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Orthopaedic Proceedings
Vol. 93-B, Issue SUPP_III | Pages 250 - 250
1 Jul 2011
Beaulé P Hack K DiPrimio G Rakhra K
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Purpose: A growing body of literature confirms that idiopathic OA is frequently caused by subtle, and often radiographically occult, abnormalities at the femoral head-neck junction or acetabulum that result in abnormal contact between the femur and acetabulum. This condition, known as femoroacetabular impingement, is a widely accepted cause of early OA of the hip. MRI is the imaging modality that is most sensitive in detecting cam morphology. There is currently little published data regarding the prevalence of abnormalities of the femoral head-neck junction in patients without hip pain or previous hip pathology. The primary aim of this project is to examine the incidence of cam morphology in a population without hip pain or pre-existing hip disease using non-contrast MRI.

Method: Two hundred asymptomatic volunteers underwent magnetic resonance imaging targeted to both hips. Subjects were examined at the time of MRI to document internal rotation of the hips at 90 degrees flexion and to assess for a positive impingement sign. The mean age was 29.4 years (range 21.4–50.6); 77.5% were Caucasian and 55.5% female. The Nötzli alpha angle was measured on oblique axial images through the middle of the femoral neck for each hip. A value greater than 50 degrees was considered consistent with cam morphology. Measurements were performed independently by two musculoskeletal radiologists.

Results: Twenty-six percent of volunteers had at least one hip with cam morphology: 20% had an elevated alpha angle on either the right or the left side, and 6% had bilateral deformity. The average alpha angle was 42.6 degrees on the right (SD=7.9) and 42.4 degrees on the left (SD=7.7). Internal rotation was negatively correlated with alpha angle (p< .05). Patients with an elevated alpha angle on at least one side tended to be male (p< .01).

Conclusion: The high prevalence of cam morphology in asymptomatic individuals is critical information in determining the natural history of FAI as well as establishing treatment strategies in patients presenting with pre-arthritic hip pain.


Orthopaedic Proceedings
Vol. 91-B, Issue SUPP_II | Pages 247 - 247
1 May 2009
Pollock JW Conway A DiPrimio G Giachino AA Hrushowy H Rakhra K
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The traditionally accepted etiology of Scapholunate Advanced Collapse (SLAC) requires traumatic rupture of the scapholunate (SL) ligament which leads to abnormal wrist kinematics and thereafter severe localised degenerative arthritis of the wrist. The purpose of this prospective blinded kinematic analysis was to demonstrate that SLAC wrist also exists in the absence of trauma, and that abnormal carpal bone kinematics (specifically, decreased lunate flexion) is the initiating factor.

Patients with SLAC and no history of upper extremity trauma were compared with an age matched control group. All patients completed a questionnaire, personal interview, and a physical examination. A specialised flexion / extension radiographic jig was designed to control for the magnitude of force and position of the wrist in all planes.

A total of thirty-five subjects (sixty-nine wrists) were retained for the study, including thirty-three non-traumatic SLAC wrists and thirty-six control wrists. The non-traumatic SLAC group had significantly different radiographic kinematic analysis compared to the control group: increased Watson Stage (2 v 0), SL gap (3.4 v 1.8mm), revised carpal height ratio (rCHR) (77 v 68), SL angle in flexion (forty-one v twenty-eight degrees), and decreased radiolunate (RL) joint flexion (nine v twenty-seven degrees). Most importantly flexion of the asymptomatic non-degenerative wrist of the non-traumatic SLAC group was distributed 70% through the lunocapitate (LC) joint and only 30% through the RL joint (p< 0.05). Conversely, flexion was more evenly distributed in the control group (48% LC and 52% RL). Non-traumatic or developmental SLAC does exist. SLAC can thus be classified into non-traumatic (developmental) and traumatic types.

Non-traumatic SLAC begins with abnormal wrist kinematics. Over time restricted lunate flexion and normal scaphoid flexion leads to increased SL angles and eventual attrition of the SL ligament and predisposes patients to SLAC despite having no history of trauma.