Total hip arthroplasty is an elective procedure, performed for the treatment of debilitating pain.  Osteoarthritis is the etiology for 60% of THA (contribution of unrecognized dysplasia is controversial), femoral neck fractures and other trauma 10%, rheumatologic causes about 10%, AVN about 10%,  is about 10% other causes.  


Gradual but progressive cartilage wear is the most common indication for THA in people over 55 yo.  Osteoarthritis is a term used in place of idiopathic arthritis, suggesting no underlying cause for the cartilage degeneration.

Yet many argue that any hip with arthritis is either morphology or underlying genetics and doctors have just not yet found the cause – the absence of evidence is not evidence of absence.  But why is all arthritis abnormal? Because all forms of arthritis possess an inflammatory component that is absent from normal aging.  Lets get technical for a moment by looking at the molecular level. 

Cartilage at the molecular level. Cartilage is best understood as meshwork that resists compressive pressure via the regulation of water. Proteoglycans attract water while collagen forms a matrix that gives a surrounding structure. 

Proteoglycans look like a tree with a trunk-branches-leaves.  The trunk is the hyaluronic acid backbone, the braches are a protein called aggrecan, and the leaves are GAGs (chondroitin and keratin sulfate) which possess a highly negative charge (from the sulfate compound) that generates an osmotic gradient to pull in water.  Proteoglycans are highly concentrated in the “deep layer” of cartilage, like a magnet at the core.

Our body use water as a shock absorber, to resist compressive loads, but the uncontrolled influx of water just creates swelling, which is not functionally useful.  Therefore, our body has created a scaffolding around the proteoglycans, made of type 2 collagen and reinforced with type 9 collagen, to limit the swelling and create “fluid pressurization”.  During joint loading, the big net of collagen holds the proteoglycans in place, and by preventing deformity, it increases pressure within the cartilage, and this pushes water out of the cartilage scaffold and into the joint space, where it lubricates.  When the joint is subsequently unloaded, the negative charges of the GAGs repel, recreating the osmotic pressure, which pulls water and nutrients back into the cartilage.  This system is called - “exchangeable water”.

Normal aging.  Over time cartilage breaks down as the body loses its anabolic response to TGF-ß . Fewer proteoglycans and GAGs are produced, which diminishes the negative charge that attracts water, so the cartilage starts drying out.  Collagen 9 decreases, so the underlying structure becomes more brittle, and cartilage end products slowly accumulate which turns the cartilage yellow.  The body increases cartilage cross-linking via the molecule “decorin”, which increases the stiffness (read: modulus of elasticity), but further increases its brittleness and decreases its overall strength (just like highly-crosslinked PE!). 

Osteoarthritis. A pro-inflammatory state forms within the joint that increases the expression of degenerative enzymes (cytokines, and proteases) that directly damage the components of cartilage. IL-1 stimulates matrix metalloproteases (degrades collagen), ADAMTS proteases, and stromelysin (degrades aggrecans).  Therefore, the early phase of arthritis sees generalized cartilage injury.  A drop in proteoglycans and aggrecans leads to free-floating GAGs.  Collagen breakdown reduces control over the osmotic gradient, and there is more permeability and swelling, which decreases stiffness and strength of the matrix, further increasing its risk for breakdown.  There is an increase in DAMPS (cartilage breakdown products), which include Hyaluronan, Fibronectant, and Collagen X.

The middle phase of arthritis is a response to this injury.  Chondrocytes try to compensate by proliferating and increasing both anabolic activity (forming ECM) and catabolic activity (removing debris). 

The late phase of arthritis, the chondrocytes are burnt out, and theres reduced chondrocyte activity, reduced anabolic activity, reduced water, and reduced compressive modulus.   

What is the stimulus for Osteoarthritis?

Recent trends toward structural etiology for hip degeneration is currently in vogue (see DDH and FAI).  Studies are being performed to better understand the role of obesity, genetics, and abnormal morphology.  Obesity may accelerate the rate of hip degeneration.  Biomechanically it increases forces across the hip.  If climbing stairs creates a force 5x body weight, then body weight exerts a significant effect on the hip (just losing 10 lbs decreases the force on the hip by 50 lbs while stair climbing).  Genetics of osteoarthritis are poorly understood.  

▪ On Exam, progressive arthritis causes the hip to be flexed, externally rotated (near all internal rotation is lost), and adducted (develop abduction contracture). These changes lead to apparent limb shortening (which can lead to percieved limb lengthening after THA).   

