Hip OA is common but not inevitable condition, increasing in prevalence with age. It is a dynamic inflammatory process, and is associated with structural defects in childhood and young adulthood, trauma, and genetic susceptibility in old age. Many studies show inconsistent links with gender, nutrition and activity levels. Only associations with significant evidence levels are considered in detail below.
DDH represents a spectrum of neonatal hip joint malformation. It affects 1-2% of newborns, but is a leading cause of early hip OA, responsible for 8.6% of all primary hip replacements and 28.8% of hip replacements in people over 6o years in Norway. Despite a national screening programme in UK over the past 40 years there has been no fall in the number of late cases of DDH and the operation rate is increasing (Sewell and Eastwood, 2011). Some cases of dysplastic hip result from altered muscle tone, for example from cerebral palsy or myelomeningocele, leading to progressive dysplastic change over time. Some hip dislocations occur before birth, while most cases of DDH are due to dysplastic acetabula. Early detection and reduction may lead to a good outcome, as a stable contained hip acetabular dysplasia may subsequently normalise following remodelling in the infant. Late identification may require open reduction with later femoral and/or acetabular osteotomies to stabilise the joint. The outcome of late open reduction is significantly worse both for hip function and future risk of hip OA.
A systematic review found an overall positive association between hip dysplasia and the development of osteoarthritis of the hip. The studies were primarily of patients age 50-60 or older. The authors suggested that in younger age groups the relation between hip dysplasia and OA or hip complaints may be much higher (Lievense et al., 2004). Another review found an association between bony abnormalities found in acetabular dysplasia and femoroacetabular impingement with hip OA. Preliminary evidence suggested that acetabular dysplasia was a risk factor for OA but prospective longitudinal studies were needed to confirm a causal relationship (Harris-Hayes and Royer, 2011).
FAI is considered a prearthritic condition in young adults. FAI is defined as a collection of bony morphological abnormalities of the hip joint that result in abnormal contact during motion. Two main lesions are described, ‘cam deformity’ and ‘pincer deformity’. In cam deformities, the femoral head-neck junction is not uniformly spherical, with a bulge in one area that impinges on the acetabular labrum as the bulge is moved into proximity with the labrum. In pincer deformities, the acetabulum is deeper, with a labral edge that comes further towards the femoral neck. Pain is typically chronic and deep, and can be aching anterior groin pain on sitting. Pain may also present during or after activity, and during activity the pain can be sharp and occasional only (Zhang et al., 2015).
There may be an inflammatory component to development of OA secondary to FAI. A small study found evidence of an inflammatory cell infiltrate (in particular mast cells and macrophages) in FAI along with significant neovascularisation. This suggests the involvement of immune pathways in events mediating hip impingement (Elias-Jones et al., 2015).
A radiographic study of patients aged 18-50 (mean age 32) presenting with hip-related symptoms showed an 87% prevalence of FAI. (Ochoa et al., 2010).
An analysis of hip morphology in the Johnston County OA project found increased risk of worsening hip OA in men due to baseline cam deformity (greater baseline AP alpha angles, higher Gosvig ratio and acetabular index) while coxa profunda was negatively associated. In women, greater baseline AP alpha angles, smaller minimum joint space width, protrusion acetabuli and triangular index sign were associated with hip OA (Nelson et al., 2015).
Around 80% of Japanese patients develop hip OA secondary to acetabular dysplasia. The rate of acetabular dysplasia is higher than in US patients and significantly higher than British patients with OA. CT and X-ray studies show an association between dysplasia and a reduced transverse pelvic inlet diameter and a hypoplastic inward wing of the ileum (Okano et al., 2014).
During childhood before closure of the growth plate, the capital femoral epiphysis can be displaced posteriorly and inferiorly on the femoral neck. This often causes significant pain and disability at the time, and if not addressed surgically it often leads to early OA of the hip. The recommended management technique is in situ pinning but this may not restore normal anatomy, leading to FAI, hip pain and early onset hip OA (Kuzyk et al., 2011). Any decision on fitness for service in the military, police or fire services should depend on minimal FAI on imaging.
