December 01, 2016
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Heterotopic ossification after total hip arthroplasty: Why that difference?

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Per Kjaersgaard-Andersen, MD
Per Kjaersgaard-Andersen

In the Cover Story of this issue of Orthopaedics Today Europe, experts across Europe detail their clinical and scientific experiences with heterotopic ossification that develop after surgical and non-surgical events in patients.

Heterotopic ossification (HO) following total hip arthroplasty (THA) has been researched in recent years and yet we still do not either understand its evolution in detail nor do we know entirely how to prevent its development. In my younger years, our team participated in this HO research, especially on how to prevent its development by adding pharmaceuticals to surgical approaches. Non-steroidal anti-inflammatory drugs (NSAIDs) have been found to be efficient to prevent the development of severe HO. However, this is not always the case. Much has been speculated on the cause of this biological variance. Some patients develop HO even though they are treated with high-dose NSAIDs. Other patients do not develop HO even though they have not been treated at all. This remains an open question.

The number of patients who develop severe HO after THA, where the pain and stiffness of a new hip is dramatic for months after surgery ending up with hip stiffness that limits range of motion, has been reduced over time. Today, we rarely see severe cases in our institution. Why is this the case? It is an open question for sure. In my clinic today, we give all patients NSAIDs for the first 10 days after surgery. The NSAIDs not only reduce postoperative pain, but also may be one of the most logical explanations for this reduction in HO.

Although HO has been meticulous researched for decades, the basics behind the development of HO after THA and its prevention with NSAIDs still need to be answered. Some years ago, we performed a study in the Danish Hip Arthroplasty Registry about patients who were treated with NSAIDs and had non-cemented total hip prostheses. In time, the patients showed an increased risk for revision due to aseptic loosening. Animal studies have shown NSAIDs can reduce the remodeling power of osteoblasts, so it is logical to expect a reduction or prevention of bony ingrowth into non-cemented implants. We followed these patients for years, yet we could not see this aseptic loosening take place. This is also an open question. The most logical explanations are differences in remodeling activity between different species and differences in surgical trauma after implants are inserted into minor animals and non-cemented femoral components are used in humans. This theory needs to be scientifically approached.

Disclosure: Kjaersgaard-Andersen reports no relevant financial disclosures.