▪On X-Ray, hip osteoarthritis is described with reference to "sclerosis" "subchondral cysts" "joint space narrowing" and any morphological changes to the joint, such as femoral head collapse (as seen in AVN, below)) or acetabular dysplasia (as seen in DDH, below). The Tönnis Grading System can be used to describe hip osteoarthritis, although its infrequently used in practice. 



Synovial cells inappropriately release cytokines that recruit immune cells and fibroblasts and create a toxic environment to cartilage [2]. The synovial cells are a primary source of the inflammation, and therefore, complete synovectomy is needed to minimize the risk of continued pain and disability [7]. 


Young Age.  On average Rheumatoid Arthritis (RA) patients are 10 years younger than typical OA patient requiring THA [3].  Greater functional demands, increased longevity requirements for the implant and higher expectations all contribute to making younger patients more challenging to treat successfully (see Patient Risk Factors – Age). 

Polyarticular Involvement.  Inflammatory Arthritis rarely affects an isolated joint. A broader view of functional goals must be addressed before a joint surgeon puts on the blinders as says “Your knee looks terrible, I can fix that and you will feel better.” The ipsilateral hip and knee are affected in up to 50% of cases, and the upper extremity (especially MCP, PIP, and also wrist joint) are involved in most cases [4].  A plan that addresses the multiple sources of disability will maximize rehab/recovery and minimize risk of complication.  Should a wrist be fused before TKA to maximize postop recovery or will TKA rehab overstress a fused wrist leading to higher risk of complication?  Can an ipsilateral hip and knee be addressed in the same hospitalization? If not, which should undergo surgery first? It is generally recommended that THA preceed TKA, as rehab from THA is less affected by a painful ipsilateral knee than vise versa.  Obtaining deep knee flexion after TKA requires adequate hip ROM, which can be compromised by a severely arthritic hip. 

RA patients commonly have c-spine instability (90%) and therefore a lateral c-spine flexion/extension x-ray are important to evaluate canal diameter (< 14 mm is risk for cord compression, and ADI >10 mm is risk for instability).  Patients with ankylosing spondylitis similarly have spine issues, notably loss of lumbar spine lordosis, which can lead to pelvic hyperextension and increased anteversion.   

Severe Deformity.  Standard implants assume that a given patient will fall within a range of anatomic “normal”, whereby variations in femoral neck angle, canal diameters, etc can be addressed by the variety of implant sizes in a normal tray.  Yet in inflammatory arthritis, its not uncommon for these patients to fall outside is “normal”.  JRA for example may present with excessive femoral anteversion, anterior bowing. Its therefore, important to obtain anatomic measurements, and consider custom implants when necessary. These patients have higher risk of acetabluar protrusion (which complicates the surgical approach and may require in situ femoral neck cut, or troch osteotomy.  it also brings the sciatic nerve closer to the surgical field).  Juvenile Rheumatoid arthritis patients commonly present with excessive femoral anteversion and anterior bowing. 

Bone Quality.  Many patients have poor bone quality secondary to disease and chronic medication (such as steroids). There is a higher risk of acetabular protrusion in THA for RA patients (10% vs. < 2% for primary OA) and even higher risk in ankylosing spondylitis (30%).  

Cementless femoral stems in THA show lower rates of loosening in RA patients [5], and yet cemented stems may be considered to reduce the higher rates of periprosthetic fracture intraop and postop[6].  Furthermore, there is a high incidence of large cystic areas that may require bone grafting.  Postoperative subsidence, particularly along the medial tibia following TKA is a concern. Aseptic loosening remains a concern for TKA and thus cemented components are recommended.

Soft Tissue Quality. Ligament attenuation may require greater implant constraint (which has the unfortunate effect of translating greater force to the bone implant interface, where the bone is also less strong, thus risking premature loosening).  However, the opposite is also seen, whereby chronic deformity leads to rigid contractures (particularly knee flexion contractures after long-term wheelchair use), which can be refractory to intraoperative correction (with approximately 30% residual deformity postop).  There are reports on preoperative serial casting to address the contracture.

Patients with ankylosing spondylitis have a high risk for developing hetertopic ossification post-op (consider giving 700 cGy within 72 hours to minimize risk). In psoriatic patients avoid any incision that includes a plaque as they are colonized by bacteria.

Systemic Disease: Higher rate of dermatitis, fragile skin, and vasculitis can lead to wound complications.  Osteopenia is common, and may lead to implant loosening, periprosthetic fractures, and implant subsidence.

Medications (immune-modulating agents) [8].

