Nonsteroidal Anti-Inflammatory Drugs and Oral Corticosteroids Mitigated the Risk of Arthrofibrosis After Total Knee Arthroplasty

Salmons, Harold I.; Payne, Ashley N; Taunton, Michael J.; Owen, Aaron R; Fruth, Kristin M.; Berry, Daniel J.; Abdel, Matthew P.

doi:10.1016/j.arth.2023.03.076

Cited by 8 publications

(3 citation statements)

References 33 publications

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“…Existing treatments for knee arthrofibrosis are limited, with clinical and in vivo evidence supporting the use of anti-inflammatory medications perioperatively to alter disease pathogenesis. 7,8,28 Identifying a medication that may be administered perioperatively to help prevent arthrofibrosis remains appealing. In the present investigation, AdipoRon, a synthetic, orally bioavailable, adiponectin mimetic, instilled in serial IV once daily doses for 6 consecutive days significantly increased (i.e., improved) PEA in a dose-dependent manner in our rabbit model of arthrofibrosis.…”

Section: Discussionmentioning

confidence: 99%

Efficacy of ADIPOR1 and ADIPOR2 peptide‐agonist AdipoRon in preventing contracture in a rabbit model of arthrofibrosis

Salmons,

Carstens,

Limberg

et al. 2024

Journal Orthopaedic Research

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AdipoRon is an adiponectin receptor 1, 2 (ADIPOR1 and ADIPOR2) agonist with potential antifibrotic effects. Whether AdipoRon can mitigate joint stiffness in a rabbit model of arthrofibrosis is unknown. We examined the efficacy of intravenous (IV) AdipoRon at mitigating contracture in a rabbit model of knee arthrofibrosis. Fifty‐six female New Zealand White rabbits were divided into three dosing groups: vehicle (dimethyl sulfoxide, DMSO), 2.5 mg/kg AdipoRon, and 5 mg/kg AdipoRon. AdipoRon, in DMSO, was administered IV preoperatively and for 5 days postoperatively (30 rabbits, Aim 1). AdipoRon was again dosed similarly after Kirschner wire (K‐wire) removal at 8 weeks (26 rabbits; Aim 2). The primary outcome of joint passive extension angle (PEA,°) was measured at 8, 10, 12, 16, and 24 weeks following index surgery. At 24 weeks, rabbits were euthanized and limbs were harvested to measure posterior capsular stiffness (N cm/°). In Aim 1, the 5 mg/kg treated rabbits had a significant increase in PEA when compared to controls at 16‐week (p < 0.05). In Aim 2, the 5 mg/kg treated rabbits had a significant increase in PEA when compared to controls at 10‐week (p < 0.05). In both aims, no significant differences were observed at later time points. Capsular stiffness was no different in any group. We are the first to report the efficacy of IV AdipoRon in a rabbit model of arthrofibrosis. We identified a significant dose‐dependent decrease in joint PEA at early time points; however, no differences were observed between groups at later time points. Clinical Significance: The present investigation provided the first assessment of AdipoRon's efficacy in mitigating knee stiffness in the current gold standard rabbit model of arthrofibrosis. Results of this investigation provided further evidence as to the potential role of AdipoRon as a preventative for arthrofibrosis in large mammals.

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Section: Discussionmentioning

confidence: 99%

Efficacy of ADIPOR1 and ADIPOR2 peptide‐agonist AdipoRon in preventing contracture in a rabbit model of arthrofibrosis

Salmons,

Carstens,

Limberg

et al. 2024

Journal Orthopaedic Research

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“…Additional support for the use of these medication classes in arthrofibrosis was provided by Salmons et al, who showed that perioperative NSAIDs, most commonly celecoxib, naproxen, and meloxicam, reduced the odds of arthrofibrosis by 33%. In comparison, oral corticosteroids (prednisone and hydrocortisone) reduced the odds of MUA by 74% 136 . It is important to note that neither the study by Premkumar et al nor that by Salmons et al reports or makes suggestions on dosages of these medications.…”

Section: Pharmacological Interventionsmentioning

confidence: 90%

Arthrofibrosis After Total Knee Arthroplasty

Ramos,

Pasqualini,

Surace

et al. 2023

JBJS Reviews

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» Arthrofibrosis after total knee arthroplasty (TKA) is the new formation of excessive scar tissue that results in limited ROM, pain, and functional deficits.» The diagnosis of arthrofibrosis is based on the patient's history, clinical examination, absence of alternative diagnoses from diagnostic testing, and operative findings. Imaging is helpful in ruling out specific causes of stiffness after TKA. A biopsy is not indicated, and no biomarkers of arthrofibrosis exist.» Arthrofibrosis pathophysiology is multifactorial and related to aberrant activation and proliferation of myofibroblasts that primarily deposit type I collagen in response to a proinflammatory environment. Transforming growth factor-beta signaling is the best established pathway involved in arthrofibrosis after TKA.» Management includes both nonoperative and operative modalities. Physical therapy is most used while revision arthroplasty is typically reserved as a last resort. Additional investigation into specific pathophysiologic mechanisms can better inform targeted therapeutics.

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“…Additionally, the incorporation of preoperative oral corticosteroids has proven to be effective in the reduction of MUA rates as well. 60 However, further research is required to know whether these benefits extend to the pediatric population.…”

Section: Preventing Arthrofibrosismentioning

confidence: 99%