Nonsteroidal Anti-inflammatory Drugs as Prophylaxis for Heterotopic Ossification after Total Hip Arthroplasty

Abstract

Heterotopic ossification (HO) is a frequent complication after total hip arthroplasty (THA). Nonsteroidal anti-inflammatory drugs (NSAIDs) have been used as routine prophylaxis for HO after THA. However, the efficacy of NSAIDs on HO, particularly selective NSAIDs versus nonselective NSAIDs, is uncertain.We searched PubMed, Embase, the Cochrane Central Register of Controlled Trials, and clinicaltrials.gov to identify randomized controlled trials with respect to HO after THA. Two reviewers extracted the data and estimated the risk of bias. For the ordered data, we followed the Bayesian framework to calculate the odds ratio (OR) with a 95% credible interval (CrI). For the dichotomous data, the OR and 95% confidence interval (CI) were calculated using Stata version 12.0. The subgroup analyses and the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) approach were used.A total of 1856 articles were identified, and 21 studies (5995 patients) were included. In the NSAIDs versus placebo analysis, NSAIDs could decrease the incidence of HO, according to the Brooker scale (OR = 2.786, 95% CrI 1.879–3.993) and Delee scale (OR = 9.987, 95% CrI 5.592–16.17). In the selective NSAIDs versus nonselective NSAIDs analysis, there was no significant difference (OR = 0.7989, 95% CrI 0.5506–1.125) in the prevention of HO. NSAIDs could increase discontinuation caused by gastrointestinal side effects (DGSE) (OR = 1.28, 95% CI 1.00–1.63, P = 0.046) more than a placebo. Selective NSAIDs could decrease DGSE (OR = 0.48, 95% CI 0.24–0.97, P = 0.042) compared with the nonselective NSAIDs. There was no significant difference with respect to discontinuation caused by nongastrointestinal side effects (DNGSE) in NSAIDs versus a placebo (OR = 1.16, 95% CI 0.88–1.53, P = 0.297) and in selective NSAIDs versus nonselective NSAIDs (OR = 0.83, 95% CI 0.50–1.37, P = 0.462).NSAIDs might reduce the incidence of HO and increase DGSE in the short-term.

NF-κB/MAPK activation underlies ACVR1-mediated inflammation in human heterotopic ossification

“…IL-6, IL-10, monocyte chemoattractant (MCP1), effluent IP10 (IFN-γ-induced protein), and macrophage inflammatory protein 1 α (MIP1-α) are also associated with heterotopic ossification from high-energy trauma (19). Antiinflammatory treatments like glucocorticoids and nonsteroidal antiinflammatory drugs (NSAIDs) are the mainstay of current treatment for heterotopic ossification (20)(21)(22)(23). Although these strategies attempt to mitigate the inflammation and subsequent bone formation, these drugs show low efficacy in blocking heterotopic ossification.…”

Demethylation of ITGAV accelerates osteogenic differentiation in a blast-induced heterotopic ossification in vitro cell culture model

“…In such cases, the incidence of HO can be as high as 63% when the mechanism of injury is a single high energy shock wave [ 14 , 15 ]. Current methods of prophylaxis, such as non-steroidal anti-inflammatory drugs [ 10 , [16] , [17] , [18] , [19] ] and radiotherapy [ 18 , 20 ], can reduce the incidence of trauma-induced HO, but are by no means a cure for the disease [ 21 , 22 ]. Thus, there is a need to develop model systems capable of breaking down the individual components causative of trauma-induced HO, to study their specific roles in disease onset, so that we can identify new therapeutics to prevent HO.…”

Cementless Primary Total Hip Arthroplasty with a Trabecular Titanium Implant: Results at Short-to-Medium-Term Follow-Up

“…Antibiotic prophylaxis with second generation cephalosporin (or clindamycin in case of beta-lactam allergy) and antithromboembolic prophylaxis was administered to every patient. Patients also received a heterotopic ossification (HO) prophylaxis, [9][10][11][12] with indomethacin 50mg twice per day for 15 days or celecoxib 200 mg once a day for 15 days for patients suffering from gastritis.…”