious draining sites can evolve into a squamous-cell type of skin cancer; this, too, is rare. Any change in the nature of the chronic drainage, or change of the nature of the chronic drainage site, should be evaluated by a physician experienced in treating chronic bone infections. Because it is important that osteomyelitis receives prompt medical attention, people who are at a higher risk of developing osteomyelitis should call their doctors as soon as possible if any symptoms arise.

Osteomyelitis for Jaw Treatment

Osteomyelitis occurs when a bone becomes infected. Though osteomyelitis most often occurs in the bones of the limbs, spine and pelvis, it can also affect the jaw. Osteomyelitis in the jaw is a rare condition that once had been thought incurable, however advances in medicine make the condition treatable. It can present itself in either acute or chronic forms. Osteomyelitis is a serious condition and if proper treatment is not sought, it can destroy your bones.

Symptoms

The symptoms for people with osteomyelitis in the jaw include pain and tenderness, swelling around the jaw, drainage in the sinus cavity, loss of teeth, discharging of pus and necrotic bones. Factors that can lead to osteomyelitis include tobacco, anaemia, viral infections and malnutrition. Since the condition exhibits symptoms that are common in many other diseases, osteomyelitis can be difficult to diagnose at first. If you have chronic osteomyelitis, debilitating fatigue is also very common symptom.

Diagnosis

If your doctor suspects osteomyelitis, he will order various tests before he can make a firm diagnosis. Though a blood test does not define an osteomyelitis diagnosis, a high level of white blood cells will indicate that body is fighting off an infection. If your osteomyelitis is advanced, an X-ray will show the extent of the damage. If you need a better image, your doctor may recommend a CAT scan or MRI. Your doctor may also remove a piece of your bone for a biopsy. This biopsy will check for the strain of bacteria that has infected your bone.

Treatment

Most often infections of the jaw are polymicrobial oral flora so a regimen of antibiotics are used to treat the infection. You doctor may prescribe penicillin, clindamycin and metronidazole. Depending on the extent of the infection, surgery may be required. Your doctor will decide which procedure is best based on the damage caused by the infection. Some bone and tissue may need to be removed, fractures repaired and rotten teeth extracted. You may also want to consult with an oral-maxillofacial surgeon to see if facial reconstruction is required.

Osteomyelitis
Osteomyelitis is a rare complication of tooth-related infections (incidence of 25 in 100,000).  In most cases, it is the result of spread of infection from a dento-
alveolar (tooth) or periodontal (pyorrhoea / gum disease) abscess or from the para-nasal sinuses, by way of continuity through tissue spaces and planes.  It occasionally occurs as a complication of jaw fractures or as a result of manipulations during surgical procedures.
Most patients are adult males with infection of the mandible (lower jaw).
Osteomyelitis of the maxilla (upper jaw) is a rare disease of neonates (newly born) or infants after either birth injuries or uncontrolled middle ear infection.
It is classified as acute or chronic osteomyelitis.
Acute Osteomyelitis
In the acute form (which rarely, may also be of hæmatogenous origin [i.e. seeded from the blood stream]), the infection begins in the medullary cavity (bone marrow) of the bone.  The resulting increase of intra-bony pressure leads to a decreased blood supply (and hence diminution of white blood cells and other immune
components) and spread of the infection, by way of the Haversian canals of the bone, to the cortical bone (definition) and periosteum (below the periosteum, a thick
fibrous two-layered membrane covering the surface of bones).  This aggravates the ischæmia (decreased blood supply), resulting in necrosis (the death of cells or tissues from severe injury or disease, especially in a localised area of the body.  Causes of necrosis include inadequate blood supply [as in infarcted tissue], bacterial infection, traumatic injury and hyperthermia) of the bone.
Acute Osteomyelitis of the Jaws — Potential Sources of
Infection

• Peri-apical infection
• A periodontal pocket involved in a fracture
• Acute gingivitis or pericoronitis (even more rarely)
• Penetrating, contaminated injuries (open fractures or
  gunshot wounds)

Important Predisposing Conditions for Osteomyelitis
Local Damage to / Disease of the Jaws

• Fractures, including gunshot wounds
• Radiation damage
• Paget's disease
• Osteopetrosis

Impaired Immune Defences

• Acute leukaemia
• Poorly-controlled diabetes mellitus
• Sickle cell anaemia
• Chronic alcoholism or malnutrition
• AIDS

• Infection from micro-organisms with great virulence.  
  In such cases, even a peri-apical abscess may be
  implicated in osteomyelitis.

