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Pathophysiology of Heterotopic Ossification

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Pathophysiology of Heterotopic Ossification PATHOPHYSIOLOGY Pathophysiology of Heterotopic Ossifi cation Michael E. Zychowicz Heterotopic ossifi cation (HO) is a pathologic condition that Up to 35% of those patients with an SCI will develop leads to the development of bone within nonosseous soft a limitation in range of motion of the affected body part tissues. A common site for HO development is at the hip. (Shehab et al., 2002 ). Between 70% and 97% of patients The bone that forms is believed to develop through stimula- will have the hip as their primary site of HO develop- tion by cellular mediators and altered neurovascular signal- ment within 2–3 weeks following SCIs. Nearly 8% of ing. Heterotopic ossifi cation can be a debilitating disease patients will go on to develop ankylosis at the hip (Teasell et al., 2010 ). Following an SCI, there appears to leading to pain, edema, and stiffness. This only compounds be a relationship with the development of HO and expe- already-debilitating comorbid conditions such as a spinal riencing muscle spasticity, a fracture, limited range of cord injury, head injury, or trauma. Several factors, includ- motion or greater than 2 weeks’ loss of consciousness ing prostaglandin E2, bone morphogenetic protein, and (Aubut, Mehta, Cullen, & Teasell, 2011). the infl ammatory process, are believed to contribute to In patients with a closed brain injury, HO occurs in the development of HO. The full scope of pathophysiology approximately 10%–20% of patients. Nearly 10% of contributing to HO is not fully understood. those who develop HO following a closed brain injury will also develop signifi cantly limited range of motion at the affected joint (Shehab et al., 2002 ). Some of the Introduction most commonly affected joints of people who develop HO following a closed brain injury include the hip, Heterotopic ossifi cation (HO) is a pathologic condition elbow, and knees (Aubut et al., 2011 ). where patients develop bone formation within nonosse- There appears to be no difference in HO develop- ous tissues. A common site for HO development is at the ment when comparing racial groups. Males and females hip. The bone that forms in tissues with HO is mature have an equal incidence of HO following some type of lamellar bone and is believed to be stimulated to develop nerve injury. Nearly 20%–30% of those patients with a through cellular mediators and altered neurovascular nerve injury will develop HO within 2–4 months signaling (Keschner & Paksima, 2007). This condition (Bossche & Vanderstraeten, 2005; Frassica et al., 2006 ). has been described in children early in the medical lit- Patients with a greater degree of trauma have a erature in 1692 (Bossche & Vanderstraeten, 2005). greater risk for the development of HO. Only 3% of Heterotopic ossifi cation was later described by Reidel in patients who have an elbow dislocation will develop 1883 and subsequently by Dejerne and Ceillier in 1918 HO. This is contrasted by nearly 20% of patients who as developing in soldiers who suffered spinal cord inju- will develop HO following a fracture and dislocation at ries (SCIs) in combat (Shehab, Elgazzar, & Collier, the elbow (Keschner & Paksima, 2007). 2002). The physiologic process in the development of Heterotopic ossifi cation is a possible complication HO is not fully understood in the scientifi c literature. following total hip arthroplasty (THA). Males generally have a greater incidence of developing HO following a Epidemiology THA than females. The incidence of HO in patients with a THA ranges between 16% and 53% (Bossche & Several conditions have been correlated with the devel- Vanderstraeten, 2005). Nearly 3% of people who opment of HO (see Table 1 ). Frequently, the bone that develop HO following a THA will be severely disabled forms in patients with HO occurs following an SCI, mus- (Vigorita, 2008 ). Up to 90% of the patients who have a culoskeletal trauma, surgical intervention, or brain injury (Frassica, Sponseller, & Wilckens, 2006). For patients with these conditions, the hip is a very common Michael E. Zychowicz, DNP, FAANP, Director, Master of Science of site for the development of HO (Bossche & Nursing Program, and Lead Faculty, Orthopedic NP Program, Duke Vanderstraeten, 2005). Patients with SCIs have approxi- University School of Nursing, Durham, NC. mately a 20%–30% chance for developing HO. This typi- The author has disclosed that he has no fi nancial interests to any com- cally will develop at a site that is distal to the SCI (Shehab mercial company related to this educational activity. et al., 2002 ). DOI: 10.1097/NOR.0b013e3182920d85 © 2013 by National Association of Orthopaedic Nurses Orthopaedic Nursing • May/June2013 • Volume 32 • Number 3 173 Copyright © 2013 