The American journal of sports medicine · 2026
Triamcinolone Acetonide Is Not Harmful to Healthy and Osteoarthritic Human Knee Cartilage.
СтатьяНазвание и аннотация: Перевод в очереди
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Porter Annie, Nguyen Julie, Peng Ying, DiStefano Steven, Asres Naod, Snyder-Mackler Lynn, Axe Michael, Lu X Lucas
Аннотация
BACKGROUND: Intra-articular triamcinolone acetonide (TA) injections are commonly used to manage joint synovitis despite reports that they accelerate cartilage degeneration. Previous studies found that TA minimally affected bovine cartilage, but effects in human cartilage remain unclear.
PURPOSE: To determine how TA in physiologically relevant concentrations influences chondrocyte viability and matrix metabolism in healthy and osteoarthritic (OA) human cartilage.
STUDY DESIGN: Controlled laboratory study.
METHODS: Human cartilage was harvested from cadaver donor knees (mean age, 38 years; 4 male) or total knee replacement remnants (mean age, 66 years; 9 female, 7 male). Samples were exposed to TA, 200 μM (0.087 mg/mL) or 1 nM, to evaluate chondrocyte viability and gene expression. A high-resolution click chemistry assay quantified glycosaminoglycan (GAG) and collagen synthesis and tracked GAG loss. Two dosing regimens were tested: a continuous 14-day exposure (multiple-injection simulation) and a 2-day exposure followed by a 14-day recovery (single-injection simulation).
RESULTS: TA did not reduce chondrocyte viability and did not increase baseline GAG loss from the cartilage samples. In healthy cartilage, TA downregulated MMP13 (mean ± SD; 1.0 ± 0.8 vs 0.4 ± 0.2; P = .04) and COL2A1 (1.0 ± 0.3 vs 0.5 ± 0.2; P = .003). In OA cartilage, 200 μM TA downregulated MMP13 (1.0 ± 0.7 vs 0.2 ± 0.3; P = .02), ADAMTS5 (1.0 ± 0.3 vs 0.4 ± 0.1; P = .03), and COL2A1 (1.0 ± 0.3 vs 0.7 ± 0.2; P = .05). A continuous 14-day 200 μM TA exposure reduced GAG synthesis by 26% in OA cartilage (P < .001) and 18% in healthy cartilage (P = .004), but 1 nM TA had no effect. Collagen synthesis was reduced only in healthy cartilage by 25% (200 μM TA; P < .001) and 21% (1 nM TA; P = .004). A single-injection simulation produced no change in GAG or collagen synthesis in healthy cartilage.
CONCLUSION: In intact human cartilage under these experimental conditions, TA had no measurable toxicity to chondrocytes and only modestly, reversibly suppressed matrix synthesis at doses far exceeding clinical exposure. Intra-articular TA poses minimal measured direct risk to cartilage integrity when used for synovitis management.
CLINICAL RELEVANCE: These findings support the clinical use of TA for synovitis while alleviating concerns about direct cartilage damage, even with multiple injections.
PURPOSE: To determine how TA in physiologically relevant concentrations influences chondrocyte viability and matrix metabolism in healthy and osteoarthritic (OA) human cartilage.
STUDY DESIGN: Controlled laboratory study.
METHODS: Human cartilage was harvested from cadaver donor knees (mean age, 38 years; 4 male) or total knee replacement remnants (mean age, 66 years; 9 female, 7 male). Samples were exposed to TA, 200 μM (0.087 mg/mL) or 1 nM, to evaluate chondrocyte viability and gene expression. A high-resolution click chemistry assay quantified glycosaminoglycan (GAG) and collagen synthesis and tracked GAG loss. Two dosing regimens were tested: a continuous 14-day exposure (multiple-injection simulation) and a 2-day exposure followed by a 14-day recovery (single-injection simulation).
RESULTS: TA did not reduce chondrocyte viability and did not increase baseline GAG loss from the cartilage samples. In healthy cartilage, TA downregulated MMP13 (mean ± SD; 1.0 ± 0.8 vs 0.4 ± 0.2; P = .04) and COL2A1 (1.0 ± 0.3 vs 0.5 ± 0.2; P = .003). In OA cartilage, 200 μM TA downregulated MMP13 (1.0 ± 0.7 vs 0.2 ± 0.3; P = .02), ADAMTS5 (1.0 ± 0.3 vs 0.4 ± 0.1; P = .03), and COL2A1 (1.0 ± 0.3 vs 0.7 ± 0.2; P = .05). A continuous 14-day 200 μM TA exposure reduced GAG synthesis by 26% in OA cartilage (P < .001) and 18% in healthy cartilage (P = .004), but 1 nM TA had no effect. Collagen synthesis was reduced only in healthy cartilage by 25% (200 μM TA; P < .001) and 21% (1 nM TA; P = .004). A single-injection simulation produced no change in GAG or collagen synthesis in healthy cartilage.
CONCLUSION: In intact human cartilage under these experimental conditions, TA had no measurable toxicity to chondrocytes and only modestly, reversibly suppressed matrix synthesis at doses far exceeding clinical exposure. Intra-articular TA poses minimal measured direct risk to cartilage integrity when used for synovitis management.
CLINICAL RELEVANCE: These findings support the clinical use of TA for synovitis while alleviating concerns about direct cartilage damage, even with multiple injections.