-NSAIDS.  Associated with a higher risk of bleeding, and while some recommended holding one week before surgery [3], other sources demonstrate no correlation between nsaids and increased transfusion risk [9].

-Steroids. Are used as maintenance medication or episodic dosing for flair ups. This is an important distinction, as patients on chronic steroids may have adrenal insufficiency and will thus require a stress dose of 50-100 mg hydrocortisone (or 10-15 mg methylprednisone IV) with postoperative taper to the preoperative dose to prevent an Addison’s Crisis [10].  Chronic steroids are associated with poor bone quality, poor wound healing and immunocompromise (with 3x increased risk of joint infection [11]).

-DMARDS. These medications have been hugely successful in slowing the progression of disease and delaying the need for TJA, decreasing the incidence of THA in RA patients by 50% since the advent of TNF-alpha inhibitors.  In patients that do require arthroplasty, these medications exhibit immunomulatory effects and thus dosing must be considered individually with regards to timing of surgery [12].  In contrast to most DMARDS, Methotrexate should not be held in the perioperative period, as studies demonstrate a higher infection rate when held[13] (with the exception of renal impaired patients, whereby it should be held 1 weeks before and after surgery).  Examining the chart indicates that joint surgeons should not simply stop all medications before surgery, but rather discuss timing with a patient’s rheumatologist, to minimize the risk of a flair in other joints after surgery, thus delaying rehab from surgery.

Outcomes: Despite the additional complexity associated with TJA for inflammatory arthritis, the outcomes are positive.  Survivorship at 10 years is about 90% (and comparable to standard OA patients) [14].  Functional scores were inferior to OA patients, however, this is hardly surprising considering the polyarticular involvement in these patients.



Most cases of AVN occur in 3-5th decade of life and are idiopathic, although its also associated with: trauma (particularly native hip dislocation – occurring in 10-25% of cases, and displaced femoral neck fractures – occurring in 15-50% of cases), alcoholism, steroid use (uncommon overall, and only 2% of patients with liver transplants, exposed to continuous , high level steroid developed symptomatic avn [16]), sickle cell disease and other coagulopathies, and autoimmune disease.  AVN is the underlying etio for 5-12% of THA cases. 


Secondary AVN occurs bilaterally in 80% of cases to be sure to examine both hips.

Hip AVN is diagnosed and staged with hip AP and frog-leg lateral, and MRI studies.  Early stages of AVN will only appear as edema on MRI.  Progression will then be seen on Hip XR as cystic and sclerotic changes in the femoral head, the “Crescent Sign” will develop (subchondral lucency which represents delamination of the cartilage, and is a poor prognostic sign), and this will be followed by femoral head collapse and progressive degeneration of the hip joint (involving both the femoral head and acetabulum).  MRI is 99% sensitive and specific for AVN of the hip. AVN is typically progressive, yet there are

Prognostic Factors for Femoral Head Collapse.

% involvement of the femoral head (proportion of cross-sectional involvement) [21].

-if <30%: low risk collapse (at 5 yrs): 5%

-if 30 – 50%: moderate risk collapse: 46%

-if >50%: high risk collapse: 83%

Combined Angle of Necrosis in the Mid-saggital + Mid-coronal cuts on MRI (this is the Modified Kerboul method). The implications on collapse was studied by Ha et al[17].

- if < 190° combined angle = low risk of collapse

-if 190 – 240° combined angle = moderate risk (50%) 

-if >240° combined angle = high risk of collapse (near 100%)

Location. AVN in the weight bearing area has the greatest impact on collapse.  One study found that 8/9 hips did not collapse when necrosis was < 2/3 of weight bearing area[18].

Edema.  When the initial MRI (at the early stage of AVN) demonstrates significant edema in the proximal femur, there is a higher risk of progression and persistent symptoms[19]. 

Pain. Proceeds collapse.


There is no proven best method of joint preservation with AVN, however, a number of approaches have emerged.  There is a lot of conflicting evidence for each treatment modality, and much of this may stem from our incomplete knowledge of the underlying cause of AVN and therefore, we are lumping together dissimilar patients for treatments.

Ficat Classification utilizes the findings on XR and MRI to stage the severity of AVN, and guide treatment (see table).

