Chronic Osteomyelitis of the Jaw - Features of Diagnosis and Treatment

Chronic osteomyelitis of the jaw

Chronic osteomyelitis of the jaw develops from an untreated acute form of the disease. This osteomyelitis is called secondary chronic. If the inflammatory process was initially sluggish and was not as clinically pronounced as acute, then this is primary chronic osteomyelitis.

Chronic osteomyelitis, like acute osteomyelitis, can be of infectious or non-infectious origin. The first, in turn, is divided into odontogenic and non-odontogenic.

In accordance with the predominance of the processes of construction or death of bone substance, 3 clinical and radiological forms of chronic odontogenic osteomyelitis of the jaws are distinguished: productive (without the formation of sequestration), destructive (with the formation of sequestration) and destructive-productive. The productive form is less common than the others, mainly at a young age.

Chronic odontogenic osteomyelitis of the jaw

Chronic odontogenic osteomyelitis of the jaw is often secondary chronic and is considered as a complication of acute odontogenic osteomyelitis. The transition from the acute stage of the disease to the chronic stage occurs on average at 4-5 weeks of illness. By this time, the manifestations of acute inflammation have passed: the swelling of the soft tissues surrounding the jaw subsides, the amount of pus released from the wound decreases, the pus itself becomes thicker, and granulation tissue forms in the wound. The patient’s general condition also normalizes: body temperature returns to normal, the patient does not complain of pain in the affected area, sleep and appetite are restored, blood tests are approaching normal values.

Figure 1. Formation of the fistula tract.

The first clinical sign that the acute stage has not been cured is the appearance of fistulas with pus in the wound area. Sometimes fistulas can open on the skin of the maxillofacial area.

Next, the formation of sequesters is observed, which, depending on their size, either exit through the fistula tracts (small) or are subject to removal by a maxillofacial surgeon (large).

Figure 2. Sequestration formation and rejection.

If the outflow of pus is disrupted and small sequesters are removed through the fistulous tracts, the chronic process worsens, the clinical picture becomes the same as in acute osteomyelitis.

The picture described above is characteristic of destructive or destructive-productive forms of osteomyelitis. The productive form is characterized by the absence of sequesters and an increase in bone tissue in the area of ​​inflammation; it occurs only in osteomyelitis of the lower jaw.

general description

Osteomyelitis of the femur is a purulent infectious inflammation of the femur that affects all elements of the bone - bone marrow, the bone tissue itself and the covering tissue of the bone - the periosteum.
If osteomyelitis occurs for the first time, it is called acute. If osteomyelitis occurs over a long period of time and periodically worsens, it is called chronic.

Osteomyelitis of any bone is always caused by the penetration of pathogenic microorganisms in various ways. It is extremely rare that osteomyelitis does not have an infectious nature and bone inflammation occurs against the background of activation of the immune system. The causes of osteomyelitis of the femur can be:

• penetration of microbes through blood vessels into the femur from a distant source of infection (hematogenous form of osteomyelitis);
• direct penetration into the bone during wounds, fractures, operations on the femur (non-hematogenous osteomyelitis).

Even 25-30 years ago, acute hematogenous osteomyelitis of the femur occurred in most cases in childhood; currently, osteomyelitis of the femur occurs with equal frequency in children and adults.

The causes contributing to the occurrence of osteomyelitis of the femur are:

• atherosclerosis of blood vessels of the lower extremities;
• chronic alcohol intoxication;
• diabetes;
• immunodeficiency.

Diagnosis of chronic odontogenic osteomyelitis

Diagnosis of chronic odontogenic osteomyelitis consists of collecting a history of the disease, examining the patient and performing radiography.

From the anamnesis we learn that the patient either suffered from acute osteomyelitis and did not seek help, or assistance was provided to him, but the acute form of the process became chronic. In both cases, further examination of the patient is carried out.

The clinical picture is very diverse, so it is difficult to accurately characterize all the signs of the disease.

Externally, the face may be asymmetrical due to soft tissue swelling or bone deformation. In the productive form, asymmetry can be caused by an increase in the volume of bone tissue.

The opening of the mouth is either normal or not fully, which is caused by inflammatory contracture of the masticatory muscles.

Lymph nodes are normal or may be slightly enlarged and painful on palpation.

When examining the oral cavity, an inflammatory infiltrate, hyperemic mucosa, the causative tooth or the socket of an extracted tooth are determined. Fistulas are found on the mucous membrane of the oral cavity or on the skin, through which formed sequestra are probed. Teeth that are mobile in acute osteomyelitis are less mobile in the chronic form of the disease.

Next, an X-ray diagnosis is carried out, preferably an orthopantomogram or radiography in two projections (direct and lateral). In the acute form of odontogenic osteomyelitis, only the source of infection is observed - thinning of the bone tissue in the area of ​​the apex of the root of the causative tooth. If the disease has become chronic, sequestration is visible on the image. But the first manifestations of the disease in the picture appear only at the end of the 2nd, and sometimes 3rd, week. The situation with the destructive form of osteomyelitis is described above.

If we talk about the productive form, then bone sequestration is not observed. But the amount of mineralized tissue increases due to the reaction of the periosteum. The patient's face becomes asymmetrical, the bone increases in volume.