The blood supply to the femoral head is tenuous, and may be compromised in childhood or adulthood, often due to trauma. Childhood AVN, sometimes called Legg-Calve-Perthes disease, or Perthes disease, usually occurs in children aged 4-10. Childhood AVN may be secondary to a slipped femoral epiphysis, and it may also arise due to rapid growth in the epiphysis causing interruption of the blood supply. Natural removal of necrotic tissue and replacement with new bone can lead to normal joint structure and function. Protection of the joint during this healing process is critical to a good outcome, and a young adult with a history of childhood AVN but with a hip joint that appears normal on X-ray should have a normal risk of OA, and be considered fit for a role in the military, police or fire services.
A Norwegian cohort study of sixty cases of childhood AVN over forty one years found 33% developed OA in the fourth decade and 55% had developed OA by the fifth decade (Heesakkers et al., 2015).
Studies show a strong familial link with hip OA, but most cannot distinguish between genetic and common environmental factors. A large twin follow-up study from the Danish Twin Register and Danish Hip Arthroplasty Register between 1995 and 2010 found a significant additive genetic component of 47%, a shared environmental component of 21% and a unique environmental component of 32%. The genetic influence increases significantly from age 60 onwards (Skousgaard et al., 2015).
A review of studies (Spector and MacGregor, 2004) suggests that for hip OA genetic factors are responsible for around 60% of cases. Studies include twin studies, adoption studies, family history and clustering studies and these also include rare genetic disorders.
Congenital factors for hip OA include a family history, being first born, breech presentation at birth, female gender, high birth weight and oligohydramnios. There may in addition be nutritional, hormonal and mechanical influences, with ligament laxity a possible factor. The overall significance of all these remains to be determined (Rhodes and Clarke, 2014).
A study of 322 patients from arthroplasty registries found a significantly increased requirement for arthroplasty on the dominant side. Cerebral laterality is a contributing factor predisposing the dominant side to hip OA (Cawley et al., 2015). This may reflect increased use of the dominant leg for example in sport, or in applying force during manual labour.
Internal reduction and fixation of femoral neck fracture can lead to cam-type FAI, particularly if there is malalignment of the fracture during fixation. A follow-up study found 75% of postoperative cases had signs of radiographic impingement, higher than expected (Wendt et al., 2013).
Significant physical activity during childhood and adolescence can lead to structural changes within the hip joint.
A cohort study of preprofessional Dutch footballers age 12-19 found that those who trained in youth before closure of the growth plate developed significant cam deformities. Training after closure showed no significant changes in strucure around the femoral head and neck (Agricola et al., 2014).
There is good evidence that high physical workload is a risk factor for OA hip. The studies showing this only find a link with frequent and long-term high levels of physical workload, not just occasional heavy manual handling.
A systematic review of workload as a risk factor was unable to estimate a quantitative dose-response relationship between workload and hip OA, but there was enough evidence to identify job-related heavy lifting as a risk factor, and the evidence suggested a risk from prolonged standing. Heavy lifting was defined as long-term frequent (44,000-95,000 lifts in one study) lifting of 10-25kg loads. No association was found between hip OA and sitting or walking at work, and there was no clear association between hip OA and stair climbing or jumping at work (Sulsky et al., 2012).
An older case-control study found that there was no clear association with sitting, bending, kneeling, squatting, walking (and walking over rough ground for greater than two hours a day), running for over an hour a day, climbing ladders, climbing more than 30 flights of stairs a day, and driving for over four hours a day. There was an OR of 2.7 (95% CI 1.0-7.3) for those standing for more than two hours a day for over forty years. There was an OR of 2.5 (95% CI 1.1-5.7) for those lifting or moving weights greater than 56lbs for over twenty years (Croft et al., 1992).