Non-surgical.  It appears that even small lesions prove problematic over time, although the results are variable (suggesting that underlying factors determining outcome have not been fully identified).  One study looking at small lesions (<10% femoral head volume) with over 10 years follow up, showed 88% symptomatic and 73% demonstrated some collapse [20].   A separate study showed only 5% collapse at 5 years in small lesions (<30% femoral head), while the overall rate of collapse (all comers) was 59% [21].  A systemic review looking at patients around 5 years follow up indicated that 66% required surgical intervention and 72% showed progression on X-ray[22].  Therefore the concensus is that non-surgical treatment (ie nonweight bearing) should have a very limited role in the treatment of AVN.

Core decompression.  The goal is to reduce pressure within the femoral head and restore vascularity to stimulate healing.  The key to core decompression is performing the procedure pre-collapse. Core decompression can be performed alone, or in conjunction with bone graft, nonvascularized fibular graft of vascularized fibular graft (VFG).  One study found lower rates of THA at a minimum of 2 years (only 42% with lesions >30% of femoral head) [23].  Another demonstrated that only 30% of patients required a second procedure, and 63% had good outcomes on XR[22].  Other studies found no difference in collapse rate in those treated with core decompression[17].  Supplementing core decompression with bone marrow aspirate[24] or BMP [25] shows some potential for slowing progression. 

Vascularized Fibular Graft (VFG). Appears to have the biggest impact on reversing disease progression.  Studies report 86% survival of precollapse hips at 7 years (vs. 30% with nonvascularized graft) [26], although it appears less successful in post-collapse hips with 44% showing progressive changes by 5 years[27].

Bisphosphonates (alendronate). Pharmacologics have been studied for treating early (pre-collapse) AVN. The results are mixed, with one study showing low incidence of collapse, and another study showing no impact on collapse or need for THA. 

THA. Outcomes of THA for AVN were historically associated with higher dislocation rates (due to better preop motion) and higher revision rates (younger, more demanding patients) [28].  However, recent studies suggest a low revision rate, and comparable to THA for osteoarthritis[29].  Hip resurfacing can also be considered in the younger patients, but its recommended only when AVN <50% of the femoral head, and standard complications like MoM and femoral neck fracture must be considered.



The indication for THA (vs. ORIF or Hemi) after a displaced femoral neck fracture is becoming more widely accepted.  The indication for THA is closely tied to chronologic age and activity age.

Chronoloigc age.  The success of ORIF decreases with increased chronologic age regardless of patient activity due to diminished blood supply.  THA demonstrated superior functional outcome and decreased revision surgery with arthroplasty (THA or hemi) in the elderly population [30-37].  Thus the debate for treating displaced femoral neck fractures in patients > 60 years old recognizes the poor outcomes of ORIF and focuses on Hemi vs. THA ... and herein lies the importance of activity age.

Activity age.  Hemi is shown to provide inferior functional scores and persistent pain in patients that place high demands on their hip. THA is considered a superior operation in the independent elderly (young activity age). There are trade offs.  There is a higher reported risk of hip instability in THA after femoral neck fracture.  The soft tissue surrounding the hip becomes tight and contracted during the gradual process of osteoarthritis and acts as a stabilizing force after THA.  In contrast, the acute event of a fracture does not allow the soft tissue to stiffen and these patients have demonstrated a higher rate of dislocation with THA from the posterior approach, although direct anterior THA or anterolateral approach may reduce this risk [38]. 

THA is often required for unsuccessful treatment of a hip fracture.

Failed Femoral Neck ORIF (5-15% nonunion, 5-15% AVN) is often the easiest to convert to THA, as the standard treatment of 3 cannulated screws can be removed through the posterolateral incision for THA.  Furthermore the femoral neck nonunion is excised with femoral preparation for the stem implant [40].  Outcomes suggest conversion failed femoral neck ORIF to THA is comparable to standard THA with 93% survivorship at 10 years (although possibly higher dislocation risk) [41].  

Failed Intertrochanteric Fracture ORIF (nonunion risk only 5%) is more complicated to revise [40].  An intramedullary nail (hip IMN) is inserted through the abductor musculature and removal often causes further injury to the abductor complex, leading to postoperative limp and possible long term abductor deficiency and subsequent risk for instability.  A screw and side plate is the preferred construct for the arthroplasty surgeon because removal can often be performed through the posterolateral approach used for the THA, and also because it preserves the abductor musculature.  The additional challenge of converting a failed Intertroch ORIF is an intertroch nonunion often requires a calcar replacing stem (about 65% of cases), and the stem must be long enough to bypass screw holes from the removed hardware which would otherwise act as stress risers.  Additionally, the fracture itself may have altered the anatomy of the proximal femur and thus increases the complexity of preparing the femur.  Outcome studies indicate that conversion of Intertroch to THA is a less successful procedure, with higher rates of instability and greater troch pain, overall 88% survivorship at 10 years [42]. 


