Characteristics that may predispose patients to HO following hip arthroscopy include capsulotomy and acetabuloplasty with osteochondroplasty for mixed-type FAI and a large amount of bone resection, although these arthroscopic procedures have not been specifically studied [3, 10]. Similarly, the proximity of periosteal disruption to damaged musculature about the hip may contribute to a high propensity for HO after other hip surgery, including hip arthroplasty, acetabular trauma, and surgical hip dislocation [11, 12]. Rath et al. [13] hypothesized that capsule repair after hip arthroscopy decreased HO by blocking the interface between the injured periosteum and necrotic or damaged muscle, while Amar et al. [14] reported that capsule repair did not seem to alter the rate of HO compared to a control group of patients in whom the capsulotomy was not repaired. In our study, most patients underwent capsulotomy or osteochondroplasty, but the incidence of HO was not as high (4.28%) as reported. In 13 of the 14 patients (92.9%), HO formation was in the central area of the arthroscopic portals placed during the primary surgery (anterior or anterolateral portion of hip joint), so we thought that gentle soft tissue handling (minimizing portal trauma and peri-articular soft tissue damage) and fluid evacuation of the bony debris from the osteochondroplasty are more important than the capsulotomy or osteochondroplasty for preventing HO after hip arthroscopy; however, we did not have sufficient patients to assess the power of this comparison, which merits further study.
Symptoms of HO include articular disability, stiffness, pain, and crepitation, but most have minimal or no clinical or functional significance. Moreover, in around 64% of patients the ectopic ossification is a self-limited naturally resolving entity that does not require surgical intervention [15]. Nevertheless, if persistent pain or limited articular activity is seen, then it is important to suspect HO, although the clinical manifestations are difficult to isolate from other sources of postoperative pain. A mechanical blockage can explain the motion pain if the HO has formed in the plane of motion, mainly anterior and lateral. In our revision hip arthroscopy for HO excision patients, the HO was located anterior to the iliopsoas in one and anterolateral to the capsule in the other. Examinations showed that severe pain was induced during hip flexion, adduction, and internal rotation. This motion pain had resolved nearly completely at 1 year and no further treatment was required at the most recent follow-up.
HO lesions must be allowed to mature fully before surgical excision. Bedi et al. [5] treated 7 of 29 patients who developed HO postoperatively with revision surgery to excise the HO a mean of 11.6 months after the prior hip arthroscopy. Beckman et al. [10] reported arthroscopic HO resection in 9 of 34 patients who developed HO at 12 months postoperatively. This 12-month period was used to ensure full maturation of the HO and to allow for adequate recovery from the prior hip arthroscopy. Animal studies show that ectopic bone formation begins within 5 days of injury [16]. In humans, ossification is evident radiographically by 6 weeks and does not progress further at 12 to 24 weeks [17, 18]. Therefore, we treated both patients who developed symptomatic HO postoperatively with revision hip arthroscopy 12 months after the prior hip arthroscopy.
The best treatment of HO is prevention. Low-dose irradiation and NSAIDs are two common methods to prevent HO. NSAIDs are thought to limit HO by inhibiting cyclooxygenase and preventing prostaglandin synthesis. This may result in the inhibition of mesenchymal cell proliferation [19] and differentiation of mesenchymal cells into osteogenic cells [20]. Various NSAIDs have been shown to decrease postoperative HO [21, 22]. Indomethacin is the most extensively studied NSAID for use in preventing HO. Bedi et al. [5] found that taking indomethacin after hip arthroscopy is effective at preventing HO, particularly in males after osteoplasty. They found that HO developed postoperatively in 29 (21 males, 8 females) of 616 hip procedures (4.7%). The HO rate for cases with and without prophylactic indomethacin was 1.8% (6 of 339) and 8.3% (23 of 277), respectively. The duration of indomethacin prophylaxis is generally 6 weeks, although some reports suggest 3 weeks is effective [20]. Ionizing radiation influences rapidly dividing cells by altering the nuclear DNA. Thus, early postoperative radiation may prevent the differentiation of some pluripotent mesenchymal cells into osteoblasts [23]. There is currently little evidence to support the routine use of prophylaxis for HO in arthroplasty patients, but some investigators recommend prophylaxis for high-risk patients [24]. In our study, all of the patients were treated with an NSAID (range 3–6 weeks) after primary hip arthroscopy and underwent prophylactic radiotherapy (10 Gy) and were prescribed indomethacin (100 mg/day, for 6 weeks) after revision hip arthroscopy.
There were several limitations to this study. First, it was a single-institution retrospective study, so the number of patients was too small to generate significant results. Second, the radiological evaluation of developing HO is subjective. To increase the objectivity, one radiologist and two orthopedic surgeons, all board certified, evaluated the radiological imaging. Third, this study did not make comparisons with a non-prophylaxis group. Fourth, although one senior surgeon performed the hip arthroscopy, some cases underwent more aggressive osteochondroplasty or a more extended capsulotomy, which resulted in more soft tissue damage and bony debris. Further well-controlled prospective studies should be conducted to address different arthroscopic techniques to reduce HO after hip arthroscopy.