Acute Osteomyelitis of the Jaws — Key Features

• Mandible mainly affected, usually in adult males
• Infection of dental origin - anærobes are important
• Pain and swelling of jaw
• Teeth in the area are tender; gingivæ (gums) are red
  and swollen
• Sometimes paræsthesia of the lip
• Minimal systemic upset
• After about 10 days, X-rays show 'moth-eaten'
  pattern of bone destruction
• Good response to prompt antibiotic treatment and
  debridement

The mandible (lower jaw), due to decreased vascularity (blood supply & flow), is
involved 6 times more often than the maxilla (upper jaw).
The mandible has a relatively limited blood supply and dense bone with thick bony
(cortical) plates.  Infection causes acute inflammation in the medullary (bone
marrow) soft tissues and inflammatory exudate (a fluid with a high content of
protein and cellular debris which has escaped from blood vessels and has been
deposited in tissues or on tissue surfaces, usually as a result of inflammation. It
may be septic or non-septic) spreads infection through the marrow spaces.  It also
compresses blood vessels confined in the rigid boundaries of the vascular canals.

Thrombosis (the formation or presence of a thrombus [a clot of coagulated blood
attached at the site of its formation] in a blood vessel) and obstruction then lead to
further bone necrosis.

Dead bone is recognisable microscopically by lacunae (a cavity, space, or
depression, especially in a bone, containing cartilage or bone cells) empty of
osteocytes (a cell characteristic of mature bone tissue.  It is derived from
osteoblasts and embedded in the calcified matrix of bone. Osteocytes are found in
small, round cavities called lacunae and have thin, cytoplasmic branches) but filled
with neutrophils (white blood cells) and colonies of bacteria which proliferate in the
dead tissue.

Pus, formed by liquefaction of necrotic soft tissue and inflammatory cells, is forced
along the medulla and eventually reaches the sub-periosteal region by resorption
(an organic process in which the substance of some differentiated structure that
has been produced by the body undergoes lysis and assimilation) of bone.  
Distension of the periosteum by pus stimulates sub-periosteal bone formation but
perforation of the periosteum by pus and formation of sinuses on the skin or oral
mucosa are rarely seen now.

At the boundaries between infected and healthy tissue, osteoclasts (a specialised
bone cell that absorbs bone) resorb the periphery of the dead bone, which eventually becomes separated as a sequestrum (a fragment of dead bone separated from healthy bone as a result of injury or disease).  Once infection starts to localise, new bone forms around it, particularly sub-periosteally.
Where bone has died and been removed, healing is by granulation with formation of
coarse fibrous bone in the proliferating connective tissue.  After resolution, fibrous
bone is gradually replaced by compact bone and remodelled to restore normal
bone tissue and structure (and function).
Piercing, deep and constant pain predominates in the clinical presentation in adults,
while low or moderate fever, cellulitis, lymphadenitis, or even trismus may also be
noted.
In the mandible, changes in sensation affecting the lower lip (paræsthesia or
dysæsthesia of the lower lip) may accompany the disease.  When the disease
spreads to the peri-osteum (definition) and the surrounding soft tissues, a firm
painful œdema (definition) of the region is observed, while the tooth becomes loose
and there is discharge of pus from the periodontium.  Radiographic examination
reveals osteolytic (definition) or radiolucent (definition) regions.
Therapy entails combined surgical (incision, drainage, extraction of the tooth and
removal of sequestrum) and chemo-therapeutic treatment (with antibiotics).
Summary of Treatment of Osteomyelitis
Essential Measures

• Bacterial sampling and culture
• Vigorous (empirical) antibiotic treatment
• Drainage
• Give specific antibiotics based on culture and sensitivities
• Give analgesics
• Debridement
• Remove source of infection, if possible

Adjunctive Treatment

• Sequestrectomy
• Decortication if necessary
• Hyperbaric oxygen*
• Resection and reconstruction for extensive bone destruction

*Mainly of value for osteo-radionecrosis and possibly, anærobic infections.

Anæsthesia of the lower lip usually recovers with elimination of the infection.  Rare
complications include pathological fracture caused by extensive bone destruction,
chronic osteomyelitis after inadequate treatment, cellulitis due to spread of
exceptionally virulent bacteria or septicæmia in an immuno-deficient patient.

Chronic Osteomyelitis

Chronic osteomyelitis is characterised by a clinical course lasting over a month.  It
may occur after the acute phase or it may be a complication of tooth-related
infection without a preceding acute phase.  The clinical presentation is milder, with
painful exacerbations and discharge of pus or sinus tracts.

Osteomyelitis - Inflammation of the Bone

The terms osteomyelitis, periostitis and ostitis are frequently used as synonyms for inflammation of the bone.

Let’s have a quick look at the definition of the terms. Since the bone itself (the calcium structure) cannot get inflamed osteomyelitis (meaning bone marrow inflammation) and periostitis (meaning bone lining inflammation) would be the correct descriptions for an inflammation of the bone. Nevertheless ostitis is becoming more and more the term used.