The two most commonly described types of Structural Pathology are Hip Dysplasia and Femoroacetabular Impingement.  They share the same foundation of abnormal hip architecture, yet they are fully distinct conditions . There is always natural variation to the shape of our bones and there is a wide spectrum that falls within "normal".  However, its becoming increasingly apparent that certain shapes of the hip can increase the risk of acute pain and future osteoarthritis.  The correlation between anatomy and symptoms, anatomy and osteoarthritis, is not clear in most cases due to confounding variables.  Yet a properly identified patient can avoid debilitating pain or the high probability of early hip arthritis by undergoing targeted procedures that re-balance the forces within the hip joint.  

1. Hip Dysplasia

by Dr. Erin Honcharuk

Background. Adolescent/Adult dysplasia, like Infantile DDH, has a higher female predominance and is commonly bilateral.

Increased acetabular obliquity leads to anterior-lateral undercoverage of the femoral head.  A smaller surface area of contact between the femoral head and acetabulum increases peak forces on the cartilage and promotes subtle hip instability that increases shear stresses on the cartilage and promotes fatigue failure of the labrum.  Chronic mechanical overload may lead to osteoarthritis. Uncorrected hip dysplasia is the most common etiology of hip OA in young patients requiring THA, with 50% of patients under 50 years with a THA have underlying dysplasia [1].

Exam. Patients may present with pain in groin or lateral hip (giving the classic “C” sign when asked to locate their pain). They may also report instability, mechanical symptoms, and activity related pain. 

Imaging. Hips that have less coverage, defined by many of the measurements discussed below, have been shown to have an increase in OA [2].

The amount of acetabular deficiency is characterized by the Lateral Center-Edge Angle and the Acetabular Inclination.  A dysplastic hip with a lateral center-edge angle < 16, an acetabular index > 15 is associated with high risk for early arthritis if treated without surgery.  The prognosis for mild dysplasia is less clearly understood.  

Surgical Treatment. "Hip Preservation" is a surgical intervention that alters the position of the acetabulum to increase coverage of the femoral head and return radiographic measurements to within a normal range. The goals of hip preservation are to correct the primary deformity, eliminate instability, prevent articular damage, and delay or prevent the onset of OA.

There are multiple preservation techniques which all utilize acetabular osteotomies to re-orienting the hip joint.  Bernese Peri-Acetabular Osteotomy (PAO) has emerged as the leading technique.  Its main advantages are that it preserves the pelvic ring, while allowing for acetabular correction in multiple planes (anterior  coverage, lateral coverage, and medialization).   

Outcomes. The outcomes of the Bernese PAO are promising.  20 year survival is about 60-80%, with the end point being hip replacement.  Importantly, a PAO does not appear to negatively impact hip arthroplasty in cases of progressive OA.  However, there is a concern that overcorrection of the acetabulum (excessive anterior coverage, the acetabulum becomes retroverted) leading to iatrogenic impingement.

Overtime, OA can still occur. Predictors of conversion to THA include surgery at older age (>35) and preoperative XRs that show poor joint congruency, or early signs of OA. Postoperative radiographs showing improved congruency and coverage have been associated with better long term outcomes. 

More recently, delayed gadolinium-enhanced MRI of cartilage (dGEMRIC) has played a role in analyzing hips concerning for dysplasia and the likelihood of success of PAO vs. conversion to THA. Glycosaminoglycans (GAGs) in articular cartilage are high-fixed-negatively charged density that provide compressive stiffness. GAGs are lost with OA. Gadopentetate (Gd-DTPA) distributes in cartilage inversely to the concentration of GAGs. So, it’s low in normal cartilage and high in degraded cartilage. It’s also been found to correlate with pain and other radiographic measurements, like the L-CEA, and may show signs of dysplasia and OA before evidence on XRs, when hip preservation may be too late anyway.  It can help predict which hips are more likely to get converted to a THA. About 570 ms is considered normal. 

However, if/when conversion to a THA occurs after PAO, it is important to consider changes in the hip from the original surgery. Correction from the PAO can often lead to a more retroverted acetabulum making exposure more difficult and requiring trimming of the anterior wall or bone grafting, and a conscious effort to achieve proper acetabular version. However, compared to patients who underwent a THA for dysplasia, there was no difference in blood loss, OR time, or complications.