An Icelandic study found an age adjusted odds ratio of 3.6 (95%CI 2.1-6.2) of total hip replacement due to OA in farmers, but no other occupations showed increased risk in men, and for women there was no increased risk for any occupation (Franklin et al., 2010). A Danish study using only occupational codes in a national registry also found that male farmers were most at risk from hip OA with an increased risk found after only one to five years in occupation (HR 1.63) rising to a threefold risk after ten years. An elevated risk of hip OA was also found in male healthcare assistants who had worked for more than ten years (HR 1.71). An increased risk of hip OA was generally considered to be related to any occupation involving heavy physical work in both men and women. (Andersen et al., 2012).
There is good evidence that trauma to a joint can substantially increase the risk of OA in that joint. Trauma may be a fracture through the joint line, disruption to ligaments around the joint, disruption to structures within the joint such as the acetabular labrum, a direct blow to the joint surfaces, or a penetrating injury to a joint. Infection of a joint may follow trauma. Any history of trauma needs to be supported by documented evidence of the event, clinical assessment at the time and the treatment received. Dislocation of the hip, fracture-dislocation of the hip and acetabular fractures are particularly likely to predispose to OA of the hip. One French study found a third of patients with these conditions developed hip OA within 1-20 years (Lequesne et al., 1993).
Vascular compromise of the femoral head can occur in adults and is associated with a variety of non-traumatic conditions including steroid therapy and alcoholism although around twenty percent of cases are idiopathic. It is also a complication of hip dislocation or femoral neck fracture. Loss of blood supply leads to death and collapse of subchondral bone. This can lead to painful synovitis and the altered shape of the femoral head often leads to early OA.
A systematic review of prevalence of OA in former elite athletes found indications that there was a higher prevalence with hip OA ranging from 2-60%, (Gouttebarge et al., 2015). Another recent review on running found no evidence that moderate running increased the risk of hip OA while the risk from intense running remained uncertain. There was insufficient literature on barefoot/minimalist running to comment (Hansen et al., 2012). Another review found no increase in risk of hip OA for recreational runners who ran 12-14 miles a week for up to 40 years while higher rates were seen in contact sports, particularly professional players (Molloy and Molloy, 2011). Overall there appears to be good evidence for an increased prevalence among elite athletes, while general sports activity is protective.
A systematic review from 2003 found none of the older published reviews assessed included clearly defined inclusion and exclusion criteria, a methodologic quality assessment or explicit criteria for assessment of the strength of evidence. This review concluded that there was moderate evidence for a positive relationship between physical sporting activity and hip OA with an OR of approximately 2. This applied particularly to running. The evidence for athletics was limited, while the evidence for soccer playing and ballet dancing was conflicting. There was a stronger associated for clinically assessed hip OA than radiographically assessed hip OA so it was felt that the findings could reflect the fact that people undertaking sport had the same degree of degeneration but more symptoms because of sporting activity, or that the symptoms reflected other causes than OA of the hip. Overall, the quality of studies was considered low (Lievense et al., 2003).
Overall there is no clear evidence to suggest military activity, or general sporting activity in the military causes hip OA.
A study showed a significant increase in risk of OA of the hip where there is an increase in bone mineral density of the hip (Nevitt et al., 1995). There is a clear inverse relationship between osteoporosis and osteoarthritis. This appears to be a combination of local factors directly related to bone density, and shared general genetic factors (Antoniades et al., 2000). Bone density is known to be also related directly to muscle mass, however genetic predisposition to increased muscle mass does not fully explain the risk of OA in high bone density; there appears to be a direct genetic factor involving bone (Arden and Spector, 1997).
Substantial obesity equates to heavy physical activity so a link between hip OA and obesity would be expected. The relationship is not as strong as for knee OA, but a recent systematic review found a significant link, with a five unit increase in body mass index (BMI) showing a relative risk of 1.11(95%CI 1.07-1.16). BMI was positively associated with hip OA defined by radiography, clinical symptoms and clinical surgery (Jiang et al., 2011).
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