Hip Osteoarthritis: Causes, Symptoms, and Treatment

What Is Hip Osteoarthritis?

Osteoarthritis (OA) of the hip is a degenerative joint condition characterized by the gradual breakdown of articular cartilage — the smooth, protective tissue that covers the femoral head (ball) and acetabulum (socket) of the hip joint. As cartilage wears away, bone rubs on bone, causing pain, inflammation, and progressive joint damage.

Hip OA affects approximately 10% of adults over 60 and is one of the leading causes of disability worldwide. When end-stage, it is one of the most common reasons for total hip replacement — one of the most successful surgical procedures in all of medicine.

Joint Anatomy

The hip is a ball-and-socket joint:

Femoral head: The "ball" at the top of the thighbone (femur)
Acetabulum: The "socket" in the pelvis
Articular cartilage: A 2–3mm layer of smooth cartilage covering both surfaces
Joint capsule: Fibrous sleeve enclosing the joint
Synovial membrane: Lines the capsule and produces synovial fluid (joint lubrication)

In OA, cartilage progressively erodes through:

Surface fibrillation and cracking
Full-thickness cartilage loss
Subchondral bone exposure and sclerosis
Osteophyte (bone spur) formation at joint margins
Joint capsule thickening and synovial inflammation

Causes and Risk Factors

Age: The strongest risk factor; OA prevalence rises sharply after 50
Obesity: Each pound of body weight translates to 3–5 lbs of hip joint force during walking — the most modifiable risk factor
Prior hip injury: Fracture, dislocation, labral tears, FAI
Female sex: Women develop hip OA more frequently, especially after menopause
Genetics: Strong heritable component to cartilage quality
Hip dysplasia (developmental): Congenital or developmental abnormal hip shape accelerates wear
Femoroacetabular impingement (FAI): Abnormal bony morphology causing cartilage damage over decades
Repetitive heavy work: Loading and impact sports

Symptoms

Groin pain: The hallmark; deep groin pain (not lateral hip/buttock) is characteristic of true hip joint pathology
Pain with activity: Walking, rising from a chair, climbing stairs
Morning stiffness: Typically resolves within 30 minutes (distinguishing OA from inflammatory arthritis)
Limited range of motion: Difficulty putting on socks and shoes, difficulty crossing legs
Antalgic gait: Limping to offload the painful hip
Referred pain: Hip OA frequently causes knee pain, thigh pain, or lower back pain — this can delay correct diagnosis
Night pain: In advanced OA, pain may disturb sleep

Diagnosis

Physical examination:

Reduced internal rotation is the first and most sensitive finding in hip OA
FADIR test (flexion, adduction, internal rotation) — reproduces groin pain
Log roll test
Abductor strength testing

X-ray: Standing AP pelvis and lateral hip X-rays are the standard imaging:

Joint space narrowing (direct measure of cartilage loss)
Subchondral sclerosis (bone thickening)
Osteophytes (bone spurs)
Subchondral cysts

MRI: For younger patients with equivocal X-rays; identifies early cartilage damage, labral tears, bone marrow edema

Treatment

Conservative Management

Weight loss: 10 lbs of weight loss reduces hip OA progression significantly
Exercise: Low-impact exercise (swimming, cycling) maintains muscle strength and joint health; strengthening hip abductors, extensors, and core
Physical therapy: Gait training, hip and core strengthening, stretching
NSAIDs: Ibuprofen, naproxen, or celecoxib for pain and inflammation
Acetaminophen: Analgesic for breakthrough pain
Assistive devices: Cane (used in the opposite hand) reduces hip joint loading
Intra-articular corticosteroid injections: Temporary pain relief; typically 2–6 months
Hyaluronic acid injections: Less evidence than for knee OA; some benefit possible

Surgical Treatment

When conservative management fails to control pain and maintain function, total hip replacement (total hip arthroplasty) is the gold standard treatment. It reliably eliminates pain and restores function for 15–25 years in most patients.