The cause of an inflammation of the bone can come from outside – (exogenous factors) or from inside (endogenous factors). When both factors occur at the same time then we speak of combined forms. The so called idiopathic factors may also be regarded as a fourth form, consisting of bone inflammations of unidentifiable origin. Exogenous factors include, for example, numerous bacteria, viruses and fungi. They are potential pathogenic agents. If these pathogens find their way into our body they can cause an inflammation. If the inflammation gets into the bone then it’s a bone inflammation.

In the case of endogenous factors the cause lies in our own bodies. For example, in the case of diabetics the raised level of sugar of a diabetic leads to ever-increasing thickening of the walls of the blood vessels and thus an ever-poorer flow of blood.

The flow of blood can get so bad that certain areas of the body are no longer reached by it any more and the affected tissues die due to lack of oxygen and will be destroyed as a consequence of an inflammatory reaction - this can also occur in the bones, as shown in the animation and that would be an example of an endogenous osteomyelitis.

X-ray of Jaw Structure

Idiopathic osteomyelitis means to the patient that, at the end of the day the doctor cannot find an adequate explanation for it.

In the area of the jaw the most common causes of bone inflammation are exogenous or, more accurately, iatrogenous (caused by the doctor). Thus often extractions and/or badly root-treated teeth lead to bone infections.

In the picture you can see an x-ray of an extraction wound (circled in blue), the bone in this area is inflamed (circled in red) – osteomyelitis. In order to diagnose osteomyelitis an x-ray is usually required. In the same picture you can see a tooth (circled in green), which has an inflammation of the bone going on at the tip of the root (circled in red), as can be seen from the dark spot.

An x-ray can provide a lot of information about the bone but if precision is needed then a CT or MRT scan is very useful. This brings us to the diagnosis of osteomyelitis - CT and MRT scans are very reliable diagnostic aids at a certain stage of the osteomyelitis but at a very early stage of the illness their usefulness is rather limited.

Nuclear medical examinations such as skeletal cintography (Tc-99m) are frequently being made use of in order to detect osteomyelitis. The radioactive element technetium will be seen to be concentrated in the areas with raised bone metabolism after being applied intravenously. This increased concentration can be seen from the outside by means of a special camera (the darker spots in the exposure). Unfortunately it is not possible with this method to distinguish between the different causes of the raised bone metabolism.

Is the cause an inflammation or only an innocent build-up of bone after all?

With the addition of special factors (marked anti-granulocyte antibodies for additional investigation) the examination can however be made more specific. Blood tests are likewise not specific and unfortunately the blood values of the inflammation do not always correlate with the values of the osteomyelitis - especially in the jaw area. A bone biopsy is usually the most reliable means of diagnosis, as this way the bone can be viewed very precisely under the microscope (histological examination), and it may be possible to isolate the offending pathogen on the culture glass (bacteriology). If this succeeds then an antibiogram can be carried out in order to find the antibiotic with which to destroy the pathogen.

Bone Scan Scintigraphy

However, biopsy has a couple of disadvantages. The examination is invasive (therefore a wound is unavoidable) and not all areas of bone can be biopsied easily. Sometimes the bacteriological investigations are not successful or it may happen that during the taking of the sample there is contamination of the sample, for example by non-specific bacteria from the mouth.

Finally, let us take a look at the treatment options for osteomyelitis. There are various treatment options available - in the worst case the affected bone must be removed but this is very seldom necessary. The most frequent and simplest treatment option is the prescription of antibiotics, which can be swallowed or applied intravenously. The latter gives a higher concentration of the active ingredient in the blood.

By means of oxygen therapy we enrich the concentration of oxygen in the blood, since within the inflamed bone there is frequently insufficient blood supply and consequently, too little oxygen, ideal conditions for the multiplication of bacteria which do not tolerate oxygen – anaerobic bacteria as they are known. Oxygen-rich blood should have an effect on them, as per the motto: a little blood but very rich.

Another very much talked about treatment is the removal of the sick bone and the filling of the resultant gap with replacement donor bone which has been enriched with an antibiotic. In the animation you can see how the donor bone with the antibiotic (shown in green here) is put in place. The inflamed bone (shown in red here) will be removed and the donor bone will be inserted in the resulting cavity. The antibiotic will then pass continually into the body over months and simultaneously the replacement bone can regenerate.

The advantage of this treatment is that far higher concentrations of medication can be placed specifically in the affected area unlike with the usual means of application (orally or intravenously). Examination over a long period of time is still needed in order to evaluate this treatment over several years.

Ideally you want to avoid it getting to that stage. At least the iatrogenic forms of osteomyelitis can be avoided through sterilisation and cleanliness in the dental clinic.

Osteomyelitis

Odontogenic infection via a root canal, a periodontal pocket or an extraction wound is the most common local cause of osteomyelitis of the jaws. Rarely, a fracture serves as in infection route. Haematogenous spread of an infective agent from another part of the body also occurs. A distinct type of osteomyelitis, osteoradionecrosis, occurs after therapeutic irradiation of oral and neck malignancies.

