Tenosynovitis - Pathogenesis

Piogenica tenosynovitis occurs by multiplication of the infectious agent in closed space the hand flexors tendons and synovial fluid culture. Natural immune response mechanisms cause edema and migration of inflammatory cells or mediators. Septic and inflammatory processes in the sheath of flexors interfering reaction mechanisms sliding rapidly, leading to adhesions and sclerosis.The final consequence is necrosis of tendon, tendon rupture and digital contracture.Inflammatory tenosynovitis is usually the result of rheumatoid arthritis and other inflammatory or degenerative processes, diabetes, and diseases of connective tissue suprauzajului.Microtraume suprauzaj syndromes causing cumulative tendon with stenosing tenosynovitis.Gonococcal infection originates from infected genital tract mucosa, rectum, or pharynx. Dissemination occurs in 3% of patients with mucosal infection. Approximately two thirds of patients with disseminated gonococcal infection develop tenosynovitis.
Suprauzaj syndromes.They show various stages of evolution leading to tenosynovitis flexors. Microtraume repetitive wear and tear is defined as lowering the possibility of adapting the tissue. Pathological stages of these syndromes include: inflammation, proliferation and finally maturation.Inflammation begins immediately after injury with the release of chemotactic and vasoactive substances. Inflammatory cells cause pain, swelling, redness and local heat. This stage can last from 48 hours to another injury. Proliferative stage lasts two weeks and is characterized by the production of collagen and matrix substances.The tendon is particularly vulnerable to damage during this period.Maturation stage lasts 12 weeks in the healing phase occurs. If at this stage fibrosis develops inflammation recurs through the re-release of inflammatory substances.Infection follows the path of lesser resistance along the tendon sheath. Infection can be introduced directly into the tendon sheath of skin through a wound or by extension most commonly in marrow and gonococcal tenosynovitis.A history of recent trauma is frequently affected area is a predisposing factor for development of tenosinovitei piogenice flexors. Suprauzajul leads to inflammation and the Quervain tenosynovitis.
Causes and Risk Factors
Quervain tenosynovitis of the thinning occurs by wear and tear of the sheath and first dorsal extensor compartment fibroosos canal collapse. Tenosynovitis flexors is considered to occur throughout the convention, but multiple etiologies have been identified.Hypertrophy trigger phenomenon is the first ring gear.Nongonococice infections are caused mainly by Staphylococcus aureus, and aerobic and anaerobic. Pasteurella multocida is common in cat bites. Eikenella corrodens appears in human bites.Animal and human bites have a component of mixed infections.Predisposing factors include diabetes, intravenous drug abuse or drug abuse, debility and arteriosclerosis obliterans. Micobacterium species can cause tenosynovitis, especially the immunocompromised.