Osteoarthritis Of The Hip


Osteoarthritis (OA) is the most common joint disorder in the world, and the prevalence of OA is expected to rise in the next few decades. Osteoarthritis is a chronic degenerative joint disease that originates in the cartilage and affects underlying bone, soft tissues, and synovial fluid. Osteoarthritis commonly affects the knee and hip. Symptomatic OA is associated with pain, stiffness, swelling, joint instability, muscle weakness, and poor health status. Symptomatic OA is the most common reason for hip surgery.


The hip joint is the synovial articulation between the head of the femur and the acetabulum of the pelvic bone.  This deep ball and socket joint allows for structural stability during weight bearing activities such as walking and running.  The acetabular labrum acts similarly to the meniscus in the knee to deepen the socket for the femoral head. Three major ligaments also help to stabilize the joint, these include: iliofemoral ligament -   Y shaped ligament which becomes taught with hip extension; ischiofemoral ligament – screws the femoral head into the acetabulum which helps to limits hyperextension; pubofemoral ligament – limits excessive abduction and extension and helps to prevent the head of the femur from sliding out of the capsule inferiorly.  



OA is the single most common joint disease, with an estimated prevalence of 60% in men and 70% in women after the age of 65 years. Osteoarthritis currently affects an estimated 40 million people in the United States alone. However, the prevalence of symptomatic osteoarthritis among Caucasians 55 and older is only about 5%. Hip osteoarthritis is less common than knee OA. Both the incidence and prevalence of hip OA are expected to rise in the coming decades as life expectancy increases, aging "baby boomer" population in America, and with the increase participation in extreme sports and activities.

Potential Etiologies1,7,9:

Osteoarthritis was previously thought to be a normal consequence of aging and actually considered to be due to "wear and tear," however, it is now widely accepted to be a result of a combination of factors that can affect any synovial joint. These factors include: biomechanics of the joint, genetics, nutrition, weight control, estrogen use, bone density, muscle weakness, and joint laxity. Risk factors can be broken into two categories: modifiable risk factors, and non-modifiable risk factors. Modifiable risk factors include: smoking because smoking with OA can lead to greater cartilage loss, weight loss since a modest amount of weight loss (10-15 lbs) can alleviate symptoms and delay OA disease progression, exercise given that muscle weakness is a risk factor for OA, and nutrition since intake of dietary antioxidants may possibly protect against OA. Non modifiable risk factors include: age and gender, sex hormones (OA incidence in women following menopause increases possibly due to estrogen defiency), genetics, generalized ligament laxity (appears to be a predisposing factor as seen in patients with Ehlers-Danlos syndrome, RA, SLE, or Marfan’s syndrome), and previous injury (since impact sports are known to increase the risk for OA this may be considered modifiable, however, previous surgery or other injury is not a modifiable risk factor).

Clinical Manifestations9

Patients with osteoarthritis will demonstrate limited range of motion with crepitus during movement, tender to palpation, joint effusion, and joint deformity. Inflammation in the joint and soft tissue may be evident on patients with increased pain. For most patients, the onset of pain will have been slow and gradual and the pain will be described as deep and boring which is worse with activity and better after rest. Stiffness may occur after prolonged periods of inactivity but usually only lasts between 5-10 minutes.

Diagnostic Tests5,9:

Although symptoms and radiographic changes do not always overlap, radiographic osteoarthritis can help to explain patient symptoms. X-rays or MRIs can be used to determine the extent of damage to the joint. Radiographic findings include joint space narrowing, osteophytes and subchondral sclerosis on plain film radiographs. These tests will easily diagnose severe OA, however moderate or early signs of OA may not be shown on the images. Joint space narrowing may predict the early stages; the normal hip joint space is 3-5mm, a reduction of greater than or equal to 0.5mm represents a clinically significant change.

Evaluation/Special Orthopedic Tests5,10:

The most commonly used outcome measures for hip OA are the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC), the lower extremity functional scale (LEFS), and the Harris Hip Scale. These tests measure patient reported function and pain and can be used to to quantify subjective data in order to check progress on patient goals and the results of treatment. To measure activity limitations and participation restriction, tests such as the 6 minute walk test, timed up and go test, self paced walk test, and stair measures can be used. Objective measures such as strength and range of motion tests can also be used to track progress.