Figure 20.
An ill-defined periapical and interdental osteolytic lesion in the mandibular anterior region three weeks after onset of clinical symptoms of osteomyelitis.

Figure 21.
Chronic suppurative osteomyelitis with three sequestra (arrows). Osteolytic as well as sclerotic areas are present.

Osteomyelitis is more common in the mandible than in the maxilla. In the mandible, it occurs predominantly in the posterior parts, the ramus included, whereas in the maxilla, it is more frequent in the anterior than in the posterior parts. In the acute phase, osteolysis is not visible radiographically until one or two weeks after the onset of clinical symptoms which are: pain, fever, local lymphadenopathy, increased white blood cell count, and teeth sensitive to percussion. Numbness of the lower lip is another common sign of mandibular osteomyelitis.

The initial radiographic changes are blurring and thinning of the trabeculae and subsequent enlargement of the bone marrow spaces. Without treatment, large volumes of the bone tissue can rapidly become involved, causing loosening of the teeth (Fig. 20).

If acute osteomyelitis becomes chronic, it is frequently possible to distinguish between chronic suppurative osteomyelitis (Fig. 21) and chronic sclerosing osteomyelitis (Fig. 22), both of which have ill-defined borders. In the suppurative form, radiolucent areas alternate with sclerotic, giving the bone a "moth-eaten" appearance. This is further enhanced when sequestra develop. In chronic sclerosing osteomyelitis, radiolucent areas occur, but there is a predominance of radiopaque changes due to the formation of sclerotic bone. The bone is often enlarged through periosteal bone formation (Figs. 22, 23). Over time, the distribution of sclerotic and radiolucent areas varies, indicating disease activity.

Figure 22.
Chronic sclerosing osteomyelitis of right mandible with some osteolytic areas. Ramus is enlarged.

a

b

Figure 23.
a) Right mandibular molars in a young patient. The alveolar bone is unevenly sclerotic; chronic sclerosing osteomyelitis.
b) Occlusal view of the same patient. Periosteal bone formation (arrow) on the buccal side of the mandible.

Fig. 1.

Cropped panoramic radiograph of suppurative osteomyelitis at the right mandible. Osteolytic change is observed from around the molar tooth roots to the body of the mandible (arrows).

How to Diagnose Osteomyelitis

Osteomyelitis is an infection of the bone, generally caused by the Staphylococcus Aureus bacteria. This bacteria infects the bones because it travels through the blood from other infected areas. It can also come directly from a wound and travel straight to the bone. A common cause of Osteomyelitis is an open fracture, where not only the bone breaks, but the skin breaks too.

Instructions

1. Perform a physical examination of the patient. Be sure to take a complete medical history and list any medications the patient is already taking. Also ask about any recent problems with the area the patient says is painful.

2. Take a blood sample to perform a blood test to pinpoint if the patient's white blood cell count is high, which is often a sign of infection. Look for signs of infection in the body, such as areas that are inflamed, red and warm.

3. Send the patient for a bone x-ray. A bone x-ray can show if there is an infection in the bone, but might not be as accurate for someone who has just started complaining of pain. If the bone x-ray does not come back positive, but the patient exhibits signs of Osteomyelitis, send them for a bone scan, which gives you a more detailed view of the bone.

4. Follow up with an MRI, if the bone scan indicates osteomyelitis. MRIs are a valuable test to run. In addition to diagnosing osteomyelitis, the MRI can also help determine how long the infection has been in the bone.

Osteomyelitis may manifest itself in acute, subacute, or chronic forms. Chronic osteomyelitis will result in variable sclerosis and deformity of the affected bone. After the age of 50, the majority of the blood supply to the mandible comes from the overlying periosteum and attached musculature, due to age and atherosclerosis-related involution of the inferior alveolar artery. With an infection of the bone, the subsequent inflammatory response will elevate this overlying periosteum, leading to a loss of the nourishing vasculature, vascular thrombosis, and bone necrosis, resulting occasionally in formation of sequestra. These become areas that are more resistant to systemic antibiotic therapy due to lack of the normal Haversian canals that are blocked by scar tissue, inflammatory exudate, and necrotic bone. At this point, not only systemic antibiotic therapy, but also surgical debridement maybe required to remove the affected bone and prevent disease propagation to adjacent areas. The relative hypoxia seen in infected bone will impair leukocyte bacterial killing, and impede fibroblastic collagen production that is required to support angiogenesis. Thus, it is not surprising that the concomitant use of hyperbaric oxygen therapy maybe beneficial in cases refractory to medical management alone or in patients with a severely compromised immune response. Generally, 20 dives (2.8-3.0 at 100% oxygen for 90 minutes) are administered preoperatively, followed by 20 dives after the debridement of necrotic tissue.

