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Last reviewed: 23.04.2024

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The term "osteomyelitis" is suggested for the inflammation of bone and bone marrow (in translation from Greek "osteomyelitis" - inflammation of the bone marrow). Currently, this term is understood as the infectious and inflammatory lesion of bone tissue (osteitis), bone marrow (myelitis), periosteum (periostitis) and surrounding soft tissue. Osteomyelitis is also defined as an infection in the bone.

Osteomyelitis is a local inflammatory process that develops in response to the invasion and proliferation of microbial bodies. The main starting point of hematogenous osteomyelitis is the endogenous invasion of microbial bodies into the medullary canal; in exogenous osteomyelitis, microbial invasion occurs as a result of a bone injury or surrounding tissue. Localization of inflammation serves as a protective reaction of the body, preventing the development of sepsis, which is possible if the mechanisms of delimitation of the purulent-necrotic process become untenable. This may be due to the high virulence and pathogenicity of microorganisms, the vastness of the lesion focus, the duration of the inflammatory process and the weakening of the protective forces of the macroorganism.

trusted-source[1], [2], [3], [4], [5], [6], [7], [8], [9]



Despite the steady progress in understanding the pathogenesis of osteoarticular infection and the introduction of modern diagnostic and treatment methods, the number of such patients in the last 30 years has no tendency to decline.

Acute hematogenous osteomyelitis is found in 2 out of 10 000 children, chronic osteomyelitis - in 2 out of 10 000 people, with the bones of the lower limbs being affected in 90% of cases. The tibia account for 50%, the femur - 30%, the fibular - 12%, the humerus - 3%, the ulnar - 3% and the radiation - 2% of the lesions of long bones. Currently, in the epidemiology of osteomyelitis of long bones trace several trends. There have been changes in the structure of hematogenous osteomyelitis. Leading industrialized countries report a decrease in the incidence of acute hematogenous osteomyelitis of long bones in children (2.9 new cases per 100 000 population per year) and Staphylococcus aureus, the main causative agent of the disease, from 55 to 31%. In countries with developed infrastructure, these diseases have become rare.

In recent years, there has been an increase in the number of patients with post-traumatic osteomyelitis. This is due, above all, to the increase in injuries, especially as a result of road accidents, with changes in microflora that can cause suppuration, and with disturbances in the human immune system. Development of bone infection is promoted by diabetes mellitus, obliterating vascular diseases, tumors, alcoholism and tobacco smoking. In adults, the main cause of osteomyelitis is a fracture of long bones. The development of this pathological condition depends on many factors and primarily on the localization and extent of bone and soft tissue damage, blood supply and innervation disorders, timeliness and quality of primary surgical treatment, antibiotic prophylaxis, choice of osteosynthesis and plastic wound closure. In this regard, the incidence of osteomyelitis varies widely - from 0.5-2% in the operative treatment of closed fractures and injuries of the upper limb to 50% and higher with open fractures of the lower leg and thigh with extensive soft tissue damage.

In modern conditions, the role of suppurative complications, including osteomyelitis, has increased, after gunshot wounds to the extremities, the main causes of which are the severity of injuries to bones and joints, as well as treatment defects committed during the stages of medical evacuation. According to the experience of post-war armed conflicts, the frequency of development of gunshot osteomyelitis is at least 9-20%.

Throughout the world, in the treatment of fractures, various types of submerged metallosteosynthesis have become widespread. Unjustified expansion of indications for operative methods in severe fractures with extensive damage to soft tissues, non-compliance with the timing and techniques of performing operations, incorrect choice of surgical manual and metalwork lead to severe purulent inflammation of bones and joints. Suppuration around the spokes and rods, as well as "spinal" osteomyelitis remain the most common complications in osteosynthesis by external fixation devices. In the world annually produce about 1 million prosthetic operations of the knee and hip joint. Therefore, a major problem, especially in developed countries, is osteomyelitis, which occurs after endoprosthetics.

trusted-source[10], [11], [12], [13], [14], [15],

Causes Osteomyelitis

What causes osteomyelitis?

In 1880, Louis Pasteur first isolated pest from the pus with osteomyelitis and named them staphylococci. Later it was established that any pyogenic microbes can cause osteomyelitis, and the clinical and morphological picture of the disease can depend on their species composition. Currently, the causative agent of acute hematogenous osteomyelitis of long bones in children is mainly monoflora (up to 95%). This is, as a rule, Staphylococcus aureus, allocated in 50-90% of cases. This microorganism remains the leading causative agent in all cases of osteomyelitis due to its osteochondrotropism and high adaptive capacity, which leads to the development of a large number of various antibiotic-resistant virulent strains and ultimately to a decrease in the effectiveness of conservative treatment.

In children up to a year, Streptococcus agalactiae and Escherichia coli are most often extracted from bone and blood, in children over one year old, Streptococcus pyogenes and Haemophilus influenzae. The cases of H. Influenzae discharge decrease in children after four years, which is connected with the use of a new vaccine against this pathogen.

