Septic arthritis pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
Septic arthritis most commonly develop as a result of hematogenous spreading of bacteria into the synovial membrane, that induces inflammatory reactions. Eventually, release of cytokines and activation of both host humoral and immunological response which damages articular surface and cartilage along with bacterial virulence factors.<ref name="pmid3288326">Klein RS (1988) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=3288326 Joint infection, with consideration of underlying disease and sources of bacteremia in hematogenous infection.] ''Clin Geriatr Med'' 4 (2):375-94. PMID: [https://pubmed.gov/3288326 3288326]</ref><ref name="pmid737020">Atcheson SG, Ward JR (1978) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=737020 Acute hematogenous osteomyelitis progressing to septic synovitis and eventual pyarthrosis. The vascular pathway.] ''Arthritis Rheum'' 21 (8):968-71. PMID: [https://pubmed.gov/737020 737020]</ref> | Septic arthritis most commonly develop as a result of hematogenous spreading of bacteria into the synovial membrane, that induces inflammatory reactions. Eventually, release of cytokines and activation of both host humoral and immunological response which damages articular surface and cartilage along with bacterial virulence factors.<ref name="pmid3288326">Klein RS (1988) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=3288326 Joint infection, with consideration of underlying disease and sources of bacteremia in hematogenous infection.] ''Clin Geriatr Med'' 4 (2):375-94. PMID: [https://pubmed.gov/3288326 3288326]</ref><ref name="pmid737020">Atcheson SG, Ward JR (1978) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=737020 Acute hematogenous osteomyelitis progressing to septic synovitis and eventual pyarthrosis. The vascular pathway.] ''Arthritis Rheum'' 21 (8):968-71. PMID: [https://pubmed.gov/737020 737020]</ref> | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Venkata Sivakrishna Kumar Pulivarthi M.B.B.S [2]
Overview
Septic arthritis most commonly develop as a result of hematogenous spreading of bacteria into the synovial membrane, that induces inflammatory reactions. Eventually, release of cytokines and activation of both host humoral and immunological response which damages articular surface and cartilage along with bacterial virulence factors.[1][2]
Pathophysiology
| Bacterial colonization and adherence into the synovium ⬇ | ||
|---|---|---|
| Mechanism of transmission | Hematogenous spread: Septic arthritis most commonly develop as a result of hematogenous spreading bacteria into the vascular synovial membrane.[1] Hematogenous spread is commonly associate with injection drug use, presence of indwelling catheters, and an underlying immunocompromised state such as HIV infection.
Determinants of hematognous seeding:[1]
Risk factors: Diabetes mellitus, HIV, immunosuppressants, intravenous drug abuse, osteoarthritis, prosthetic joint, rheumatoid arthritis.[3][4][5] Direct inoculation: Direct inoculation of microorganisms may occur during deep penetrating injuries, intra-articular steroid injection, arthroscopy or prosthetic joint surgery, particularly in association with knee and hip arthroplasties.[2][6][5] Risk factors: Previous history of intra-articular injection, prosthetic joint: early and delayed, recent joint surgery.[3] Contiguous spread: Bone infection such as osteomyelitis can spread by breaking through its outer cortex and then into the intracapsular region that lead to joint infection. | |
