Witbreuk M, van Kemenade F J, van der Sluijs J A, Jansma E P, Rotteveel J, van Royen B J
Department of Orthopaedic Surgery, Research Institute MOVE, VU University Medical Center, De Boelelaan 1117, P.O. Box 7057, 1081 HV Amsterdam, The Netherlands.
Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands.
J Child Orthop. 2013 Jun;7(3):213-23. doi: 10.1007/s11832-013-0493-8. Epub 2013 Mar 30.
Puberty, obesity, endocrine and chronic systemic diseases are known to be associated with slipped capital femoral epiphysis (SCFE). The mechanical insufficiency of the physis in SCFE is thought to be the result of an abnormal weakening of the physis. However, the mechanism at the cellular level has not been unravelled up to now.
To understand the pathophysiology of endocrine and metabolic factors acting on the physis, we performed a systematic review focussing on published studies reporting on hormonal, morphological and cellular abnormalities of the physis in children with SCFE. In addition, we looked for studies of the effects of endocrinopathies on the human physis which can lead to cause SCFE and focussed in detail on hormonal signalling, hormone receptor expression and extracellular matrix (ECM) composition of the physis. We searched in the PubMed, EMBASE.com and The Cochrane Library (via Wiley) databases from inception to 11th September 2012. The search generated a total of 689 references: 382 in PubMed, 232 in EMBASE.com and 75 in The Cochrane Library. After removing duplicate papers, 525 papers remained. Of these, 119 were selected based on titles and abstracts. After excluding 63 papers not related to the human physis, 56 papers were included in this review.
Activation of the gonadal axis and the subsequent augmentation of the activity of the growth hormone-insulin-like growth factor 1 (GH-IGF-1) axis are important for the pubertal growth spurt, as well as for cessation of the physis at the end of puberty. The effects of leptin, thyroid hormone and corticosteroids on linear growth and on the physis are also discussed. Children with chronic diseases suffer from inflammation, acidosis and malnutrition. These consequences of chronic diseases affect the GH-IGF-1 axis, thereby, increasing the risk of the development of SCFE. The risk of SCFE and avascular necrosis in children with chronic renal insufficiency, growth hormone treatment and renal osteodystrophy remains equivocal.
SCFE is most likely the result of a multi-factorial event during adolescence when height and weight increase dramatically and the delicate balance between the various hormonal equilibria can be disturbed. Up to now, there are no screening or diagnostic tests available to predict patients at risk.
已知青春期、肥胖、内分泌及慢性全身性疾病与股骨头骨骺滑脱(SCFE)相关。SCFE中生长板的机械功能不全被认为是生长板异常弱化的结果。然而,迄今为止细胞水平的机制尚未阐明。
为了解作用于生长板的内分泌和代谢因素的病理生理学,我们进行了一项系统综述,重点关注已发表的关于SCFE患儿生长板激素、形态和细胞异常的研究。此外,我们查找了内分泌疾病对人类生长板影响的研究,这些影响可导致SCFE,并详细关注生长板的激素信号传导、激素受体表达和细胞外基质(ECM)组成。我们在PubMed、EMBASE.com和Cochrane图书馆(通过Wiley)数据库中从建库至2012年9月11日进行检索。检索共产生689篇参考文献:PubMed中有382篇,EMBASE.com中有232篇,Cochrane图书馆中有75篇。去除重复论文后,剩余525篇。其中,基于标题和摘要选择了119篇。排除63篇与人类生长板无关的论文后,本综述纳入56篇论文。
性腺轴的激活以及随后生长激素 - 胰岛素样生长因子1(GH - IGF-1)轴活性的增强对青春期生长突增以及青春期结束时生长板的闭合很重要。还讨论了瘦素、甲状腺激素和皮质类固醇对线性生长和生长板的影响。患有慢性疾病的儿童会出现炎症、酸中毒和营养不良。这些慢性疾病的后果会影响GH - IGF-1轴,从而增加发生SCFE的风险。慢性肾功能不全、生长激素治疗和肾性骨营养不良患儿发生SCFE和缺血性坏死的风险仍不明确。
SCFE很可能是青春期多因素事件的结果,此时身高和体重急剧增加,各种激素平衡之间的微妙平衡可能被打破。迄今为止,尚无筛查或诊断测试可用于预测有风险的患者。