Abstract:Heterotopic ossification (HO) after hip arthroscopy is the abnormal formation of mature lamellar bone within extra skeletal soft tissues. HO may lead to pain, impaired range of motion and possibly revision surgery. There has been a substantial amount of recent research on the pathophysiology, prophylaxis and treatment of HO associated with open and arthroscopic hip surgery. This article reviews the literature on the aforementioned topics with a focus on their application in hip arthroscopy.
“…Six hips (12%) developed heterotopic ossification (Brooker Grade I and II). This is well within the rate reported in the literature [ 1 ] and according to Daum et al [ 14 ], these grades are functionally irrelevant. No revision surgery hat to be performed because of that reason.…”
Section: Discussionsupporting
confidence: 90%
“…The aim of this study was to report on the 7-year followup of patients undergoing hip arthroscopy for treatment of symptomatic FAI with trimming of the head-neck junction and/or acetabular rim, including treatment of the labrum. We asked the following questions: (1) What is the clinical and radiographic outcome at a mean 7-year followup of arthroscopically treated symptomatic FAI; (2) what is the cumulative 7-year survivorship of arthroscopically treated FAI; and (3) what are factors associated with revision surgery?…”
Section: Discussionmentioning
confidence: 99%
“…We therefore asked: (1) What are the clinical and radiographic outcomes at a mean 7-year followup; (2) what is the cumulative 7-year survivorship (hips free from conversion to THA, progression of osteoarthritis as increased by one or more points on Tönnis score, or poor clinical outcome as a Merle d'Aubigné score of < 15 points) of hips with symptomatic FAI treated arthroscopically; and (3) what are factors associated with revision surgery?…”
Section: Introductionmentioning
confidence: 99%
“…Questions/purposes (1) What are the clinical and radiographic outcomes at a mean 7-year followup; (2) what is the cumulative 7-year survivorship, using the endpoints of THA, progression of osteoarthritis according to Tönnis, or …”
“…Six hips (12%) developed heterotopic ossification (Brooker Grade I and II). This is well within the rate reported in the literature [ 1 ] and according to Daum et al [ 14 ], these grades are functionally irrelevant. No revision surgery hat to be performed because of that reason.…”
Section: Discussionsupporting
confidence: 90%
“…The aim of this study was to report on the 7-year followup of patients undergoing hip arthroscopy for treatment of symptomatic FAI with trimming of the head-neck junction and/or acetabular rim, including treatment of the labrum. We asked the following questions: (1) What is the clinical and radiographic outcome at a mean 7-year followup of arthroscopically treated symptomatic FAI; (2) what is the cumulative 7-year survivorship of arthroscopically treated FAI; and (3) what are factors associated with revision surgery?…”
Section: Discussionmentioning
confidence: 99%
“…We therefore asked: (1) What are the clinical and radiographic outcomes at a mean 7-year followup; (2) what is the cumulative 7-year survivorship (hips free from conversion to THA, progression of osteoarthritis as increased by one or more points on Tönnis score, or poor clinical outcome as a Merle d'Aubigné score of < 15 points) of hips with symptomatic FAI treated arthroscopically; and (3) what are factors associated with revision surgery?…”
Section: Introductionmentioning
confidence: 99%
“…Questions/purposes (1) What are the clinical and radiographic outcomes at a mean 7-year followup; (2) what is the cumulative 7-year survivorship, using the endpoints of THA, progression of osteoarthritis according to Tönnis, or …”
“…HO occurs after severe trauma or in patients with a rare genetic disorder known as fibrodysplasia ossificans progressiva (FOP) . HO is often triggered by trauma, including musculoskeletal injuries, spinal cord damage or burns, and inflammation associated with traumatic injury . It is most prevalent around large joints, such as the hip and elbow joints.…”
Heterotopic ossification (HO) refers to the pathological formation of ectopic bone in soft tissues, it occurs following severe trauma or in patients with a rare genetic disorder known as fibrodysplasia ossificans progressiva. The pathological process of HO formation is a two-step mechanism: inflammation and destruction of connective tissues, followed by bone formation. The latter is further subdivided into three stages: fibroproliferation/angiogenesis, chondrogenesis, and osteogenesis. Currently, therapeutic options for HO are limited. New potential therapeutics will most likely arise from a more detailed understanding of the signaling pathways implicated in each stage of ectopic bone formation and molecular targets that may be effective at both the early and late stages of HO. Bone morphogenetic protein (BMP) signaling is believed to play a key role in the overall HO process. Recently, the mammalian target of rapamycin (mTOR) signaling pathway has received attention as a critical pathway for chondrogenesis, osteogenesis, and HO. Inhibition of mTOR signaling has been shown to block trauma-induced and genetic HO. Intriguingly, recent studies have revealed crosstalk between mTOR and BMP signaling. Moreover, mTOR has emerged as a factor involved in the early hypoxic and inflammatory stages of HO. We will summarize the current knowledge of the roles of mTOR and BMP signaling in HO, with a particular focus on the crosstalk between mTOR and BMP signaling. We also discuss the activation of AMP activated protein kinase (AMPK) by the most widely used drug for type 2 diabetes, metformin, which exerts a dual negative regulatory effect on mTOR and BMP signaling, suggesting that metformin is a promising drug treatment for HO. The discovery of an mTOR-BMP signaling network may be a potential molecular mechanism of HO and may represent a novel therapeutic target for the pharmacological control of HO.
Acquired heterotopic ossifications (HO) arising as a result of various traumas, including injury or surgical interventions, often result in pain and loss of motion. Though triggers for HO have been identified, the cellular source of these heterotopic lesions as well as the underlying mechanisms that drive the formation of acquired HO remain poorly understood, and treatment options, including preventative treatments, remain limited. Here, we explore the cellular source of HO and a possible underlying mechanism for their spontaneous osteogenic differentiation. We demonstrate that HO lesions arise from tissue-resident PDGFRα+ fibro/adipogenic progenitors (FAPs) in skeletal muscle and not from circulating bone marrow-derived progenitors. Further, we show that accumulation of these cells in the tissue after damage due to alterations in the inflammatory environment can result in activation of their inherent osteogenic potential. This work suggests a mechanism by which an altered inflammatory cell and FAP interactions can lead to the formation of HO after injury and presents potential targets for therapeutics in acquired HO.
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