Surgical Management of Shoulder Heterotopic Ossification.
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ABSTRACT:
SUBMITTER: Hallock J
PROVIDER: S-EPMC6848966 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Heterotopic ossification (HO) is a diverse pathologic process, defined as the formation of extraskeletal bone in muscle and soft tissues. HO can be conceptualized as a tissue repair process gone awry and is a common complication of trauma and surgery. This comprehensive review seeks to synthesize the clinical, pathoetiologic, and basic biologic features of HO, including nongenetic and genetic forms. First, the clinical features, radiographic appearance, histopathologic diagnosis, and current methods of treatment are discussed. Next, current concepts regarding the mechanistic bases for HO are discussed, including the putative cell types responsible for HO formation, the inflammatory milieu and other prerequisite "niche" factors for HO initiation and propagation, and currently available animal models for the study of HO of this common and potentially devastating condition. © 2019 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.
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Project description:Heterotopic ossification (HO, also termed myositis ossificans) is the formation of extra-skeletal bone in muscle and soft tissues. HO is a tissue repair process gone awry, and is a common complication of surgery and traumatic injury. Medical strategies to prevent and treat HO fall well short of addressing the clinical need. Better characterization of the tissues supporting HO is critical to identifying therapies directed against this common and sometimes devastating condition. The physiologic processes of osteogenesis and angiogenesis are highly coupled and interdependent. However, few efforts have been made to document the vascular patterning within heterotopic ossification. Here, surgical pathology case files of 29 human HO specimens were examined by vascular histomorphometric analysis. Results demonstrate a temporospatial patterning of HO vascularity that depends on the "maturity" of the bony lesion. In sum, human HO demonstrates a time- and space-dependent pattern of vascularization suggesting a coupled pathophysiologic process involving the coordinate processes of osteogenesis and angiogenesis. Further imaging studies may be used to further characterize vasculogenesis within HO and whether anti-angiogenic therapies are a conceivable future therapy for this common condition.
| S-EPMC5529164 | biostudies-literature
Project description:Heterotopic Ossification (HO) is a potential long-term complication in orthopaedic surgery. It is commonly classified according to the Brooker classification, which is based on radiological findings. To our knowledge the correlation of histological features to the Brooker grade is unknown as is the association between HO and the indication for revision. The aim of this paper is to analyze the ossification grade of HO tissue in patients undergoing revision hip and knee arthroplasty and to propose a histologically based classification system for HO. We also assess the relationship between the grade of HO and the indication for revision (septic and aseptic revision). From January to May 2019 we collected 50 human HO samples from hip and knee revision arthroplasty cases. These tissue samples were double-blinded and sent for histopathological diagnostic. Based on these results, we developed a classification system for the progression of HO. The grade of ossification was based on three characteristics: Grade of heterotopic ossification (Grade 1-3), presence of necrosis (N0 or N1) and the presence of osteomyelitis (HOES-Score Type 1 to 5). Demographic data as well as surgical details and indication for surgery was prospectively collected from clinical records. Fifty tissue samples were harvested from 44 hips and 6 knee joints. Of these 33 exhibited Grade I ossifications (66%), followed by 11 Grade II (22%) and one Grade III (2%). Necrosis was noted in two tissue samples (4%) and 2 more had osteomyelitis findings according to HOES-Score. Six samples (12%) with radiologically suggestive of HO turned out to be wear-induced synovitis, SLIM Type 1. Of these cases 16 were septic (32%) and 34 aseptic (68%) revisions. Most of the HO tissue samples were classified as a low-grade. High-grade ossification-Score is rare. Higher grades of ossification seem to be associated with septic revision cases. Wear-induced synovitis potentially influences HO development. A histological scoring system for ossification grading can be derived from the data presented in this study.
