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
Entry of the organism into bone is the first step in the development of osteomyelitis and occurs by three main mechanisms; hematogenous seeding, contiguous spread of infection to bone from adjacent soft tissue, and direct inoculation from trauma or orthopedic surgery (including prostheses).[1][2]
Microbial and host factors contributing to the pathological process of the disease may vary from one patient to another. In children, the long bones are usually affected. Acute osteomyelitis almost invariably occurs in children. In adults, the vertebrae and the pelvis are most commonly affected, possibly due to the compromised host resistance as a result of debilitation, intravenous substance abuse, infectious root-canaled teeth, or other disease or drugs (e.g., immunosuppressive therapy).
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 prostheses).
Pathogenesis
Several factors contributing to the pathogenesis of osteomyelitis include microbial factors and host factors.
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]
- Biofilm pathogens are more resistant to host defense and are able to survive longer than usual.[3]
Host factors
Host factors that may contribute to the pathogenesis of osteomyelitis are subdivided into factors that are involved in hematogenous spread and factors that may contribute to contiguous spread.
Hematogenous spread
- The pathogen colonizes the metaphysis of a large long bone below 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 observed 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 trigger inflammation and due to this inflammatory process, intraosseous pressure inside the tight bone matrix increases and may lead to thrombosis of bone vasculature that finally results in bone death.
- If the 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 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 around the dead area, resulting in the separation of the dead area of bone from the surrounding living bone, ultimately, forming theSequestrum.
- When periosteal stripping occurs, the resulting periosteal reaction produces a shell of new bone; the Involucrum, around the dead bone.
Associated conditions
- Factors that may commonly complicate osteomyelitis are fractures of the bone, amyloidosis, endocarditis, or sepsis.
- 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 often 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
- ↑ 1.0 1.1 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 2.2 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.