Classification Criteria for Osteoarthritis of the Hip

Clinical (history, physical examination, laboratory) classification criteria for osteoarthritis of the hip, classification tree format
1. Hip pain
2a. Hip internal rotation <15 degrees
2b. ESR greater than or equal to 45mm/hour
3a. Hip internal rotation greater then or equal to 15 degrees,
3b. Pain on hip internal rotation,
3c. Morning stiffness of the hip greater than or equal to 60 minutes
3d. Age greater than 50 years

Combined clinical (history, physical examination, laboratory) and radiographic classification criteria for osteoarthritis of the hip, traditional format
Hip pain and,
At least 2 of the following three features:
- ESR <20mm/hr
- Radiographic femoral or acetabular osteophytes
- Radiographic joint space narrowing (superior, axial, and/or medial)

Conservative Treatment3,5,9,11:

The goals of conservative treatment include:

  • Pain reduction
  • Education
  • Optimization of joint function and ability to perform tasks of active daily living (ADL's)

In order to reduce pain analgesics and non-steroidal anti inflammatories are often prescribed in the initial phases of OA. As the disease progresses steroid injections may be recommend to reduce pain while the patient continues with physical therapy for strengthening. Often these drugs are avoided due to the risk of gastrointestinal bleeding. Some alternative medicine approaches include glucosamine or chondroitin, however the effectiveness of these supplements is often debated with more current evidence leading to the fact that these are not effective.

Physical Therapy Management of Hip OA

Surgery & Post-op Treatment2:

Surgical treatment may be recommended if conservative treatment has failed and the patient is in the later stages of osteoarthritis. Surgery is considered if the pain is affecting the patient's sleep patterns or if the pain is constant and severe. During a total hip replacement the orthopedic surgeon will remove the damaged cartilage and bone, and replace the structures with metal, plastic, or ceramic. Typically the tools are designed so that bone will grow into the components and to help secure the replacement. Depending on the type of surgery, there may be movement precautions during and after recovery. Preoperative education, and post operative physical therapy should be performed in order to further aide in the patient recovery. Most patients who undergo a total hip replacement report significantly improved pain and function.

Additional Web Based Resources:

1. Arden N, Nevitt MC. Osteoarthritis: Epidemiology. Best Pract Res Clin Rheumatol. 2006;20(1):3-25. doi: 10.1016/j.berh.2005.09.007.
2. American Academy of Orthopaedic Surgeons. http://orthoinfo.aaos.org/topic.cfm?topic=a00377. Reviewd April, 2009. Accessed December, 2011.
3. Bennell KL, Hinman RS. A review of the clinical evidence for exercise in osteoarthritis of the hip and knee. J Sci Med Sport. 2011;14(1):4-9. doi: 10.1016/j.jsams.2010.08.002.
4. Cheung PP, Gossec L, Dougados M. What are the best markers for disease progression in osteoarthritis (OA)?Best Pract Res Clin Rheumatol. 2010;24(1):81-92. doi: 10.1016/j.berh.2009.08.009.
5. Cibulka MT, White DM, Woehrle J, et al. Hip pain and mobility deficits—hip osteoarthritis: Clinical practice guidelines linked to the international classification of functioning, disability, and health from the orthopaedic section of the american physical therapy association. J Orthop Sports Phys Ther. 2009;39(4):A1-25. doi: 10.2519/jospt.2009.0301.
6. Drake R, Vogl W and A Mitchell. Gray’s Anatomy for Students Churchill Livingstone, 2nd edition. Elsevier; 2009.
7. Felson DT, Chaisson CE. Understanding the relationship between body weight and osteoarthritis. Baillieres Clin Rheumatol. 1997;11(4):671-681.
8. Fransen M. Exercise for osteoarthritis of the hip. Cochrane Database of Systematic Reviews. 2009(3).http://search.ebscohost.com/login.aspx?direct=true&db=chh&AN=CD007912&site=ehost-live.
9. Goodman CG, Fuller KS. Pathophysiology: Implications for the physical therapist, 3rd edition. St Louis, MO: Saunders Elsevier; 2009.
10. Magee DJ. Orthopedic physical assessment. 5th ed. St. Louis, MO: Saunders Elsevier; 2008.
11. Wandel S, Juni P, Tendal B, et al. Effects of glucosamine, chondroitin, or placebo in patients with osteoarthritis of hip or knee: Network meta-analysis. BMJ. 2010;341:c4675. doi: 10.1136/bmj.c4675.
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