19 Hip Osteoarthritis
Etiology of Hip Osteoarthritis
I. Primary “idiopathic” hip osteoarthritis (OA):
Historically described as “wear and tear” or overuse.
Common age-related changes, although routine use over time does not account for all aspects of the pathology.
Genetic predisposition 1 :
More common in females.
Possible link to Collagen IX gene (Col9A) phenotype.
II. Secondary OA:
Post slipped capital femoral epiphysis.
Dysplasia of the hip: shallow acetabular socket resulting in edge loading and increased articular contact forces.
Sequela of Legg–Calvé–Perthes disease with resulting femoral head irregularities (the square peg in a round hole):
Development often depends on containment of the femoral head and congruency of the ultimate joint through adolescence and adulthood.
Posttraumatic arthritis: prior damage to chondrocytes, labrum, or osseous structures.
Septic arthritis: infection and inflammatory response resulting in articular damage.
III. Femoroacetabular impingement (FAI):
Cam impingement: prominent bone present at the femoral head–neck junction leading to cartilage damage with hip motion.
Pincer impingement: excessively deep socket or retroversion leading to bony impingement.
Combination FAI frequently demonstrates features of both aspects of the impingement spectrum:
Ganz and several others have suggested that subtle changes in hip anatomy, such as that seen in FAI, lead to abnormal contact forces and progressive changes of the osteochondral and labrocapsular structures.
This concept proposes that idiopathic OA is unrecognized or subtle forms of these secondary diagnoses.
IV. Differential diagnosis: other conditions leading to hip degeneration:
Avascular necrosis of the femur:
Vascular compromise to the femoral head resulting in subchondral osteonecrosis and collapse, cartilage damage, and deterioration.
Risk factors include trauma, corticosteroid use, alcohol abuse, hematologic conditions, irradiation, and cytotoxic insults.
Inflammatory arthritis: constellation of conditions leading to joint destruction in the setting of varying degrees of inflammation:
Rheumatoid arthritis: polyarthropathy with characteristic stigma including prolonged morning stiffness and morphology changes to hands/feet.
Systemic lupus erythematosus: “lupus”:
Systemic inflammatory condition that affects multiple body parts including skin, brain, kidney, heart, lungs, and joints. Malar rash is a common facial finding.
Hallmark stiffness at multiple body parts most notably in the sacroiliac joints and spine.
Referred back pain:
Often presents as pain in the buttocks and follows a radiating pattern below the level of the knee.
This can present with back pain, or neurologic changes of motor or sensory or both.
A corticosteroid injection into the hip can be useful to distinguish hip versus referred spinal pathology.
I. Macroscopic changes:
Loss of articular cartilage leading to increased contact forces and high coefficient of friction.
Results in eburnation of bone, activation of ossification centers, osteophyte formation, and labral degeneration.
Coxarthrosis—“hip joint inflammation”—misnomer as inflammatory process is not always a major factor:
Loss of proteoglycan content within articular cartilage. 2
II. Microscopic changes:
Loss of proteoglycan bonds to hyaluronic acid:
Increased type VI collagen replaces normal type II collagen.
Increased keratin sulfate–decreased chondroitin sulfate composition of glycosaminoglycans.
INCREASED water content up to 90%.
Elevated proteolytic enzymes 3 :
Metalloproteinases present in joint fluid.
Cathepsins B and D overexpression.
Nitric oxide synthase pathway activation.
Inflammatory cytokines upregulated:
Interleukin 1-beta (IL-1β)
Tumor necrosis factor α (TNF-α).
Upregulation of growth factors:
Fibroblast growth factor-2 (FGF-2) decreases aggrecanase activity and upreglulates metalloproteinases.
Transforming growth factor B1 (TFG-B1).
The end result is articular cartilage changes and chondrocyte apoptosis ( Fig. 19.1 ).
I. Pain quality:
Most frequently patients present with deep groin pain—progressively worsening with the severity of the disease.
“C sign” can represent a deep and difficult-to-localize pain: vague pain described by cupping hand around the lateral hip in a “C” shape to describe the location.
Buttocks, thigh, or knee pain may also be present but may represent other pathologies such as lumbar pathology, trochanteric bursitis, or vascular compromise.
Worsened by increased activity or trauma:
Tends to be worse with prolonged inactivity and then attempted motion.
Too much of any one activity is difficult (standing too long, sitting too long, etc.).
II. Character of symptoms:
The patient may note leg length differences as the disease pattern progresses.
Forward flexion through pelvis—hip contracture.
Poor rotational motion is common—particularly internal rotation:
Difficulty donning socks or shoes.
Hard time getting into/out of low chairs or toilet, stair climbing, getting in and out of cars.
Notable feeling with weather and barometric pressure changes.
Symptoms present in the morning or the first few steps after sitting for too long:
Additional symptoms such as:
Radiating pain into the knee.
Throbbing while at rest.
Prolonged stiffness in the morning may suggest inflammatory arthritis or avascular necrosis.
Night pain should trigger thoughts of tumor or infection.
Clinical evaluation of the hip should take a systematic approach. This requires in-depth knowledge of the local anatomy, as well as a variety of techniques to localize the cause. These specialized examination techniques, when combined with a good clinical history, can allow accurate diagnosis. 4
I. Gait pattern changes and limping:
The patient’s gait should be observed without the use of a walking aid if the patient can manage. This may reveal specific patterns of disease as follows:
Antalgic gait: shortened stance phase on affected leg to minimize joint reactive forces on painful joint.
Trendelenburg gait: consequence of abductor weakness manifesting as leaning (shifting body weight) over the weak side to prevent the need of pelvic support by the affected gluteal muscles.
Positive foot progression angle: foot externally rotated (suggests external rotation contracture).
Requirement of an assistive device to maintain balance or minimize pain (best when used in the contralateral hand).
Look for lumbar hyperlordosis with walking or hunched-over gait due to hip flexion contracture.
II. Range of motion:
Limited hip motion:
Hip rotation should be assessed at 90 degrees of flexion and compared with contralateral hip.
Pelvis should be stabilized to prevent lumbosacral motion with examination.
Difficulty with external rotation, hip extension, adduction, abduction, or hip flexion often with obligate external rotation.
Limited internal rotation: posterior capsular contracture, FAI.
Obligate external rotation (sits with legs crossed).
Hip flexion contracture (Thomas’ test): both hips are flexed up and the affected side is allowed to extend until the end point or pelvic tilt is noted.
III. Provocative maneuvers:
Trochanteric tenderness may signal bursitis or abductor tendonitis and may occur simultaneously with hip OA.
Passive straight leg raise sign performed to rule out referred back symptoms.
Resisted straight leg raise (Stinchfield’s test) with reproduction of pain.
Pain with “figure 4” position (Patrick’s test).
IV. Leg length differences: noted at either the iliac crests, the tibial tubercles, or the malleoli:
This can be measured using calibrated blocks with subjective or radiographic assessment for length equality.
Direct palpation of the iliac crests in a neutral stance.
Measurement of the medial malleoli with respect to one another or by measuring from a fixed distance (such as anterosuperior iliac spine [ASIS]) to the malleoli:
Apparent leg length—measure from the umbilicus to the medial malleoli.
True leg length—measure from the ASIS to the medial malleoli.