| Role of bacterial products in pathogenesis | Bacterial attachment protein receptors termed as microbial surface components recognizing adhesive matrix molecules (MSCRAMMs) that attach host joint extracellular matrix proteins such as collagen, laminin, elastin etc. and promote colonization and initiate the infectious process.[7][8] The role of bacterial products is activation of host immune response and deteriorate the tissue destruction.[9] | |
| Escape mechanism developed by pathogen | Adherence of pathogen to fibronectin on host tissue with its fibronectin receptors[10] ⬇ Internalization of pathogen by host mechanisms such as pseudopod formation or through receptor-mediated endocytosis via clathrin-coated pits[11] After internalization pathogen into the host cells such as osteoblasts, it survives intracellularly and induces apoptosis in the other cells through the activation of host immune response[12] | |
| Host immune response | Due to rapid proliferation of bacteria predesposes to activation of host acute inflammatory response
⬇ Synovial cells releases host inflammatory cytokines such as IL-1 and IL-6 into the synovium[13] ⬇ Activation of acute phase reactants by Interleukins[14] ⬇ Acute phase reactants bind to pathogen and promote opsonization and phagocytosis and activates complement system[15] ⬇ Phagocytosis of pathogen by macrophages, synovial cells and neutrophils with the release of inflammatory cytokines such as tumor necrosis factor, IL-6 and nitric oxide.[16] |
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| Humoral immunity and adaptive immunity also activates by superantigens of pathogens and promote clearance of pathogen by releasing Interferon-gamma, IL-4, IL-10 that reduces the host mortality and joint destruction.[17][18] | ||
| Joint destruction | As long as the immune system is able to remove the pathogen from synovium quickly, host is able to protect the joint. If immunosystem is weak or it is unable to clear the pathogen quickly, there is a potent activation of immune system that causes the joint destruction. | |
| Potent activation of immune system and release of cytokines and oxygen free radicles[19]
⬇ Activation and release of Metalloproteinases, Lysosomal enzyames and proteolytic enzymes from lysosomes, neutrophils and other inflammatory cells[20] ⬇ Further damage of joint by bacterial toxins[21] ⬇ Infectious process and inflammatory response lead to joint effusion[22][23][24] ⬇ Increased intra-articular pressure ⬇ Mechanical obstruction to the joint blood supply ⬇ Further destruction of bone and cartilage |
References
- ↑ 1.0 1.1 1.2 Klein RS (1988) Joint infection, with consideration of underlying disease and sources of bacteremia in hematogenous infection. Clin Geriatr Med 4 (2):375-94. PMID: 3288326
- ↑ 2.0 2.1 Atcheson SG, Ward JR (1978) Acute hematogenous osteomyelitis progressing to septic synovitis and eventual pyarthrosis. The vascular pathway. Arthritis Rheum 21 (8):968-71. PMID: 737020
- ↑ 3.0 3.1 3.2 Kaandorp CJ, Van Schaardenburg D, Krijnen P, Habbema JD, van de Laar MA (1995) Risk factors for septic arthritis in patients with joint disease. A prospective study. Arthritis Rheum 38 (12):1819-25. PMID: 8849354
- ↑ 4.0 4.1 Weston VC, Jones AC, Bradbury N, Fawthrop F, Doherty M (1999) Clinical features and outcome of septic arthritis in a single UK Health District 1982-1991. Ann Rheum Dis 58 (4):214-9. PMID: 10364899
- ↑ 5.0 5.1 Le Dantec L, Maury F, Flipo RM, Laskri S, Cortet B, Duquesnoy B et al. (1996) Peripheral pyogenic arthritis. A study of one hundred seventy-nine cases. Rev Rhum Engl Ed 63 (2):103-10. PMID: 8689280
- ↑ Gray RG, Tenenbaum J, Gottlieb NL (1981) Local corticosteroid injection treatment in rheumatic disorders. Semin Arthritis Rheum 10 (4):231-54. PMID: 6787706
