45Antibiotic Therapy of Septic Bursitis: Its Implication in the Treatment of Septic Arthritis
Arthritis and Rheumatism (1981) · G Ho Jr, E Y Su
This prospective study investigated the clinical course of septic bursitis (primarily olecranon, prepatellar, and infrapatellar bursae) treated with antibiotics and serial needle aspiration. Among 25 patients, those who received treatment within 2 weeks of symptom onset achieved culture sterility in about 1 week. Longer delays led to prolonged infection despite adequate therapy. All 19 patients who received 5 additional days of antibiotics after confirmed sterility were cured. The study confirms that infection of the bursa itself is a direct and treatable cause of bursitis, and that early intervention is essential to avoid prolonged inflammation. The findings have broader implications for managing bacterial infections in other joint-related structures.
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29Surgery Does Not Improve Long-Term Outcomes in Degenerative Meniscus Tears
British Journal of Sports Medicine (2020) · Raine Sihvonen, Mika Paavola, Antti Malmivaara, Ari Itälä, Antti Joukainen, Juha Kalske, Heikki Nurmi, Jaanika Kumm, Niko Sillanpää, Tommi Kiekara, Aleksandra Turkiewicz, Pirjo Toivonen, Martin Englund, Simo Taimela, Teppo L N Järvinen
This 5-year follow-up of the FIDELITY randomized, placebo-surgery controlled trial assessed the long-term effects of arthroscopic partial meniscectomy (APM) in 146 adults with degenerative medial meniscus tears. Compared to placebo surgery, APM showed no benefit in knee symptoms, function, or pain reduction, but was associated with a slightly higher risk of radiographic knee osteoarthritis. The findings suggest that APM does not offer long-term advantages and may accelerate joint degeneration in this population.
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37Local and Systemic Side Effects of Corticosteroid Injections for Musculoskeletal Indications
AJR American Journal of Roentgenology (2024) · Sarah I. Kamel, Humberto G. Rosas, Tetyana Gorbachova
This comprehensive review outlines both local and systemic adverse effects associated with corticosteroid injections used for musculoskeletal conditions. Local side effects include post-injection flare, skin hypopigmentation and atrophy, infection, tendon rupture, accelerated progression of osteoarthritis, and osseous injury. Systemic side effects encompass adrenal suppression or insufficiency, facial flushing, hypertension, hyperglycemia, and osteoporosis. The authors emphasize the importance of recognizing these potential side effects when counseling patients and planning individual injections. The review highlights the need for further research regarding the long-term complications of continuous corticosteroid use, particularly concerning osseous effects.
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93Prostaglandin E2 Drives Inflammation and Pain in Tendinopathy
Arthritis Research & Therapy (2019) · Bergqvist F, Carr AJ, Wheway K, Watkins B, Oppermann U, Jakobsson PJ, et al.
This laboratory study investigated the role of prostaglandins, specifically prostaglandin E2 (PGE2) and prostacyclin, in driving inflammation and pain in human tendinopathy. The researchers examined tendon biopsies from patients with symptomatic tendinopathy or tendon rupture, as well as healthy comparator tendons. They found that diseased tendon tissue showed increased expression of enzymes responsible for producing prostaglandins, including COX-1 and COX-2, which are the exact enzymes that NSAIDs like ibuprofen work to block. When tendon cells from diseased tissue were stimulated with an inflammatory trigger, they released large amounts of PGE2, while cells from healthy tendons did not. The researchers determined that PGE2 sustains inflammation and pain in tendon disease, while prostacyclin appears to have a protective role. Importantly, when diseased tendon cells were treated with naproxen, a standard NSAID, both PGE2 and prostacyclin production were inhibited. This study provides direct molecular evidence that the inflammatory pathway targeted by NSAIDs is active and driving pain in tendinopathy. The COX enzymes that NSAIDs inhibit are upregulated in diseased tendons, and the PGE2 they produce is responsible for sustaining the inflammatory cycle. This supports the targeted use of NSAIDs to reduce PGE2-driven inflammation in tendon conditions, while also highlighting the importance of dose control to avoid suppressing the potentially protective prostacyclin pathway.
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