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Nonsteroidal anti-inflammatory drugs have been widely prescribed for orthopaedic patients to relieve pain and chronic inflammation. However, it has been demonstrated that NSAIDs suppress bone repair and remodeling in vivo. We have reported that ketorolac inhibits bone repair in vivo and its critical effective timing is at the early stage of endochondral ossification. Our previous results showed that ketorolac and indomethacin inhibit osteoblast proliferation in vitro, suggesting that this effect may be one of the mechanisms contributing to the suppressive effect of NSAIDs on bone remodeling. Cell proliferation and death of osteoblasts should be well regulated through some relative apoptotic and mitotic factors during normal bone remodeling process. Accordingly, we proposed that the induction of osteoblastic cell death of NSAIDs might be one of the mechanisms involving their suppressive effect on bone remodeling in vivo. In this study, we investigated whether NSAIDs arrest osteoblastic cell cycle and/or induce cell death. Whether the mechanism was mediated through prostaglandin (PG) pathway. We tested the effects of ketorolac, indomethacin, diclofenac, piroxicam on cell cycle kinetics, cytotoxicity, and cell death pattern in osteoblast-enriched cultures derived from fetal rat calvaria. Our results showed that ketorolac and indomethacin arrested cell cycle at G₀/G₁ phase. All the 4 NSAIDs had cytotoxic effects and these effects were concentration dependent. The sequence of the cytotoxic effects of these four NSAIDs at 10^-4 M were indomethacin > diclofenac > ketorolac > piroxicam. Both PGE₁ and PGE₂ (10^-10 -10^-8 M) also significantly elevated the LDH leakage of osteoblasts, while PGF_2α had no significant effect. These results revealed that the cytotoxic effects of NSAIDs on osteoblasts might not be through inhibiting prostaglandin synthesis. They may be through PG-independent pathways. The results from flow cytometry followed by AnnexinV-FITC and propidium iodide double staining showed that 24 hours treatment of all the 4 NSAIDs (10^-6 and 10^-4 M) significantly induced both apoptosis (p<0.01) and necrosis (p<0.01, or p<0.05) in osteoblast cultures. These effects of NSAIDs on cell cycle arrest and cell death induction in osteoblasts may be one of the important mechanisms contributing to their suppressive effect on bone repair and bone remodeling in vivo.

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Background: The purpose of this meta-analysis is to provide an evidence-based overview of the effectiveness of corticosteroid injection for the treatment of stenosing tenosynovitis (trigger digits). We have analysed only randomised control trials (RCTs) which compared the effectiveness of corticosteroid injections with control injections.

Methods: The Cochrane Library, PubMed, Medline, Web of Science and Scopus were searched to identify relevant studies. The keywords for search in the database were (‘stenosing tenosynovitis’ OR ‘trigger finger’) AND injections. After screening titles and abstracts of these studies, full-text articles of studies that fulfilled the selection criteria were obtained. For the meta-analysis, we determined the pooled mean failure rate, odds ratio (OR), relative risk (RR) and 95% confidence intervals (CI) for the risk of failure rate between the corticosteroid injection group and the control group through the random-effects model.

Results: Six RCTs were found that involved 368 participants. The corticosteroid injection group included 190 patients and 178 patients were included in the control group. The pooled estimate of successful treatment in the corticosteroid injections group was 63.68 ± 5.32% and that in the control group was 27.53 ± 11.52%. The pooled RR of treatment failure between the corticosteroid injection group and the control group was 0.49 (95% CI 0.40–0.60). The pooled OR of treatment failure between the corticosteroid injection group and the control group was 0.18 (95% CI 0.08–0.44). All the included studies reported either mild or no complications with corticosteroids or placebo injections.

Conclusions: In the treatment of stenosing tenosynovitis, the corticosteroid injections have better outcomes compared to the control injections and this meta-analysis provides significant evidence of the effectiveness of corticosteroid injection for stenosing tenosynovitis with minimal adverse effects.

Level of Evidence: Level II (Therapeutic)

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used for their analgesic, antipyretic, and anti-inflammatory properties. However, they are also associated with a broad spectrum of hypersensitivity reactions, ranging from mild cutaneous manifestations to severe systemic responses. The complex nature of these reactions and their underlying mechanisms pose challenges in diagnosis and management.

We review the clinical evidence to six distinct clinical phenotypes of NSAID hypersensitivity, including: NSAID-induced urticaria/angioedema or anaphylaxis (SNIUAA), NSAID-exacerbated respiratory disease (NERD), NSAID-exacerbated cutaneous disease (NECD), NSAID-induced urticaria/angioedema (NIUA), food-dependent NSAID-induced hypersensitivity reactions (FDNIH), and selective NSAID-induced delayed reactions (SNIDR). This review aims to provide a comprehensive review of NSAID hypersensitivity reactions based on clinical phenotyping, which can aid in understanding and managing these adverse events.