THA in the dysplasic population without undergoing PAO is also more technically changing than a standard primary THA due to the shallow, more vertical acetabulum, with poor anterior bone stock. The severity of dysplasia can be described by the Crowe Classification, which reports worsening hip subluxation due to the dysplasia. A Crowe 4 is complete hip dislocation, which can cause a pseudoacetabulum above the normal hip center.  This can make proper cup placement more difficult. When evaluating the soft tissues, there can be muscle contracture or elongation of the capsule.   

References1. Clohisy JC, Dobson MA, Robison JF, Warth LC, Zheng J, Liu SS, et al. Radiographic structural abnormalities associated with premature, natural hip-joint failure. J Bone Joint Surg Am. 2011;93 Suppl 2:3-9.

2. Murphy SB, Ganz R, Muller ME. The prognosis in untreated dysplasia of the hip. A study of radiographic factors that predict the outcome. J Bone Joint Surg Am. 1995;77(7):985-9.

2. FAI (femoroacetabular impingement)

FAI is an incongruent ball-and-socket leading to repetitive impingement at terminal hip motion.  It is a recognized cause of hip pain and a risk factor for future arthritis [1-3].

Background. There is always natural variation to the shape of our bones and there is a wide spectrum that falls within "normal".  However, its becoming increasingly apparent that certain hip morphology can increase the risk of acute pain and future osteoarthritis.  The correlation between anatomy and symptoms, anatomy and osteoarthritis, is not clear in many cases due to confounding variables.  Yet a properly identified patient can avoid debilitating pain or the moderate probability of early hip arthritis by undergoing targeted procedures that re-reshape the hip joint.  

The abnormal shape can be femur-based, called Cam Impingement, and is due to an aspherical head (increased anterior-lateral contour) or reduced head-neck offset that causes the prominent part of the head to cause repetitive “outside-in” microtrauma, also know as an inclusion type injury, meaning that the asphericity enters the joint and damages the cartilage. Cam impingement is most common in young, athletic males, and may be associated with a subclinical SCFE that was missed in childhood [4-6].

The abnormal shape can be acetabulum-based, called Pincer Impingement, whereby an area of rim over-coverage causes repetitive trauma via direct impact of the rim against the femoral neck.  The pincer impingement may be caused by acetabular retroversion, general over-coverage, or protrusio.   This linear contact between the rim and head-neck junction causes anterior-superior labral separation and chondral damage of the acetabulum (similar to Cam impingement).  Chronic leverage of the head in the acetabulum creates chondral injury in the ‘contre-coup’ region of the posteroinferior acetabulum. Pincer deformities are more common in middle-aged women. The lesions created are also smaller than those from cam deformities, and, thus, more benign.

FAI can also be a combined Cam-Pincer deformity.

Importantly, the pathology of FAI is not only created by abnormal anatomy, but also by vigorous activity particularly at the extremes of motion.  Impingement occurs at terminal motion, and daily activity rarely pushes the hip to this limit.  Therefore, FAI is most commonly seen in athletes, even though subtle abnormalities of hip morphology may present commonly in the general population.

Association with Osteoarthritis (natural history). Solomom suggested that over 90% of hip OA can be to attributed to underlying etiology: mechanical, traumatic, inflammatory, or metabolic [7].  Ganz and others expanded on this theory by defining pathologic hip morphology (hip dysplasia and FAI) [8, 9].

Patients with FAI demonstrate peripheral cartilage degeneration in contrast to primary hip arthritis, which shows a central distribution. [10] [11]

It has been reported that 40% of people who develop OA have a pistol-grip deformity.  There are many studies that examine the hip morphology of patients under 60 yo with “idiopathic” osteoarthritis and identified high incidence of “abnormal” parameters [12].  Between 40 – 90% of patients under 60 yo with end-stage OA have significant FAI morphology.

There is an association [13] [14] [15] [16]. Particularly the association between an increasing alpha-angle in Cam impingement (over 60°) and more severe arthritis at time of arthroscopy [17] [18].  MRI studies also identified cartilage damage with CAM deformity despite normal x-ray [19] [20].

What is the association? The cause and effect of FAI is less clear. Some studies suggest a high incidence of Cam or Pincer morphology in non-OA patients [21], suggesting FAI may not be a direct cause in many cases, but rather result of selection bias. 

Some believe it is a normally occurring variant in active populations.  Reports of FAI athletic teams – ballet 90%, hockey 68% [22], 50% youth soccer [23], 48% track and field [24] show a high prevalence of “abnormal” hip morphology. The number that progress to clinically relevant OA will assuredly be less.  Abnormal morphology in the general population was seen in 15% of men, 7% of women [21] [25].  