Radiographic imaging may be deceptively unremarkable in acute osteomyelitis, particularly with plain x-rays. Computed tomography (CT) scanning is the standard for evaluating the bone for sequestrum formation. Generally, one sees areas of lytic destruction and overlying periosteal reaction. It is much more common to find cortical plate disruption in the buccal plate than in the lingual plate. Technetium⁹⁹ bone scanning is often positive within 24 hours of an acute infection. Unfortunately, persistent uptake maybe present for 2 years after eradication of osteomyelitis. Gallium^-67 scanning normalizes after successful treatment of mandibular osteomyelitis.

In acute osteomyelitis, or in chronic forms without evidence of formation of sequestra, culture-driven antibiotic therapy is important to allow for disease eradication and decrease the likelihood of formation of antibiotic resistant strains resulting from inadequate subtherapeutic antibiotic therapy. Occasionally, repeated cultures may be required to allow for pathogen isolation, especially in cases of chronic osteomyelitis. Open biopsy of the bone allows for the most accurate culture results. Alpha hemolytic streptococcus, often in conjunction with oral anaerobes, is the most commonly isolated organism noted today. Although acute osteomyelitis is often adequately treated with a culture-driven 6- to 8-week course of antibiotic therapy, chronic osteomyelitis generally requires surgical debridement as well. Antibiotic therapy should be continued for 4 to 6 weeks from the date of last debridement, from resolution of the patient's symptom complex and/or normalization of the gallium scan (if performed). Refractory osteomyelitis may benefit from the addition of hyperbaric oxygen therapy. Vancomycin or clindamycin are generally effective in the treatment of group A or B streptococci. However, as stated, culture-driven antibiotic therapy is required. With the propagation of multidrug-resistant varieties, treatment with nontraditional antibiotic regimens, such as fluroquinolones, may be required. Attention to optimal management of any underlying systemic immunocompromising conditions, such as diabetes mellitus, steroid usage, and HIV infection is important in all cases.

Clinical features, Radiographic features and treatment of Chronic Osteomyelitis of mandible

Clinical feature:
1. Site: Mandible
2. At early stage:
a. General constitutional symptoms:
• Intermittent fever
• Malaise
• Nausea, vomiting
• Anorexia
b. Pain:
• Deep seated
• Paresthesia of the lower lip

Radiology of Chronic OML• Facial cellulitis

• Trismus
• Swelling
3. Established case of OML:
a. Deep pain
b. Loosening of involved teeth
c. Pain on percussion
d. Sensitivity
e. Purulent discharge of pus
f. Regional lymphadenopathy
g. Trismus
Radiological feature:
1. In early stage, there are no findings
2. The changing begins 4-6 weeks after infection
3. In ate stage of Osteomyelitis, we find sequesterum, involucrum, scattered area, moth eaten appearance in conventional radiograph.
4. For specialized image, we do: CT scan, Radionucleido bone scan, Positron emission tomography.

Treatment:
1. Conventional treatment:
a. Complete bed rest
b. Supportive therapy:
• Nutritional support
• High protein diet
• High calorie and multivitamin diet
c. Rehydration by IV fluid
d. Blood transfusion
e. IV antimicrobial agent
2. Surgical treatment:
a. Incision and drainage   b. Extraction of the offending tooth   c. Debridement of the affected area by irrigating with H2O2 and normal saline  d. Sequestrectomy e. Decortication f. Saucerisation  g. Resection
Post operative care:
1. Continuous use of antibiotics
2. Analgesics
3. Adequate hydration
4. Complete bed rest
5. Follow up

Suppurative mandibular osteomyelitis

Suppurative mandibular osteomyelitis refers to agents that invasion of the mandible, the bone tissue as a whole, including the periosteum, cortical bone, bone marrow and the blood vessels, nerves, inflammation, alveolar abscess, periodontitis, and the third molar crown weeks go far odontogenic infection from which the highest incidence of mandibular osteomyelitis.

Disease Overview

When agents that invaded the jaw, will cause the entire jaw organizations, including the periosteum, cortical bone, bone marrow, and one of the blood vessels, nerve inflammation range of leisure, known as purulent maxillary osteomyelitis. Classification of Diseases 1 performance classification, according to the clinical pathology of suppurative odontogenic mandibular osteomyelitis lesions originating in the maxillary central cancellous bone and bone marrow, known as the Central osteomyelitis, lesions originating in the periosteum and cortical bone of the jaw around the , called the edge of osteomyelitis, according to the nature of the lesions can be divided into acute and chronic phase, the scope of the validation can be divided into localized or diffuse suppurative disease cause of mandibular osteomyelitis of up to alveolar abscess, periodontitis, third molar pericoronitis go far odontogenic infection from, followed by invasive infection due to a comminuted fracture or gunshot wound in open injury to bone by the blood circulation of sepsis or sepsis infection. this situation occurred in the maxilla of the infants and young children, very few of the infection of facial skin or oral mucosa directly affect the jaw. put the treatment of oral cancer or nasopharyngeal carcinoma, osteomyelitis common major pathogens Staphylococcus aureus bacteria, followed by Streptococcus, a few other pyogenic bacteria, stereotypes of mixed infections. pathophysiology of mandibular osteomyelitis compared with the previous mandibular osteomyelitis is more common condition than maxillary bone marrow serious, this is because the upper jaw bone dense fascia and strong muscles, present jaw infection, pus is not left around the puncture drainage poor blood supply of the mandible, infection of vascular thrombosis, it is easy to form a large sequestrum. diagnostic tests 1, details incidence and its treatment, consultation, attention to the relationship with the teeth, identify pathogen teeth. 2, with or without empyema sense of volatility, can be used to puncture confirmed suspicious when pus for bacterial culture and antibiotic sensitivity determination. fistula, exploration probes and other instruments with or without sequestrum sequestrum separation, X-ray, chronic identifying bone destruction, with or without sequestrum formation or infection of the low toxicity to the bone cortical hyperplasia. .

