Hip OA Flashcards
Forces through the hip
1) standing
2) walking level normal
3) walking up stairs
4) running
1) 0.5 body weight
2) 2.4 x body weight
3) 2.5 body weight
4) 3-4 x body weight
Primary OA Risk factors
- wear and tear
- obesity: for every added lbs of BW an additional 3 lbs may act at the hip
- age: mid age to elderly
- overuse and abuse: sports/occupation
Secondary OA: risk factors/what is it
- follows a traumatic injury
- Disease
- Anatomic alignment
- capsular tightness/hypomobility
what traumatic injuries can cause secondary OA
- hip dislocation
- hip fracture
(femoral head, femoral neck, intertrochanteric, subtrochanteric/shaft)
What conditions can lead to DJD of the hip
- congenital hip dysplasia/dislocation
- Legg Perthes: osteochondrosis - 3-10 y/o
- slipped capital femoral epiphysis 10-16 y/o
Anatomic alignment issues that can cause OA
- abnormal forces at the hip
- excessive anteversion, retroversion
- leg length asymmetry = longer leg has an increase forces on superior lateral acetabulum and femoral head
- femoral-acetabular impingement
Hip angle of inclination
- forces are not ideally located on the hip when there is an abnormal angle
- coxa vara = <125
- coxa valga = >125
Anteversion/retroversion
- neck torsion angle
- normal = 15 anterversion
- excessive anteversion = >15
- retroversion <15
Femoral acetabular impingement
- CAM impingement: large FH and small acetabulum
- Pincer type impingement: larger overhanging acetabulum
- combination of pincer and CAM
- these may result in degeneration of the hip joint labrum and articular cartilage
How can a tight capsule of the hip or hypomobilty cause secondary OA
- increase compressive forces in a smaller contact area
- “shock loading” = compression in a small contact area coupled with the high compressive forces of WB
- decreased movement of synovial fluid/distribution of nutrients
- leads to less nutrients to articular cartilage
Effect of a hip flexor contracture on standing
BW is more anterior
- more joint reaction forces due to glute max needing to contract
- increase in forces to hip joint in area of thinner articular cartilage
How does articular degeneration occur?
- decrease in GAGs, proteoglycans and H2O biding capacity
- chondrocytes turn off = dont keep up with attrition of cells
- cartilage collagen fibers thinner, stiffer, less elastic
- decreased ability to deform, absorb shock, decrease force attenuation
- increase forces to subchondral bone causing sclerosis
what else can happen with OA in addition to degradation of articular cartilage
- osteophytes at joint margins leading to irritation of synovial capsule
- inflammation/synovitis/thickened synovium leads to capsular fibrosis which decreases ROM and nutrition
- cycle of progression
Hip OA diagnosis
- DX: X-ray in standing
- decreased joint space = loss of articular cartilage
- sclerosis on the subchondral bone (related to the increase in forces)
- pseudocytes: synovial fluid pushed into bony porous areas
- osteophytes at joint margins
Hip OA signs in the history and interview
Complaints of:
- pain in groin, anterior thigh, lateral thigh, posterior thigh
- pain worsens with WB or increase hip stresses
Signs:
- decrease ROM = difficulty with donning socks and shoes, squatting, stairs
- gradual onset/post trauma
- morning stiffness (1/2 hr), better mid-day with movement
- increased pain end day due to excessive activity and WB
Hx:
- childhood hip pathology