In patients with acute post-traumatic osteomyelitis arising from open fractures with extensive damage to soft tissues, mixed aerobic-anaerobic associations are sown with a predominance of Gram-negative microorganisms, mainly Pseudomonas aeruginosa. Microbial contamination in the lesion, as a rule, is 106-108 microbial bodies in 1 g of bone tissue.

In chronic osteomyelitis, Gram-positive cocci of the genus Staphylococcus with a predominance of Staphylococcus aureus play a leading aetiological role, the seeding frequency of which depends on the stage of the process and ranges from 60 to 85%. In a chronic inflammatory process, staphylococci can be presented in monocultures or as part of aerobic-anaerobic associations. Gram-negative and anaerobic bacteria replace staphylococci, which are more resistant to widespread antibacterial drugs than gram-positive bacteria.


How does osteomyelitis develop?

Osteomyelitis can be caused by hematogenous spread of infection, direct penetration of microorganisms into the bone or from an adjacent, external focus of infection. In posttraumatic osteomyelitis, direct penetration of microbial flora occurs, due to tissue damage and blood supply disorders. The development of this form of osteomyelitis directly depends on the invasion of microorganisms, their number, species, virulence and the degree of damage to soft tissues. After adverse effects on the protective-adaptive reactions of the organism of various physical, biological factors and concomitant diseases, its ability to show an effective response to contain infection is reduced, which can contribute to the development of the initial stage of the disease.

Deep long-term infection of the bone is maintained due to the presence of a devascularized cortical layer, which is surrounded by bacteria. It acts as a foreign body, which serves as the main cause of osteomyelitis in most open fractures. Post-traumatic osteomyelitis, in addition to the usual pathogenic microorganisms, can also be caused by non-pathogenic staphylococcus and anaerobic cocci. They at the time of injury fall on the devitalized areas of the cortical layer and here, under anaerobic conditions, contribute to the sequestration and development of osteomyelitis. Such bone infection develops often after open fractures.

A number of systemic and local factors affect the immune response, metabolism and local blood supply in the development of osteomyelitis. Systemic factors include poor nutrition, impaired renal and hepatic function, diabetes mellitus, chronic hypoxia, immune diseases, malignant diseases, elderly and senile age, immunosuppression and immunodeficiency, splenectomy, viral infection, alcoholism and smoking. Local factors such as chronic lymphedema, venous stasis, vascular lesions, arteritis, severe scarring, fibrosis, pathology of small vessels and neuropathy also contribute to the development of infection.

Acute osteomyelitis is characterized as a purulent infection, accompanied by edema, vascular stasis and thrombosis of small vessels. In the acute period of the disease due to local inflammation, intraosseous and periosteal blood supply is violated, large fragments of the dead bone (sequestrants) are formed. The existence of infected, non-viable tissues and ineffective reaction of the macroorganism, as well as inadequate treatment lead to chronic illness. With the transition of the purulent process to the chronic stage, a gradual change in the microbial landscape takes place. The dominant role is played by the low-vulvalent strains of Staphylococcus epidermidis and Staphylococcus aureus.

Necrosis of bone tissue is an important feature of acute post-traumatic osteomyelitis. The dead bone slowly dissolves under the action of granulation tissue enzymes. Resorption occurs most rapidly and in early periods at the junction of live and necrotic bone. The dead spongy bone with localized osteomyelitis slowly resolves. The dead part of the cortical bone gradually separates from the living bone, forming a sequester. Organic elements in the dead bone are largely destroyed by the action of proteolytic enzymes produced by macrophages or polymorphonuclear leukocytes. Due to the violation of blood supply, the dead bone visually seems lighter than the live one. Small parts of the non-viable spongy bone dissolve within 2-3 weeks, sequestration of the cortical part may take months.

Morphological features of chronic osteomyelitis are the presence of necrosis of bone tissue, the formation of new bone and exudation of polymorphonuclear leukocytes, to which a large number of lymphocytes, histiocytes and sometimes plasma cells are attached. The presence of a dead bone often causes the formation of fistulas, through which pus enters the surrounding soft tissues and eventually leaves the surface of the skin, forming a chronic fistula. The density and thickness of the newly formed bone can gradually increase, forming part or all of the new diaphysis under relatively favorable conditions. Two parallel processes develop for many weeks or months, depending on the size of the necrosis, the extent and duration of the infection. Enlarged endostal bone can close the medullary canal.

After removal of the sequester, the remaining cavity can be filled with a new bone. This is especially common in children. Post-traumatic, secondary osteomyelitis develops as a result of damage to tissues caused by trauma, on the one hand, and by invasion and development of microorganisms, on the other. The lack of sufficient stabilization of the damaged bone leads to the development and spread of purulent infection, the formation of secondary necrosis and sequestration.

Most authors hold the opinion about the advisability of treating extensive wounds in patients with open fractures without early closure of the wound surface, which gives rise to the problem of fighting acute purulent infection. A long period of open management of such wounds is fraught with a real threat of osteomyelitis. Thus, the main reasons for the development of posttraumatic osteomyelitis in patients with open fractures should be considered:

  • untimely and inadequate surgical treatment of the lesion;
  • inferior, incorrectly chosen method of fixation;
  • long-existing extensive wound;
  • incorrect assessment of the degree of soft tissue damage;
  • insufficient postoperative control.

