New insights into the biomechanics of Legg-Calvé-Perthes’ disease

Pinheiro, Manuel; Dobson, Catherine; Perry, Daniel C.; Fagan, Michael J.

doi:10.1302/2046-3758.72.bjr-2017-0191.r1

Cited by 13 publications

(13 citation statements)

References 44 publications

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“…This provides evidence of its role in the enteropathogenesis of the LCPD. Recently, Pinheiro et al[ 65 ] proposed a biomechanical model that further supports a combined role of both ischemic condition, skeletal immaturity and altered biomechanics. Also, studies on hip osteonecrosis in piglets confirmed this aetiology[ 66 - 69 ].…”

Section: Resultsmentioning

confidence: 99%

“…Mechanical stress-induced ischemia was found to be a possible aetiology of LCPD also using several animal models[ 70 - 72 ] and experimental analysis models[ 65 , 73 , 74 ]. One particular study performed by Suehiro et al[ 49 ] involving Wistar Kyoto rats reported how repetitive mechanical stress on the femoral heads from 5 wk to 9 wk of age played an important role in the aetiology of osteonecrosis.…”

Section: Resultsmentioning

confidence: 99%

“…Mechanical-induced ischemia is one of the most supported hypotheses for the aetiology of LCPD[54,61,75-77]. Emerging evidence is supporting a role of repetitive mechanical stress to the epiphysis and de subsequent ischemia, as stated in different experimental models[65-69,73,74]. In addition, the association with ADHD[30-34,36] and hyperactive modification of behaviour could be easily explained with repetitive activity-induced mechanical stress.…”

Section: Discussionmentioning

confidence: 99%

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Aetiology of Legg-Calvé-Perthes disease: A systematic review

Pavone

Chisari

Vescio

et al. 2019

WJO

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BACKGROUNDLegg-Calvé-Perthes disease (LCPD) is a clinical condition affecting the femoral head of children during their growth. Its prevalence is set to be between 0.4/100000 to 29.0/100000 children less than 15 years of age with a peak of incidence in children aged from 4 years to 8 years. LCPD aetiology has been widely studied, but it is still poorly understood.AIMTo analyse the available literature to document the up-to-date evidence on LCPD aetiology.METHODSA systematic review of the literature was performed regarding LCPD aetiology, using the following inclusion criteria: studies of any level of evidence, reporting clinical or preclinical results and dealing with the aetiology or pathogenesis of LCPD. Two reviewers searched the PubMed and Science Direct databases from their date of inception to the 20th of May 2018 in accordance with the Preferred Reporting Items for Systemic Reviews and Meta-Analyses guidelines. To achieve the maximum sensitivity of the search strategy, we combined the terms: ‘‘Perthes disease OR LCPD OR children avascular femoral head necrosis” with “pathology OR aetiology OR biomechanics OR genetics” as either key words or MeSH terms.RESULTSWe include 64 articles in this review. The available evidence on LCPD aetiology is still debated. Several hypotheses have been researched, but none of them was found decisive. While emerging evidence showed the role of environmental risk factors and evidence from twin studies did not support a major role for genetic factors, a congenital or acquired predisposition cannot be excluded in disease pathogenesis. One of the most supported theories involved mechanical induced ischemia that evolved into avascular necrosis of the femoral head in sensible patients.CONCLUSIONThe literature available on the aetiology of LCPD presents major limitations in terms of great heterogeneity and a lack of high-profile studies. Although a lot of studies focused on the genetic, biomechanical and radiological background of the disease, there is a lack of consensus on one or multiple major actors of the etiopathogenesis. More studies are needed to understand the complex and multifactorial genesis of the avascular necrosis characterizing the disease.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Aetiology of Legg-Calvé-Perthes disease: A systematic review

Pavone

Chisari

Vescio

et al. 2019

WJO

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“…Hip joint · Femur head necrosis · Classification · Age of onset · Osteotomy die in der Durchschnittsbevölkerung nur im Verhältnis 1:15.000 vorkommen [3]; -Gefäßanomalien führen durch eine geringer ausgebildete vordere Gefäßanastomose besonders zwischen dem 3. und 10. Lebensjahr [4] oder andere Gefäßanomalien, die bei Jungen häufiger auftreten [5], zu einer Minderdurchblutung mit mehrfachem Mikroinfarktgeschehen; -konstitutionelle Faktoren mit genetischer oder erworbener, passagerer Skelettalterretardierung reduzieren bei später Ossifikation den Blutfluss zu den epiphysären Gefäßen durch den Druck des Körpergewichts und lösen so rezidivierende ischämische Infarkte aus [6,7]; -biomechanisch durch vertikale Belastung verursachte Mikrofrakturen der subchondralen Knochenlamelle mit sekundärer Ischämie.…”