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Project description:Heterotopic ossification (HO) is defined as the process by which trabecular bone forms outside of the skeletal structure, occupying space in soft tissue where it does not normally exist. The current popular prophylactic treatment modalities include non-steroidal anti-inflammatory drugs (NSAIDs) and radiation therapy, although the literature remains inconclusive as to which is superior. Additionally, both treatments can lead to adverse effects to the patient. Recently there have been several studies attempting to identify new aspects of the etiology of heterotopic bone formation and introduce new prophylactic modalities with increased efficacy and fewer side effects. For this review, we selectively retrieved articles from Medline published from 1958-2008 on the prophylaxis of HO with the aim of assisting readers in quickly grasping the current status of research and clinical aspects of HO prophylaxis.
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Project description:Optimal surgical management of anterior shoulder instability remains controversial. There is a need to assess the most recent trends for primary and revision shoulder stabilization surgery using a national database significantly larger than those previously utilized.Most shoulder stabilization procedures are performed arthroscopically. Examining revision procedures, we hypothesized that open procedures would result in decreased revision stabilizations compared with arthroscopic procedures and that most revision procedures would be open Bankart or bone transfer procedures regardless of the index procedure technique.Descriptive epidemiology study.The MarketScan Database was searched using International Classification of Diseases-Ninth Revision (ICD-9) and Current Procedural Terminology (CPT) codes to identify patients who underwent any shoulder stabilization procedure between 2008 and 2012. Regression analysis was used to evaluate trends between patient groups. The Cochran-Armitage trend test was used to identify differences in trends seen yearly. Odds ratios (ORs) were calculated to compare the likelihood of undergoing a revision stabilization procedure.A total of 66,564 shoulder stabilization procedures were identified from 2008 through 2012: 60,248 arthroscopic stabilization procedures (90.5%) and 6316 open stabilization procedures (9.5%), including 1623 bone block procedures. Arthroscopic stabilization procedures increased in total number and percentage of all procedures in each year of the study. Bone block procedures increased in number each year, although other open procedures decreased during the study period. Males underwent more stabilization procedures, while patients between the ages of 10 and 19 years were most likely to undergo any procedure. Patients who underwent bone block stabilization were significantly less likely to undergo a second stabilization procedure during the study period when compared with open Bankart repair (OR, 0.582; 95% CI, 0.405-0.836; P < .05) and arthroscopic Bankart repair (OR, 0.587; 95% CI, 0.418-0.824; P < .05). No statistically significant difference in revision stabilization was seen when comparing arthroscopic versus open Bankart repair (OR, 0.934; 95% CI, 0.863-1.139).Although the number of arthroscopic shoulder stabilization surgeries continues to increase, our data show a consistent increase, not seen in prior studies, in the number of bone block procedures. Contrary to some studies, there was no significant difference in the likelihood of a second procedure between patients initially undergoing arthroscopic compared with open Bankart repair.
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Project description:Trauma-induced heterotopic ossification (HO) occurs after severe musculoskeletal injuries and burns, and presents a significant barrier to patient rehabilitation. Interestingly, the incidence of HO significantly increases with repeated operations and after resection of previous HO. Treatment of established heterotopic ossification is challenging because surgical excision is often incomplete, with evidence of persistent heterotopic bone. As a result, patients may continue to report the signs or symptoms of HO, including chronic pain, nonhealing wounds, and joint restriction. In this study, we designed a model of recurrent HO that occurs after surgical excision of mature HO in a mouse model of hind-limb Achilles' tendon transection with dorsal burn injury. We first demonstrated that key signaling mediators of HO, including bone morphogenetic protein signaling, are diminished in mature bone. However, upon surgical excision, we have noted upregulation of downstream mediators of osteogenic differentiation, including pSMAD 1/5. Additionally, surgical excision resulted in re-emergence of a mesenchymal cell population marked by expression of platelet-derived growth factor receptor-α (PDGFRα) and present in the initial developing HO lesion but absent in mature HO. In the recurrent lesion, these PDGFRα+ mesenchymal cells are also highly proliferative, similar to the initial developing HO lesion. These findings indicate that surgical excision of HO results in recurrence through similar mesenchymal cell populations and signaling mechanisms that are present in the initial developing HO lesion. These results are consistent with findings in patients that new foci of ectopic bone can develop in excision sites and are likely related to de novo formation rather than extension of unresected bone. Stem Cells Translational Medicine 2017;6:799-806.
