Chen and Chmell Journal of Medical Case Reports 2011, 5:453 http://www.jmedicalcasereports.com/content/5/1/453 of cartilage and subchondral bone. Images taken after the surgery revealed a successful procedure (Figure 3). Discussion After delaying treatment for several months for unclear reasons, our patient presented with mild HO on his initial radiographs. The subsequent trauma of the pri- mary surgery to repair his patellar tendon was most likely a catalyst for the extensive additional HO that crippled his right knee mobilization. There are no docu- mented cases of HO secondary to patellar tendon repair. The aggressive nature of this patient’s HO may be attributable to his T8M diagnosis. Chromosome 8 has been linked to certain BMPs. BMPs are part of the transforming growth factor beta (TGFb) superfamily and play an important role in postnatal bone development [9]. BMP-1, located at 8p21, may explain the presence Figure 3 Lateral X-ray of the patient’s right knee after surgery to accomplish arthrodesis. Page 3 of 4 of abnormal bone formation in our patient with T8M [10]. BMP-1 has a unique structure and may play a role in activating other BMPs [10]. Extensive research is being conducted to better understand the biochemistry of these proteins. Basic standards for HO prophylaxis have been rela- tively well established, but specifics are still debated. Current methods include non-steroidal anti-inflamma- tory drug (NSAID) treatment with indomethacin or localized radiation therapy. A recent study concluded that indomethacin is the gold standard for HO prophy- laxis following total hip arthroplasty and, furthermore, is the only drug proven to be effective against HO fol- lowing acetabular surgery [11]. Although radiation therapy has been shown to be slightly more costly than NSAIDs, other studies suggest that morbidities and quality of life differences associated with NSAIDs are difficult to quantify, and radiation therapy may remain the preferred prophylaxis of HO after total hip arthro- plasty [11,12]. Conclusion It is our opinion that this patient’s T8M status placed him at higher risk for developing HO postoperatively. There are no reports of HO as a complication of patel- lar tendon rupture or repair. A link between these pathological phenomena could explain the extensive HO in our patient and allow us to anticipate similar out- comes in T8M patients. Consent Written informed consent was obtained from the patient’s mother for publication of this case report and any accompanying images. A copy of the written con- sent is available for review by the Editor-in-Chief of this journal. Authors’ contributions AC participated as an observer in the case described, performed an extensive literature review and was primarily responsible for writing the manuscript. SC was the attending physician for the case described and provided guidance throughout the literature review and writing process. Both authors have read and approved the final manuscript. Competing interests The authors declare that they have no competing interests. Received: 19 February 2010 Accepted: 12 September 2011 Published: 12 September 2011 References 1. Hannallah D, Peng H, Young B, Usas A, Gearhart B, Huard J: Retroviral delivery of Noggin inhibits the formation of heterotopic ossification induced by BMP-4, demineralized bone matrix, and trauma in an animal model. J Bone Joint Surg Am 2004, 86-A(1):80-91. 2. Balboni TA, Gobezie R, Mamon HJ: Heterotopic ossification: Pathophysiology, clinical features, and the role of radiotherapy for prophylaxis. Int J Radiat Oncol Biol Phys 2006, 65(5):1289-1299.