Examining a rather homogenous population of 1,000 young males in the Swiss military, 24% incidence based on MRI of cam-type deformity, which increased to 60% if they presented with low hip internal rotation (<25°) [26].  There was correlation between these Cam deformities and risk for hip disease – 2.3x risk for cystic changes and 2.8x risk for labral tears [27].  While this demonstrates a risk for MR associated pathologic changes, it is not an association with arthrosis (joint disease seen on xray) or arthritis (clinically significant degenerative joint disease). This study was not likely to show degenerative changes in such a young population, as degeneration takes decades to occur, yet by showing signs of early hip damage, it hints at risk for future OA.  Nonetheless, there is no good quality study to demonstrate a direct correlation between FAI and OA.

There is controversy about the generally high incidence of FAI.  There is always person-to-person variation in bone morphology, and the more measurements made, the more chance that something will be “abnormal”.  The challenge with FAI is the large gray area of morphology that may be abnormal but is probably within “normal”, meaning not clinically significant variation.  Furthermore, the aforementioned study examining the Swiss military, demonstrated a 40% incidence of asymptomatic antero-lateral labral tears, suggesting that general wear occurs in an active population and may not be directly caused by FAI [27]

There are some studies that evaluate patients with hip pain and mild arthritis [28], or a sampling of the normal population, and identify FAI (particularly the alpha angle) as a risk factor for future THA [29].  The majority of pathologic hips demonstrated signs of arthrosis without an endpoint of end-stage DJD or THA, questioning whether FAI leads to clinically significant disease, requiring surgical intervention. Beyond the elevated alpha angles, it is less clear what additional risk factors are associated with progression to clinically significant OA.

History and Physical. Most patients are young, active individuals.  Patients present with groin pain and may report that it travels to their buttock or greater trochanter. It may initiate after minor trauma, but tends to be insidious in onset. The pain can be intermittent and exacerbated by excessive demand on the hip from athletic activities or even from prolonged walking or sitting. They often will have delay in diagnosis, mild-moderate, prolonged, and generalized groin symptoms.

On physical examination, patients may present with a limp.  They can have decreased ROM, particularly with internal rotation; the impingement test has been found to correlate with surgical findings of FAI. This maneuver is done with the patient supine, the hip is flexed to 90 degrees and then internally rotated. Passive adduction brings the femoral neck in contact with the acetabular rim and if it increases pain, this is suggestive of anterior impingement. Posterior impingement is tested with the provocative test. The patient is supine with the leg hanging free off the bed to create extension at the hip. The hip is then externally rotated. Pain in this position is positive for posteroinferior impingement.

Imaging. XRs of FAI can often be normal or only show subtle changes.  This is due to the location of the Cam deformity.  The most common location is at the 1 o'clock position, which cannot be seen on AP or lateral view of the femur.  The 2nd most common location is at the 2 o'clock position, which can be seen on a lateral X-ray, and 3rd most common is at the 12 o'clock position, which can be seen on AP x-ray.  Thus, while the x-ray can pick up some cases of offset, it misses the most common site of occurence.

A reduced offset at the femoral neck/head junction and changes to the acetabular rim from ossification of the labrum, as seen with a double line or os acetabuli, can be seen. Herniation pits are fibrocystic changes of the anterosuperior femoral neck visualized as round or oval radiolucencies with thin zones of sclerosis. These are signs of acquired degenerative changes.

Evaluation for coxa profunda or protrusio acetabuli is done on an AP pelvis as an AP hip can change the projection. The acetabular fossa is medial to the ilioischial line with coxa profunda, but the femoral head is still lateral. With protrusio, both the acetabular fossa and femoral head lay medial. 

MR arthrogram is also used for evaluation. Labral pathology can be identified both on degree and position. The labrum can be described as detached, with separation of the labral-bone interface; as showing an intrasubstance tear, where there is fluid or contrast extending into the labrum; or as denuded, where it is absent.  

The alpha angle can be measured on axial oblique views or using an axial reconstruction of the images.  The angle is between a line down the center of the femoral neck and a line to “Point A”.  Point A is the anterior point where the distance from the center of the head (HC) exceeds the radius of the femoral head. There is debate over the value of this measurement, where the sensitivity, specificity, positive and negative predictive values have been reports as 39.3%, 70.1%, 54.7%, and 53.5% [30]. In this study, the best test was actually the clinical impingement test. Furthermore, a wide neck, osteophytes, and posterior displacement of the head can all increase the alpha angle. The cutoff has been debated, between 50 and 55 degrees.