Section: Introductionunclassified

Diagnostik und Therapie des Morbus Perthes

Strobl

2020

Monatsschr Kinderheilkd

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ZusammenfassungDie Behandlung des M. Perthes stellt aufgrund der ungeklärten Ätiologie sowie der unterschiedlichen Verlaufsformen und Behandlungskonzepte eine Herausforderung dar. Die Prognose ist abhängig von klinischen und radiologischen Parametern. Aktuelle Behandlungsansätze zielen in frühen Krankheitsstadien auf die Verbesserung der Durchblutung des Femurkopfes und später auf die Vergrößerung des Bewegungsumfangs sowie die Verminderung der vertikal einwirkenden Kräfte durch Teilentlastung und chirurgisch verbesserte Einstellung des Femurkopfes in der Gelenkpfanne ab. Da einerseits ein hoher Prozentsatz an Spontanremissionen ohne Deformitäten des Gelenks, andererseits ein hohes Risiko für eine schwere Koxarthrose mit der Notwendigkeit eines frühen Gelenkersatzes sowohl nach konservativen als auch nach operativen Verfahren zu beobachten sind, werden die Behandlungsmethoden kontrovers diskutiert.

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“…Decreased blood supply [8] and vascular occlusion [9] occur in the development of human ONFH; however, molecular events underlying the pathological reaction are poorly characterized. In experimental ONFH models, the dephosphorylation of elF2, an endoplasmic reticulum stress regulator, increases angiogenic factor vascular endothelial growth factor (VEGF) production and angiogenesis, slowing femoral head injury during the surgery-mediated ONFH [10].…”

Section: Introductionmentioning

confidence: 99%

S100 Calcium Binding Protein A9 Represses Angiogenic Activity and Aggravates Osteonecrosis of the Femoral Head

Lian

Kuo

et al. 2019

IJMS

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Ischemic damage aggravation of femoral head collapse is a prominent pathologic feature of osteonecrosis of the femoral head (ONFH). In this regard, S100 calcium binding protein A9 (S100A9) is known to deteriorate joint integrity, however, little is understood about which role S100A9 may play in ONFH. In this study, a proteomics analysis has revealed a decrease in the serum S100A9 level in patients with ONFH upon hyperbaric oxygen therapy. Serum S100A9 levels, along with serum vascular endothelial growth factor (VEGF), soluble vascular cell adhesion molecule-1 (sVCAM-1), interleukin-6 (IL-6), and tartrate-resistant acid phosphatase 5b levels were increased in patients with ONFH, whereas serum osteocalcin levels were decreased as compared to healthy controls. Serum S100A9 levels were increased with the Ficat and Arlet stages of ONFH and correlated with the patients with a history of being on glucocorticoid medication and alcohol consumption. Osteonecrotic tissue showed hypovasculature histopathology together with weak immunostaining for vessel marker CD31 and von Willrbrand factor (vWF) as compared to femoral head fracture specimens. Thrombosed vessels, fibrotic tissue, osteocytes, and inflammatory cells displayed strong S100A9 immunoreactivity in osteonecrotic lesion. In vitro, ONFH serum and S100A9 inhibited the tube formation of vessel endothelial cells and vessel outgrowth of rat aortic rings, whereas the antibody blockade of S100A9 improved angiogenic activities. Taken together, increased S100A9 levels are relevant to the development of ONFH. S100A9 appears to provoke avascular damage, ultimately accelerating femoral head deterioration through reducing angiogenesis. This study provides insight into the molecular mechanism underlying the development of ONFH. Here, analysis also highlights that serum S100A9 is a sensitive biochemical indicator of ONFH.

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New insights into the biomechanics of Legg-Calvé-Perthes’ disease

Cited by 13 publications

References 44 publications

Aetiology of Legg-Calvé-Perthes disease: A systematic review

Aetiology of Legg-Calvé-Perthes disease: A systematic review

Diagnostik und Therapie des Morbus Perthes

S100 Calcium Binding Protein A9 Represses Angiogenic Activity and Aggravates Osteonecrosis of the Femoral Head

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