- ↑ Herrmann M, Vaudaux PE, Pittet D, Auckenthaler R, Lew PD, Schumacher-Perdreau F et al. (1988) Fibronectin, fibrinogen, and laminin act as mediators of adherence of clinical staphylococcal isolates to foreign material. J Infect Dis 158 (4):693-701. PMID: 3171224
- ↑ Rydén C, Tung HS, Nikolaev V, Engström A, Oldberg A (1997) Staphylococcus aureus causing osteomyelitis binds to a nonapeptide sequence in bone sialoprotein. Biochem J 327 ( Pt 3) ():825-9. PMID: 9581562
- ↑ Yacoub A, Lindahl P, Rubin K, Wendel M, Heinegård D, Rydén C (1994) Purification of a bone sialoprotein-binding protein from Staphylococcus aureus. Eur J Biochem 222 (3):919-25. PMID: 8026501
- ↑ Lammers A, Nuijten PJ, Smith HE (1999) The fibronectin binding proteins of Staphylococcus aureus are required for adhesion to and invasion of bovine mammary gland cells. FEMS Microbiol Lett 180 (1):103-9. PMID: 10547450
- ↑ Essawi T, Na'was T, Hawwari A, Wadi S, Doudin A, Fattom AI (1998) Molecular, antibiogram and serological typing of Staphylococcus aureus isolates recovered from Al-Makased Hospital in East Jerusalem. Trop Med Int Health 3 (7):576-83. PMID: 9705193
- ↑ Ram S, Mackinnon FG, Gulati S, McQuillen DP, Vogel U, Frosch M et al. (1999) The contrasting mechanisms of serum resistance of Neisseria gonorrhoeae and group B Neisseria meningitidis. Mol Immunol 36 (13-14):915-28. PMID: 10698346
- ↑ Koch B, Lemmermeier P, Gause A, v Wilmowsky H, Heisel J, Pfreundschuh M (1996) Demonstration of interleukin-1beta and interleukin-6 in cells of synovial fluids by flow cytometry. Eur J Med Res 1 (5):244-8. PMID: 9374445
- ↑ Osiri M, Ruxrungtham K, Nookhai S, Ohmoto Y, Deesomchok U (1998) IL-1beta, IL-6 and TNF-alpha in synovial fluid of patients with non-gonococcal septic arthritis. Asian Pac J Allergy Immunol 16 (4):155-60. PMID: 10219896
- ↑ Verdrengh M, Tarkowski A (1998) Granulocyte-macrophage colony-stimulating factor in Staphylococcus aureus-induced arthritis. Infect Immun 66 (2):853-5. PMID: 9453655
- ↑ Sakiniene E, Bremell T, Tarkowski A (1997) Inhibition of nitric oxide synthase (NOS) aggravates Staphylococcus aureus septicaemia and septic arthritis. Clin Exp Immunol 110 (3):370-7. PMID: 9409638
- ↑ Hultgren O, Kopf M, Tarkowski A (1999) Outcome of Staphylococcus aureus-triggered sepsis and arthritis in IL-4-deficient mice depends on the genetic background of the host. Eur J Immunol 29 (8):2400-5. PMID: 10458752
- ↑ Puliti M, von Hunolstein C, Bistoni F, Mosci P, Orefici G, Tissi L (2000) Influence of interferon-gamma administration on the severity of experimental group B streptococcal arthritis. Arthritis Rheum 43 (12):2678-86. <2678::AID-ANR7>3.0.CO;2-A DOI:10.1002/1529-0131(200012)43:12<2678::AID-ANR7>3.0.CO;2-A PMID: 11145025
- ↑ Roy S, Bhawan J (1975) Ultrastructure of articular cartilage in pyogenic arthritis. Arch Pathol 99 (1):44-7. PMID: 1111494
- ↑ Riegels-Nielsen P, Frimodt-Møller N, Sørensen M, Jensen JS (1989) Antibiotic treatment insufficient for established septic arthritis. Staphylococcus aureus experiments in rabbits. Acta Orthop Scand 60 (1):113-5. PMID: 2929280
- ↑ Smith RL, Schurman DJ, Kajiyama G, Mell M, Gilkerson E (1987) The effect of antibiotics on the destruction of cartilage in experimental infectious arthritis. J Bone Joint Surg Am 69 (7):1063-8. PMID: 3654698
- ↑ Mitchell M, Howard B, Haller J, Sartoris DJ, Resnick D (1988) Septic arthritis. Radiol Clin North Am 26 (6):1295-313. PMID: 3051098
- ↑ Nelson JD, Koontz WC (1966) Septic arthritis in infants and children: a review of 117 cases. Pediatrics 38 (6):966-71. PMID: 5297142
- ↑ Knights EM (1982) Infectious arthritis. J Foot Surg 21 (3):229-33. PMID: 6749955