A review of environmental factors implicated in human developmental dysplasia of the hip

Abstract

PurposeDevelopmental dysplasia of the hip (DDH) is common, and the term encompasses a spectrum of anatomical abnormalities of the hip in which the femoral head displaces from the acetabulum. These abnormalities may be congenital or develop during infancy and/or childhood. Neither the prenatal and postnatal factors that predispose to hip instability nor the determinants of its resolution or persistence are well characterised. A multifactorial pathogenesis of DDH is commonly accepted and identified risk factors include a family history, being first born, breech presentation, female gender, high birth weight and oligohydramnios 1. Further to genetic factors, a number of nutritional, hormonal and mechanical influences on ligament laxity have been hypothesised.MethodsA comprehensive search was conducted using NICE Healthcare Databases Advanced Search and Google Scholar engines, and the terms “nutrition”, “environmental”, “risk factors”, “CDH” and “DDH”. Wherever possible, evidence from randomised controlled trials, systematic reviews and expert review articles published in the medical and veterinary literature was considered.ResultsThe relationship between a number of hormones and biochemical markers of nutritional status and the development of DDH has been repeatedly hypothesised upon in the last 45 years. Of those most frequently cited are calcium, vitamins C and D, and relaxin hormone. The evidence for these potential risk factors is provided mainly by canine studies, with a paucity of consistent or strong evidence in humans.ConclusionsDDH is common and remains a leading cause of hip osteoarthritis in young adults. Neonatal clinical screening programmes for this condition have been in practice since the 1950s, albeit with varying levels of sensitivity. This review summarises current understanding of some of the most frequently cited nongenetic hypothesised risk factors, the significance of which remain to be determined.

Serum prolidase activity and oxidative–antioxidative status in patients with developmental dysplasia of the hip and its relationship with radiographic severity

“…A multifactorial pathogenesis of DDH is commonly accepted. 21 There are several studies on the pathological differences in collagen content, and distribution and metabolism of the joint capsule and ligaments in patients with DDH. [22][23][24][25] Pathological changes were documented in an anatomical study of six infants with DDH that included a loss of proteoglycans and an increase in collagen deposition in the lateral acetabular roof, manifesting as a ridge of degenerating acetabular cartilage.…”

Spontaneous dog osteoarthritis — a One Medicine vision

“…Presentation. Hip dysplasia is a common risk factor for both human and dog OA [28][29][30][31] . An estimated 20-40% of idiopathic human hip OA is caused by developmental dysplasia of the hip (DDH) 32 , with many patients requiring joint replacement later in life 1,33,34 .…”

Differential effects of altered patterns of movement and strain on joint cell behaviour and skeletal morphogenesis

“…There are multiple conditions for which abnormal or reduced movement are causal; including developmental dysplasia of the hip (DDH), which affects 1.3 per 1000 births1, 2, arthrogryposis which affects around 1:4000 births 3 and fetal akinesia deformation sequence (FADS) which affects 1:15,000 births4, 5. Additionally, there is evidence that early changes to joint shape lead to osteoarthritis (OA) later in life 6 . This can arise if conditions such as DDH are uncorrected 7 , but also subtle changes to hip shape have been identified as conferring increased risk of OA8, 9.…”