Clinical symptoms

Symptoms characteristic of central mandibular osteomyelitis, acute early inflammation is often restricted to the alveolar bone or bone marrow of the mandibular body, and then invasion of mandible, from the center to the edges of cortical bone and periosteum. 2. stage, patients may feel a severe toothache, pain along the trigeminal nerve distribution area for radiation lesions of the gingival mucosa hyperemia and edema, teeth percussion pain and loose, and may have gingival sulcus overflow pus or the formation of alveolar abscess , this stage of the lesion has not been timely drainage, the infection will continue to spread to the medullary cavity, can cause diffuse osteomyelitis or perforation of cortical bone formation in subperiosteal abscess, then patients with systemic poisoning symptoms became worse, and this when patients with serious manifestations of anemia, dehydration, exhaustion, body temperature increased to 39 ~ 40 ℃, blood test white blood cells increased significantly, local pain and soft tissue swelling in the affected region of the majority of teeth to loosen, some patients would be a serious concurrent disease, such as sepsis, intracranial infections, such as inflammation has not yet been brought under control, the maxilla infection can cause suppurative maxillary sinusitis and infraorbital cheek, or zygomatic, or pterygopalatine concave, temporal, concave and other regional proliferation. mandibular infection can spread to the inferior alveolar nerve caused by the lower lip numbness spread to the jaw weeks, stimulate the open jaw muscles, causing limited mouth opening, can be complicated by the jaw weeks more space infection, so that the face was seen in the swelling, and finally inflammation in the formation of blood clots within the jaw, resulting in jaw nutritional disorders and necrosis, and thus transferred to the chronic phase. 6, transferred from the acute to the chronic phase of about 2 to 3 weeks later, the pain and other systemic symptoms have begun reduced, but the mouth gums can form multiple fistula and pus. sequestrum with healthy bone will be in about a month later, new bone layer, caused by the separation of the sequestrum with healthy bone. this stage without surgical removal of involved regional fistula pus prolonged unhealed, can sometimes have a small piece of sequestrum discharged from the fistula osteomyelitis of the mandible can cause large sequestrum formation of pathogenic pathologic fracture, marginal mandibular osteomyelitis clinical features , limitations with young people, the lesions occurred, with chronic symptoms, does not appear large sequestrum. 2, occurred in young people under the jaw, the lesion is more limited spread of the infection pathway is not the first damage to bone marrow, but in the periosteum inflammation or subperiosteal abscess on the basis of the first involving the cortical bone, but also to the deep development involving the bone marrow, but rarely large sequestrum formation of the infections originated in the mandibular third molar crown Zhou Yan, can cause masseter muscle space infection subperiosteal abscess, resulting in the mandible of the ascending branch and corner Nutrition disorders of the cortical bone necrosis, showing chronic symptoms, local mild chronic inflammatory swelling and pitting edema due to masseter muscle and pterygoid muscle involvement, and limited mouth opening. pericoronitis infection if not controlled, often repeatedly made. 5, the edge of mandibular osteomyelitis after repeated anti-inflammatory medication, could easily lead to pathogen resistance, the formation of low toxicity and infection jaw inflammation.