by National Association of Orthopaedic Nurses. Unauthorized reproduction of this article is prohibited. NNOR200393.inddOR200393.indd 117373 110/05/130/05/13 33:01:01 PPMM TABLE 1. CONDITIONS CORRELATED WITH HETEROTOPIC History and Physical Findings OSSIFICATION DEVELOPMENT Patients who develop HO will typically complain of Atherosclerosis Tumors somewhat nonspecifi c symptoms. Erythema, warmth, Trauma Spinal cord injury edema, fever, and unexplained increasing pain are some of the most common initial symptoms (Frassica et al., Head injury Infection 2006 ; Keschner & Paksima, 2007). Nearly 80% of Bone marrow transplant Joint arthroplasty patients who develop HO will have a rather benign Burns Spondyloarthropathies course with symptoms resembling an infl ammatory dis- order, cellulitis, phlebitis, or a deep vein thrombosis Note . Adapted from Orthopaedic Pathology (2nd ed.), by V. J. Vigorita, 2008 , Philadelphia, PA: Lippincott Williams & Wilkins. (Bossche & Vanderstraeten, 2005; Shehab et al., 2002 ). The signs and symptoms a patient with HO com- plains of will typically begin 1–3 months following a THA following an acetabular fracture will develop HO precipitating injury. The patient who develops HO will at the hip (Bossche & Vanderstraeten, 2005). progress from the initial symptoms of swelling to The development of HO in children is generally less develop a palpable mass as well as induration and stiff- than that for adults. Children also frequently have a ness (Bossche & Vanderstraeten, 2005). Ossifi cation spontaneous resolution of their symptoms. Children within tissues may lead to muscle pain, spasm, and with fi brodysplasia ossifi cans progressiva can poten- guarding (Frassica et al., 2006 ). tially develop HO following administration of DTP Loss of function, tissue breakdown, limited motion, immunization (Bossche & Vanderstraeten, 2005). ankylosis, nerve compression, and vascular compression Some additional causes for HO include multiple scle- are possible complications of the ossifi cation that occurs rosis, sickle cell disease, hemophilia, tetanus, and burns. with HO. Ossifi cation can lead to compression of vascu- Some patients will experience an idiopathic develop- lar structures and subsequent increased hydrostatic ment of HO. Patients can develop HO in the kidney, gas- pressure and edema or an effusion distal to the ossifi ed trointestinal tract, and uterus as well as following lesion (Bossche & Vanderstraeten, 2005). Ankylosis can abdominal surgery (Shehab et al., 2002 ). Following occur in approximately 10% of patients with HO, leading abdominal surgery, the greatest incidence of HO occurs to functional diffi culties with mobility and activities of in men older than 55 years (Christofi , Raptis, Kallis, & daily living (Keschner & Paksima, 2007; Shehab et al., Ambasakoor, 2008). 2002 ). Some patients may complain of neuropathic pain, numbness, tingling, and loss of function due to nerve entrapment within the HO (Shehab et al., 2002 ). Risk Factors Several risk factors increase the likelihood for develop- ing HO. A history of prior HO increases a patient's risk Diagnostic Testing and Imaging for future development of HO (Bossche & Approximately 2–3 weeks following the onset of HO, Vanderstraeten, 2005; Keschner & Paksima, 2007). A serum alkaline phosphatase (ALP) will be elevated possible unknown genetic cause may lead to an (Frassica et al., 2006 ). Alkaline phosphatase is a glyco- increased risk for the development of HO. Patients with sylated protein, or glycoprotein, that is produced by ankylosing spondylitis, Paget's disease, heterotopic bone, renal, hepatic, intestinal, and placenta cells. In osteoarthritis, and disseminated idiopathic skeletal bone, ALP is located primarily in the plasma membrane hyperostosis (DISH) have an increased risk of develop- of osteoblasts (Vigorita, 2008 ). Serum ALP is generally ing HO (Keschner & Paksima, 2007). A possible link produced and released by osteoblasts during the bone may exist between developing HO and human leuko- formation phase of the bone turnover cycle. Pathologic cyte antigen B18, B27, and DW7 (Bossche & conditions that increase bone formation or bone turn- Vanderstraeten, 2005). over will increase serum ALP. These include conditions Surgical procedures can increase a patient's risk for such as Paget's disease, fracture healing, osteoblastic developing HO (Xue et al., 2011 ). Patients have an tumor, osteomalacia, rickets, hyperparathyroidism, and increased risk for development of HO following a THA HO (Jacobs, DeMott, & Oxley, 2004). or trochanteric osteotomy. Not only does the surgical Prostaglandins (PGs) are typically thought of as a procedure increase the risk for HO, but the surgical major component of the inflammatory process lead- approach can increase the risk. A lateral approach to ing to pain stimulation, neutrophil
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