| S-EPMC5442786 | biostudies-literature
Project description:Heterotopic ossification (HO) is a pathological phenomenon in which ectopic lamellar bone forms in soft tissues. HO involves many predisposing factors, including congenital and postnatal factors. Postnatal HO is usually induced by fracture, burn, neurological damage (brain injury and spinal cord injury) and joint replacement. Recent studies have found that patients who suffered from bone fracture combined with severe traumatic brain injury (S-TBI) are at a significantly increased risk for HO occurrence. Thus, considerable research focused on the influence of S-TBI on fracture healing and bone formation, as well as on the changes in various osteogenic factors with S-TBI occurrence. Brain damage promotes bone formation, but the exact mechanisms underlying bone formation and HO after S-TBI remain to be clarified. Hence, this article summarises the findings of previous studies on the relationship between S-TBI and HO and discusses the probable causes and mechanisms of HO caused by S-TBI. The translational potential of this article: A better understanding of the probable causes of traumatic brain injury-induced HO can provide new perspectives and ideas in preventing HO and may support to design more targeted therapies to reduce HO or enhance the bone formation.
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Project description:Heterotopic ossification (HO) is a disabling condition associated with neurologic injury, inflammation, and overactive bone morphogenetic protein (BMP) signaling. The inductive factors involved in lesion formation are unknown. We found that the expression of the neuro-inflammatory factor Substance P (SP) is dramatically increased in early lesional tissue in patients who have either fibrodysplasia ossificans progressiva (FOP) or acquired HO, and in three independent mouse models of HO. In Nse-BMP4, a mouse model of HO, robust HO forms in response to tissue injury; however, null mutations of the preprotachykinin (PPT) gene encoding SP prevent HO. Importantly, ablation of SP(+) sensory neurons, treatment with an antagonist of SP receptor NK1r, deletion of NK1r gene, or genetic down-regulation of NK1r-expressing mast cells also profoundly inhibit injury-induced HO. These observations establish a potent neuro-inflammatory induction and amplification circuit for BMP-dependent HO lesion formation, and identify novel molecular targets for prevention of HO.
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Project description:Heterotopic ossification (HO), or bone formation in soft tissues, is often the result of traumatic injury. Much evidence has linked the release of BMPs (bone morphogenetic proteins) upon injury to this process. HO was once thought to be a rare occurrence, but recent statistics from the military suggest that as many as 60% of traumatic injuries, resulting from bomb blasts, have associated HO. In this study, we attempt to define the role of peripheral nerves in this process. Since BMP2 has been shown previously to induce release of the neuroinflammatory molecules, substance P (SP) and calcitonin gene related peptide (CGRP), from peripheral, sensory neurons, we examined this process in vivo. SP and CGRP are rapidly expressed upon delivery of BMP2 and remain elevated throughout bone formation. In animals lacking functional sensory neurons (TRPV1(-/-) ), BMP2-mediated increases in SP and CGRP were suppressed as compared to the normal animals, and HO was dramatically inhibited in these deficient mice, suggesting that neuroinflammation plays a functional role. Mast cells, known to be recruited by SP and CGRP, were elevated after BMP2 induction. These mast cells were localized to the nerve structures and underwent degranulation. When degranulation was inhibited using cromolyn, HO was again reduced significantly. Immunohistochemical analysis revealed nerves expressing the stem cell markers nanog and Klf4, as well as the osteoblast marker osterix, after BMP2 induction, in mice treated with cromolyn. The data collectively suggest that BMP2 can act directly on sensory neurons to induce neurogenic inflammation, resulting in nerve remodeling and the migration/release of osteogenic and other stem cells from the nerve. Further, blocking this process significantly reduces HO, suggesting that the stem cell population contributes to bone formation.
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