Chronic odontogenic osteomyelitis of the lower jaw

Chronic odontogenic osteomyelitis of the lower jaw often affects only the alveolar part of the bone, less often the body or branch of the jaw. Due to the structural features, the disease is severe with the formation of small and large sequesters. Often, the destruction of bone tissue leads to a pathological fracture (the bone breaks with a weak “blow” to the jaw).

Chronic odontogenic osteomyelitis of the upper jaw

Chronic odontogenic osteomyelitis of the upper jaw develops faster and is easier than in the lower jaw. Sequestra are formed in 3-4 weeks, while in the lower jaw - in 6-8 weeks. With the diffuse nature of the disease, destruction of the anterior wall of the maxillary sinus or even the lower edge of the orbit is possible.

Incidence (per 100,000 people)

Treatment of chronic odontogenic osteomyelitis of the jaw

Treatment of chronic odontogenic osteomyelitis of the jaw is complex and includes surgical intervention and drug treatment.

I. During exacerbation of chronic osteomyelitis, the symptoms of acute inflammation are first relieved. If the causative tooth has not been removed previously, then it must be removed this time. Adjacent mobile teeth are trepanned and splinted, if not removed according to indications (after assessing their viability and x-ray examination). Sanitation of the oral cavity is mandatory and all chronic sources of infection are removed to prevent complications during subsequent procedures.

To facilitate the outflow of pus, fistulas or wounds are expanded, and primary surgical treatment of subosseous and perimandibular purulent foci is performed.

An important part of the surgical stage of treatment is sequestrectomy. After evaluating the radiograph, the formed sequesters are removed. Removal is performed through an intraoral or extraoral incision. Large sequestra in the area of ​​the body and ramus of the lower jaw, as well as in the area of ​​the infraorbital margin and zygomatic bone, are removed extraorally. Sometimes large necrotic areas of bone are broken into several parts for ease of removal. Incisions are made along the natural folds of the face for better aesthetics.

After removal of sequesters, attention is paid to granulations and sequestral capsule. Using a curettage spoon or even a milling cutter, pathological tissue is removed until the signs of healthy bone are revealed: alveolar bleeding, white bone, hard bone tissue.

The free space is filled with a biosynthetic osteotropic drug: kolapol, kolapan, etc. The wound is tightly sutured, drainage is left. The stitches are removed after 7-10 days.

II. Next, let's move on to drug treatment. As with other purulent diseases, etiotropic, pathogenetic and symptomatic treatment is carried out.

To eliminate the cause of the disease, the surgeon removes the causative teeth. But the infection remains in the blood, so the patient is prescribed antibacterial drugs: macrolides, cephalosporins. It is also worth prescribing the patient antifungal agents (Deflucan 150 mg once a week).

Since the patient’s immunity is reduced, it is recommended to prescribe immune drugs such as thymalin, T-activin, levomisol, staphylococcal toxoid.

In case of extensive damage to bone tissue, the patient is recommended to follow a gentle diet to prevent a pathological fracture of the jaw.

To reduce the symptoms of inflammation, detoxification and anti-inflammatory therapy is carried out. Physical therapy exercises and physiotherapy are individually selected for the patient to restore function.

Chronic osteomyelitis of the jaw. Outcomes and complications

Outcomes:

• Favorable - if the patient contacts a maxillofacial surgeon in a timely manner and receives adequate treatment, the patient’s full recovery is possible.
• Unfavorable – if treatment is insufficient and the patient contacts a doctor late, the following may occur:
• Exacerbation of the disease
• Jaw deformity,
• Jaw fracture - occurs due to minor physical impact, from which a healthy jaw would not be damaged,
• Complications of osteomyelitis: Abscesses and phlegmon of soft tissues of the face,
• Thrombosis of facial vessels and cavernous sinus,
• Mediastinitis,
• Death.

Etiology

The main causative agent of osteomyelitis is Staphylococcus aureus, but damage can also be caused by streptococci, pneumococci, Pseudomonas aeruginosa, etc. Osteomyelitis is the result of hematogenous spread of infection from another source. For example, carious teeth, sinusitis, tonsillitis, pyoderma, infected wounds. Infection can also be acquired through contact through open injuries and deep abscesses.

Risk factors for the spread of processes are: chronic infections, diabetes mellitus, somatic diseases, hypothermia, any reactions that contribute to a decrease in immunity.

Symptoms

Acute osteomyelitis appears very suddenly. If children are small, then they are noted to be moody and lethargic. They don’t want to eat, they don’t sleep well, and their temperature rises. If the child is older, then he may feel unwell, general weakness, and may complain of toothache.

When the disease is still in its early stages, the following manifestations may be present:

• bone pain. Initially it has a local character, and then diffused;
• the oral mucosa swells, hyperemia is noted;
• on the side that is affected, the soft tissues become swollen;
• the face becomes asymmetrical;
• chewing muscles may spasm.

If an injury occurs, signs of the disease appear after 3-5 days. The child feels much worse, the temperature rises, and pus may also be released if the mucous membrane has been damaged.

Classification

Osteomyelitis can be classified according to location, route of penetration, and severity of the process.

If we talk about the course of the disease, then there is an acute or chronic type.

If we are talking about how the bone tissue became infected, then it is worth noting three types of osteomyelitis - post-traumatic, hematogenous, odontogenic.

If we take into account the localization of the purulent process, then it is worth distinguishing between the disease of the lower jaw and the upper jaw.