Adult Hip Dysplasia (DDH)

The hip is a ball-and-socket joint between the femoral head and the acetabulum. In a normal hip the socket covers the ball deeply, like a half-bowl over a sphere. In dysplasia the socket is shallow, often tilted up and outwards, so the femoral head is only partially contained. The result is that load passing through the joint is not spread evenly across the cartilage but concentrated on the edge of the socket and the labrum (the ring of cartilage around the socket rim).

The condition exists on a spectrum from mild lateral undercoverage to frank dislocation. The term "developmental dysplasia of the hip" (DDH) is preferred to "congenital dysplasia" because the joint is often stable at birth but develops abnormally as the child grows, and many cases are not detectable on the newborn or six-week hip checks.

Adult acetabular dysplasia is approximately nine times more common than infantile DDH diagnosed at screening. A normal childhood examination does not rule out dysplasia presenting later. Many adults are told for years that their groin pain is "muscular" before the underlying structural problem is identified on a properly oriented standing pelvic X-ray.

The fundamental problem in dysplasia is that the acetabular socket does not develop deeply enough. The exact reasons are multifactorial: genes, the position of the baby in the womb, hormone exposure, and rarely childhood conditions like Perthes disease or a slipped epiphysis can all contribute.

The most important risk factors are:

• Female sex. Women are affected approximately four times more often than men, partly because of the effect of maternal relaxin on the developing fetus, and partly because the female pelvic geometry is different.
• Family history. Sibling risk is around 6 per cent, parental risk 12 per cent, and approximately 36 per cent if both a parent and a sibling are affected.
• Breech presentation at birth. Particularly frank breech with the hips flexed and knees extended.
• Firstborn status. A tighter uterus in the first pregnancy limits fetal hip movement.
• Childhood swaddling. Tight wrapping of the legs in extension and adduction during infancy increases dysplasia risk. The Royal College of Paediatrics recommends "hip-healthy" swaddling that allows hip flexion and abduction.
• Neuromuscular conditions in childhood. Cerebral palsy, spina bifida, and similar conditions can cause acquired dysplasia.
• Maternal hormones. Maternal relaxin contributing to ligamentous laxity in the fetus, particularly in girls.

Many adults are diagnosed in their 20s, 30s, or 40s with no family history and no childhood risk factors recorded. The dysplasia was simply mild enough to be silent until adult loading and activity brought it to attention.

The treatment options sit on a spectrum that depends mainly on age and the state of the cartilage. Mr Hussain will guide you through which option fits your case.

• Targeted physiotherapy. Posterolateral hip strengthening (gluteus medius and minimus) first, progressing from short-lever to long-lever exercises. Compensates for the under-covered femoral head by improving dynamic stability. Strongest evidence base of any non-surgical intervention.
• Activity modification. Avoid pivoting, deep flexion loading, and high-impact sport. Many patients can find a sustainable activity level that minimises symptoms.
• NSAIDs. Topical and oral, used for symptom flares.
• Weight management. Reduces joint loading and slows symptom progression.
• Periacetabular osteotomy (PAO). The gold-standard joint-preserving operation for symptomatic dysplasia in patients whose cartilage is preserved. The Bernese (Ganz) PAO cuts and reorients the acetabulum to provide proper coverage of the femoral head. Indicated typically under age 40 to 45, with preserved cartilage (Tönnis grade 0 or 1), LCEA under 20 degrees, a congruent reducible hip, and no major femoral head asphericity. Long-term outcomes are good in suitable patients, with hip survivorship around 76 per cent at 10 years and 63 per cent of hips preserved and minimally symptomatic at long-term follow-up in published Boston cohorts.
• Hip arthroscopy. Used for selected cases of borderline dysplasia (LCEA 18 to 25 degrees), particularly when a labral tear is the dominant symptom. Mid-term outcomes are comparable with PAO in some series; the decision is driven by the Tönnis angle, instability features, and labral pathology rather than the LCEA alone.

Mr Hussain performs hip replacement and hip resurfacing but does not personally perform PAO. Appropriate younger patients are referred to a specialist hip preservation surgeon. The orthopaedic community has a small number of high-volume PAO centres in the UK that achieve the best results.

If you take prescribed medication, particularly blood-thinners or anti-inflammatories, please review Mr Hussain's patient guide on medications to pause before hip or knee surgery as you approach a surgical decision.

Mr Hussain trained in both hip replacement and hip resurfacing and is one of a relatively small group of UK surgeons who offer both approaches in selected dysplasia patients. The choice depends on the Crowe grade, age, sex, bone quality, and femoral head size.

For a deeper comparison of the two techniques covering recovery, return to sport, and implant choice, read Mr Hussain's patient guide on hip resurfacing versus total hip replacement. Active patients considering resurfacing may also find returning to sport after hip resurfacing useful for setting realistic expectations.