Signs and symptoms

In particular, according to the clinical pathology of suppurative odontogenic mandibular osteomyelitis lesionsoriginating in the maxillary centralBone trabecular and bone marrow, known as the Central osteomyelitis lesions originating in the periosteum and cortical bone of the jaw around, known as the edge of osteomyelitis according to the nature of the lesions can be divided into acute and chronic phase, according to The scope of the validation can be divided into localized or diffuse. central mandibular osteomyelitis: the maxilla than the mandible more common in teeth with severe pain, persistent, and radiating pain along the trigeminal nerve distribution. teeth and adjacent teeth loose, percussion pain, vestibular groove fullness, cheek swelling. mandibular alveolar abscess, the pus is not easy worn develop into acute diffuse osteomyelitis and lack of drainage, the patients with systemic symptoms get worse, fever, chills, leukocyte, dehydration and other toxic manifestations. mandibular osteomyelitis refers to agents that invaded the jaw, causing the entire bone tissue, including periosteum, cortical bone, bone marrow and the blood vessels, nerve inflammation, Chinese medicine called 'bone slot wind 'or' wear gills were sharply acute onset of high fever, increased white blood cells, can shift to the left. body poisoning, and with general malaise, headache, loss of appetite and other symptoms can occur in patients toothache, and the pain along the trigeminal nerve distribution area of radiation, and can quickly spread to the adjacent teeth. the short term, there may be multiple tooth mobility, periodontal pocket pus, inferior alveolar nerve by inflammatory damage to the lower lip numbness due to the spread of inflammation to the surrounding maxillofacial swelling which can occur, such as infection spread to the masticatory muscles can be trismus such as infection control in a timely and quickly to the infraorbital, inferior temporal, the pterygopalatine concave and by the mandibular foramen caused the wing jaw space infection. systemic complications such as sepsis, and intracranial infection may also occur.

Disease etiology

Suppurative osteomyelitis of jaw up to the alveolar abscess, periodontitis, the third molar pericoronitis go far odontogenic infection from, followed by open injury due to comminuted or anger injury caused by bone invasive infection, sepsis or infections, sepsis and blood circulation more than occurred in the maxilla of infants and young children, very few of the infection of facial skin or oral mucosa directly affect the jaw. major pathogens Staphylococcus aureus, followed by Streptococcus few other pyogenic bacteria stereotypes mixed infection.

Pathophysiological

Mandibular osteomyelitis compared with maxillary osteomyelitis more common condition than the maxilla bone marrow serious, this is because the upper jaw bone is dense, and some surrounding fascia and strong muscles, present jaw infection, pus left After puncture drainage poor blood supply of the mandible, infection of vascular thrombosis, easy to form a large sequestrum.

Diagnostic tests

A detailed consultation incidence after treatment, and attention teeth identify pathogen teeth.

2, with or without empyema sense of volatility suspicious can be used for puncture confirmed. 3, pus for bacterial culture and antibiotic sensitivity determination, with or without fistula, probes and other instruments to probe whether the sequestrum sequestrum separation. 5, X-ray, the chronic phase to identify bone destruction, with or without sequestrum formation or infection of the low toxicity of the bone cortex hyperplasia type.

Disease Prevention

No special

Safety Tips

1, the disease mostly occurs in the infant's maxillary marginal mandibular osteomyelitis: more common in young people, the acute phase is difficult to find common chronic phase 2, the timely treatment of the crown Zhou Yan, the periapical Yandeng odontogenic infection to prevent occurrence of mandibular osteomyelitis. has formed should be a thorough treatment to avoid to chronic osteomyelitis, in the acute phase.

Treatment programs

Acute systemic antibiotics, local incision and drainage or removal of loose teeth, diffuse patient performance Decline thirsty, systemic poisoning, severe anemia, in addition to general supportive therapy, but also a small amount of multiple transfusions and enhance systemic resistance to the chronic phase sequestrum curettage and extraction of teeth lesions mainly purulent maxillary bone marrow after a course of inflammation, and generally can be divided into two phases of acute and chronic phase. to The sequestrum began to take shape used to be collectively referred to as the acute phase by the onset, generally about 3 to 4 weeks if the infection fails to be completely controlled in the acute phase, into the chronic phase. must be used in sufficient quantities and effective antimicrobial treatment. use drugs in order to control the infection in the acute phase, use of antibiotics against Staphylococcus aureus and mixed infections, the other based on bacterial culture and susceptibility to choose effective antibiotics. In the initial stages of infection, but also with the physical therapy. When the infection into the suppuration of Early incision and drainage. wait for his condition slightly eased, the mouth opening slightly improved, should try to extraction, so that the pus from the socket to get the drainage, to prevent the spread of infection in the bone of acute suppurative osteomyelitis oncoming acute, severe illness, can cause blood and brain complications, and therefore close observation, as early as the appropriate emergency treatment of acute systemic application of antibiotics, local incision and drainage removal of loose teeth mainly diffuse patient performance decline thirsty, systemic poisoning, severe anemia, in addition to general supportive therapy, but also a small amount of multiple transfusions, enhanced systemic resistance to the chronic phase to sequester scrape and lesions in tooth extraction based. 1, the disease occurred in the maxilla of infants and young children. marginal mandibular osteomyelitis: more common in young people, the acute phase is difficult to find common chronic phase. and timely treatment of pericoronitis, periapical go far odontogenic infection, on the prevention of mandibular osteomyelitis. such as formation of osteomyelitis in the acute phase should be a thorough treatment so as not to become chronic. acute phase of infection control, enhance the body resistance-based, anti- infection drugs should be selected according to the sensitivity of pathogenic bacteria. mandibular osteomyelitis more mixed bacterial infection, it is appropriate in order to use broad-spectrum antibiotics. In addition, as has been clear for odontogenic infection, early removal of the lesions teeth in order to facilitate drainage, to avoid more extensive bone destruction. case of subperiosteal abscess or infection jaw week gap, it is timely incision in chronic phase, the lesion has been limited or has been sequestrum formation, while the surgical treatment of the main supplemented by drug treatment. marginal mandibular osteomyelitis are generally large sequestrum formation, mostly for the proliferation of subperiosteal cortical bone, the texture is more loose, and should be completely clear, pus foci of cortical bone surface where infection and the granulation organizers should be scraping, postoperative use of antibiotics to control infection in 7 to 14 days to avoid relapse.

