Osteomyelitis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1],Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]
Overview
Pathogens can involve the bone by 3 ways. Hematogenous seeding, contiguous spread of infection to bone from adjacent soft tissue and direct inoculation from trauma or orthopedic surgery (including prosthetics).
Microbial factors and host factors are contributing to pathological process of disease that may vary from one patient to another.
Pathophysiology
Entry of the organism into bone is the first step in osteomyelitis and occurs by three main mechanisms:[1][2]
- Hematogenous seeding
- Contiguous spread of infection to bone from adjacent soft tissue
- Direct inoculation from trauma or orthopedic surgery (including prosthetics).
Pathogenesis
Several factors contributing to pathogenesis of osteomyelitis include,
Microbial factors
- Etiologic pathogen possesses numerous cell-wall associated adhesins mediating specific attachment to a wide variety of extracellular matrix proteins found in bone including, fibronectin, laminin, osteopontin, bone matrix sialoprotein and collagen.[2]
- After attachment to the bone matrix, direct toxin effect of pathogen may lead to tissue necrosis.
- Adherent bacterial growth leads to the formation of a biofilm (an adherent consortium of micro-organisms enmeshed in an exocellular polysaccharide).[3]
- Biofilmed pathogens are more resistant to host defense and are able to survive longer than usual.[3]
Host factors
Hematogenous spread
- The pathogen most commonly localizes to the metaphysis of a large long bone just beneath the growth plate.
- In adults, after closure of the growth plate, the metaphyseal and epiphyseal vessels establish reconnections so bacteria entering the nutrient artery are directed to the vascular loops beneath the articular cartilage.
- Accordingly, acute hematogenous osteomyelitis in infants and adults often affects the epiphysis.
- In children the growth plate acts as an barrier and the infection is limited to the metaphysis.[4]
- Extension across the growth plate is impeded in children but after closure of growth palate, joint involvement becomes possible.
- In the spine, blood-borne pathogens usually localize to the subchondral regions of the vertebral body.
contiguous spread
- In contiguous spread, bone adjacent to a cutaneous or mucosal ulcer or soft tissue abscess are affected.
- It is more commonly seen in the setting of periodontal and sinus disease, cellulitis of diabetic feet, epidural abscess, decubitus ulcer, or septic arthritis.[5][6]
- In this setting the inflammatory process must first destroy the periosteum or articular surface before it accesses the bone.
- Unlike hematogenous osteomyelitis, the cortex instead of the medullary cavity is initially infected, and the site at which this occurs influences the rapidity of spread and extent of disease.
Pathologic process
- Pathogens triggers inflammation and due to this inflammatory process, intraoseous pressure inside the tight bone matrix increases and may lead to thrombosis of bone vasculature that finally results in bone death.
- If infection progresses, pus may track to other areas of the bone along the medullary canal or through the Haversian systems in cortical bone from the medulla to the outer surface of the cortex and form a subperiosteal abscess.
- This may contribute to a bacteremia or it may track out into the soft tissues and eventually form abscesses or a sinus tract draining to the outside.
- Dead bone accelerates biofilm formation.
- Both the inflammatory cytokines and mediators released during infection, and in some cases bacterial products themselves, can trigger bone resorption either by osteoclast activation or by stimulating phagocytic cells to take on a bone-resorbing phenotype.[7]
- Bone loss starts from around the dead area and will cause separating it from the surrounding living bone and ultimately, to form the sequestrum.
- At the same time, where periosteal stripping has occurred, the resulting periosteal reaction produces a shell of new bone, the involucrum, around the dead bone.
Factors that may commonly complicate osteomyelitis are fractures of the bone, amyloidosis, endocarditis, or sepsis.
In children, the long bones are usually affected. In adults, the vertebrae and the pelvis are most commonly affected.
Acute osteomyelitis almost invariably occurs in children. When adults are affected, it may be because of compromised host resistance due to debilitation, intravenous drug abuse, infectious root-canaled teeth, or other disease or drugs (e.g. immunosuppressive therapy).
Osteomyelitis is a secondary complication in 1-3% of patients with pulmonary tuberculosis. In this case, the bacteria generally spread to the bone through the circulatory system, first infecting the synovium (due to its higher oxygen concentration) before spreading to the adjacent bone. In tubercular osteomyelitis, the long bones and vertebrae are the ones which tend to be affected.
Gross Pathology
Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology.
Microscopic Pathology
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References
- ↑ Gristina AG, Oga M, Webb LX, Hobgood CD (1985). "Adherent bacterial colonization in the pathogenesis of osteomyelitis". Science. 228 (4702): 990–3. PMID 4001933.
- ↑ 2.0 2.1 Clarke SR, Foster SJ (2006). "Surface adhesins of Staphylococcus aureus". Adv. Microb. Physiol. 51: 187–224. doi:10.1016/S0065-2911(06)51004-5. PMID 17010697.
- ↑ 3.0 3.1 Gristina AG, Costerton JW (1984). "Bacterial adherence and the glycocalyx and their role in musculoskeletal infection". Orthop. Clin. North Am. 15 (3): 517–35. PMID 6472832.
- ↑ Jansson A, Jansson V, von Liebe A (2009). "[Pediatric osteomyelitis]". Orthopade (in German). 38 (3): 283–94. doi:10.1007/s00132-008-1402-6. PMID 19305968.
- ↑ Bluestein D, Javaheri A (2008). "Pressure ulcers: prevention, evaluation, and management". Am Fam Physician. 78 (10): 1186–94. PMID 19035067.
- ↑ van Asten SA, La Fontaine J, Peters EJ, Bhavan K, Kim PJ, Lavery LA (2016). "The microbiome of diabetic foot osteomyelitis". Eur. J. Clin. Microbiol. Infect. Dis. 35 (2): 293–8. doi:10.1007/s10096-015-2544-1. PMC 4724363. PMID 26670675.
- ↑ Lau YS, Wang W, Sabokbar A, Simpson H, Nair S, Henderson B, Berendt A, Athanasou NA (2006). "Staphylococcus aureus capsular material promotes osteoclast formation". Injury. 37 Suppl 2: S41–8. doi:10.1016/j.injury.2006.04.008. PMID 16651071.