The timely removal of wound exudate during the temporary and final closure of the wound surface is of great importance for the prevention of osteomyelitis with open fractures. The accumulation of wound exudate also serves as one of the reasons for the development of secondary necrosis.

Analysis of the causes of posttraumatic osteomyelitis confirms the fact that submersion metallo-osteosynthesis is one of the factors influencing the frequency of development of purulent complications with open fractures and development of osteomyelitis. It is known that its use with open fractures with massive soft tissue damage, especially on the lower leg, sharply increases the risk of infection. Especially clearly this pattern is traced in gunshot fractures, which determined the opinion of a number of experts on the need to prohibit the use of submerged osteosynthesis in this type of injury.

Despite the fact that alloys used to make fixatives are considered to be immunologically inert, sometimes cases of "intolerance" of metals are observed. In severe cases, the result of such a reaction is the clinical picture of acute inflammation with fistula formation and secondary infection. This process is based on the formation of haptens - substances that arise as a result of biotransformation of the metal and the connection of its molecules with proteins, which creates the prerequisites for sensitization. Starting point for this process is the surface destruction of the implant as a result of oxidation by peroxide compounds, phagocytosis or mechanical destruction (in case of stability of bone fragments or friction of the fixative elements with each other). Sensitization to the metal can exist initially or develop as a result of submerged metallosteosynthesis.

A new stage in the deepening of knowledge about osteomyelitis is connected with the study of its pathogenesis at different levels of organization: submolecular, molecular, cellular and organ. The study of the main causative agents of osteomyelitis, such as Staphylococcus aureus, made it possible to identify extracellular and intracellular microbial mechanisms of aggression and invasion with which bacteria cause and support infection, directly damage bone cells, disrupt the protective immune response of the organism, and reduce the effectiveness of antibiotics. In recent years, actively studying the role of cytokines, one of the regulators of cellular and humoral immunity. A new, unknown earlier role of bone-producing cells - osteoblasts, capable of inducing antigen-specific activation of immune cells and inflammatory mediators in response to intracellular invasion of microorganisms in bone tissue is also shown. However, it should be noted that not everything is finally understood in the pathogenesis of osteomyelitis, taking into account a wide range of its manifestations. Many putative pathogenetic mechanisms are at the level of hypotheses.

Symptoms Osteomyelitis

How does osteomyelitis manifest?

As a rule, a detailed anamnesis is often enough to diagnose osteomyelitis. Children with hematogenous osteomyelitis may exhibit acute signs of infection, including fever, irritability, fatigue, weakness and local signs of inflammation. However, the atypical current is often met. In children with hematogenous osteomyelitis, soft tissues enveloping the affected bone are able to localize the infectious process. The joint is usually not infectious. In adults with hematogenous osteomyelitis, indeterminate signs are usually found, including prolonged pain and low-grade fever. There is also a high fever, chills, edema and flushing over the affected bone. With contact osteomyelitis, there is often limited bone and joint pain, hyperemia, swelling and exudation around the injury site. Signs of severe systemic inflammatory reaction, such as fever, chills and evening sweats, may be present in the acute phase of osteomyelitis, but they are not observed in the chronic phase. Both hematogenous and contact osteomyelitis can go to the chronic stage. She is observed constant pain, exudation and a small fever. Near the foci of infection, fistulous strokes are often found. If the fistulous course closes, the patient may develop an abscess or an acute common soft tissue infection.



According to the clinical course and duration of the disease, osteomyelitis is traditionally divided into acute and chronic. According to the pathogenetic principle, osteomyelitis is divided into hematogenous and post-traumatic, which can develop as a result of mechanical, operating, gunshot trauma of both bone tissue itself and surrounding soft tissues. Hematogenous osteomyelitis can manifest primarily chronic course (Brody's abscess, sclerosing Garre's osteomyelitis, Ollier's albuminous osteomyelitis).

Convenient for practical application is the clinico-anatomical classification of osteomyelitis of long bones in adults, adopted at the University of Texas Medical Department - Classification by Czerny-Madera. Classification is based on two principles: the structure of bone lesions and the patient's condition. According to this classification, structural bone lesions are conditionally divided into four types:

  • I type (medullary osteomyelitis) - lesion over a large extent of the structures of the medullary cavity of the long bone with hematogenous osteomyelitis and with suppuration after intramedullary osteosynthesis;
  • II type (superficial osteomyelitis) - damage only to the cortical bone, which usually occurs with direct infection of the bone or from an adjacent focus of infection in soft tissues; septic joint is also classified as superficial osteomyelitis (osteochondritis);
  • III type (focal osteomyelitis) - damage to the cortical bone and structures of the medullary canal. However, with this type of lesion, the bone is still stable, because the infectious process does not extend to the entire diameter of the bone;
  • IV type (diffuse osteomyelitis) - damage to the entire bone diameter with loss of stability; an example is an infected false joint, an osteomyelitis after an open, multi-lobed fracture.

trusted-source[16], [17], [18], [19], [20], [21]

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