Clinical manifestations

Clinical presentation of osteonecrosis of the jaw. (A) Typical lesion of osteonecrosis of the jaw showing exposed infected bone involving the mylohyoid ridge. (B) Osteonecrotic bone below a dental implant. (C) Spontaneous exfoliated teeth with underlying exposed dead bone. (D) Operative picture showing well-demarcated dead bone involving the whole alveolus. (From Badros A, Weikel D, Salama A, et al. Osteonecrosis of the jaw in multiple myelomoa patients: clinical features and risk factors. J Clin Oncol 2006;24:948; with permission. Copyright © 2006 by American Society of Clinical Oncology.)

Suppurative mandibular osteomyelitis from the clinical course of disease, pathogens, routes of infection and lesions involving the siteCan be manifested as acute and chronic stages, and often divided into two types of central and edge (a central mandibular osteomyelitis is usually odontogenic inflammation spread to the bone marrow, spread to the bone from the jaw center around cortex and periosteum in the bone marrow of early acute inflammation is often restricted to the alveolar bone or the mandibular body, patients feel severe toothache, pain along the trigeminal nerve distribution of radiation lesions of the gingival mucosa hyperemia and edema, teeth that is, obvious pain and loose, and can gingival sulcus septic overflow or the formation of alveolar abscess. acute phase has not been timely drainage, infections continue to spread to the medullary cavity can cause disseminated osteomyelitis or perforation of cortical bone formation in subperiosteal abscess. exacerbate symptoms of systemic poisoning at this time, the body temperature to 39 ~ 40 ℃, blood test white blood cells increased significantly, local pain and soft tissue swelling the affected regions the majority of loose teeth. If the inflammation is not brought under control, the maxillary infection can cause purulent maxillary sinusitis and infraorbital, buccal, zygomatic or pterygopalatine concave, temporal concave and other areas to spread. mandibular infection can spread to the inferior alveolar nerve caused by the lower lip numbness spread to the jaw week to stimulate the open jaw muscles, causing limitation of mouth opening can be complicated by the infection of the jaw week more than the gap, so that the face was seen in the swelling, and finally inflammation in the formation of blood clots within the jaw, resulting in nutritional disorders of the jaw and necrosis, and thus transferred to the chronic phase. turn by the acute phase into the chronic phase of about two to three weeks later, pain and other systemic symptoms began to ease, but the mouth gums can form more than one fistula and pus out about a month later, the sequestrum with healthy bone between the new bone layer, causing the separation of the sequestrum with healthy bone without surgical removal of involved regional fistula pus prolonged unhealed, can sometimes have a small piece of sequestrum discharged from the fistula. osteomyelitis of the mandible can cause large piece of dead bone formation, can be pathogenic pathological fractures appear bite (occlusal disorders. Suppurative mandibular osteomyelitis (two marginal mandibular osteomyelitis spread of the infection pathway is not the first damage to bone marrow, but the basis of periostitis or subperiosteal abscess the first involving the cortical bone occurred in adolescents mandible, more limited lesions, infections originated in the mandibular third molar pericoronitis inflammation, caused by the masseter muscle space infection and subperiosteal abscess, resulting in lower jaw of the ascending branch and the corner of cortical bone nutritional barriers necrosis. clinical manifestations of chronic symptoms, the symptoms of the acute phase of infection and jaw week gap coexist but often overlooked in local mild chronic inflammatory swelling and pitting edema due to the chewing muscles and wing muscle involvement and limited mouth opening. lesions confined to the cortical bone, or to the deep development involving the bone marrow, but rarely large sequestrum formation. pericoronitis infections if not controlled, often repeatedly made by anti-inflammatory drugs after treatment, could easily lead to pathogen resistance, the formation of low toxicity and infection, no obvious purulent and sequestrum formation process and significant cortical hyperostosis, sclerosis and periosteal thickening of cortical bone lysis little part the formation of small abscess and granulation tissue. cortical hyperplasia of the mandibular ascending branch of the Ministry of mandibular angle can cause facial asymmetry, X-ray showed obvious subperiosteal hyperostosis.