            -MEN alpha: Pathologic: > 83; Borderline: 69-82, normal < 68.

            -WOMEN: Pathologic > 57, borderline: 51-56, , normal < 5

Treatment. Nonoperative treatment includes activity modification by restriction of athletics and general demand on the hip.  Therapy to increase ROM and strength is often not helpful or counterproductive.

Surgical treatment aims to improve clearance for hip motion and alleviation of femoral abutments against the acetabular rim. Open treatment has mostly been done with the surgical hip dislocation, which requires a greater trochanter osteotomy and careful preservation of the blood supply to the femoral neck. However, it does allow for 360° inspection and treatment of the acetabulum and femoral head. To address the femoral head, an excision osteoplasty is normally done. There is often a clear demarcation between normal femoral articular cartilage and the area of the head subjected to FAI. The hyaline cartilage may show fraying and furrowing and areas of reddish or blue hue. The acetabulum rim is also usually treated with resection osteoplasty. In cases of retroversion causing FAI, the role for a reverse PAO has also been discussed. Patients are usually toe touch weight bearing for 8 weeks to allow for full healing.

More recently, arthroscopic management of these pathologies has increased in popularity. For arthroscopic resection of a cam lesion, complications do exist, including residual cam lesion, over-resection of the femoral neck, femoral neck fracture, AVN, and capsular adhesion. For the acetabulum, procedures entail accessing the joint capsule, identifying the impinging lesion, protecting uninjured labrum, resection of bony impingement, and reattachment of uninjured labrum to the bony rim.

Treatment is more successful in patients with less signs of arthritis. Patients with Tonnis grade 2 or 3 may have temporary relief in pain, but no long-term difference with conversion to THA.  Furthermore, patients with more retroversion have a decreased, albeit still clinical, improvement compared to those with normal or ante-version [31]. The role for a reverse PAO versus just arthroscopic procedures needs to be further delineated in this patient population.


1.         Sankar, W.N., et al., Femoroacetabular impingement: defining the condition and its role in the pathophysiology of osteoarthritis. J Am Acad Orthop Surg, 2013. 21 Suppl 1: p. S7-S15.

2.         Sankar, W.N., T.H. Matheney, and I. Zaltz, Femoroacetabular impingement: current concepts and controversies. Orthop Clin North Am, 2013. 44(4): p. 575-89.

3.         Sankar, W.N., et al., Staging of hip osteoarthritis for clinical trials on femoroacetabular impingement. J Am Acad Orthop Surg, 2013. 21 Suppl 1: p. S33-8.

4.         Bedi, A., et al., Assessment of range of motion and contact zones with commonly performed physical exam manoeuvers for femoroacetabular impingement (FAI): what do these tests mean? Hip Int, 2013. 23 Suppl 9: p. S27-34.

5.         Bedi, A., et al., Elevation in circulating biomarkers of cartilage damage and inflammation in athletes with femoroacetabular impingement. Am J Sports Med, 2013. 41(11): p. 2585-90.

6.         Bedi, A. and B.T. Kelly, Femoroacetabular impingement. J Bone Joint Surg Am, 2013. 95(1): p. 82-92.

7.         Solomon, L., Patterns of osteoarthritis of the hip. J Bone Joint Surg Br, 1976. 58(2): p. 176-83.

8.         Harris, W.H., Etiology of osteoarthritis of the hip. Clin Orthop Relat Res, 1986(213): p. 20-33.

9.         Ganz, R., et al., The etiology of osteoarthritis of the hip: an integrated mechanical concept. Clin Orthop Relat Res, 2008. 466(2): p. 264-72.

10.       Wagner, S., et al., Early osteoarthritic changes of human femoral head cartilage subsequent to femoro-acetabular impingement. Osteoarthritis Cartilage, 2003. 11(7): p. 508-18.

11.       Reiman, M.P., et al., Diagnostic accuracy of clinical tests for the diagnosis of hip femoroacetabular impingement/labral tear: a systematic review with meta-analysis. Br J Sports Med, 2015. 49(12): p. 811.

12.       Kowalczuk, M., et al., Does Femoroacetabular Impingement Contribute to the Development of Hip Osteoarthritis? A Systematic Review. Sports Med Arthrosc, 2015. 23(4): p. 174-9.

13.       Ganz, R., et al., Femoroacetabular impingement: a cause for osteoarthritis of the hip. Clin Orthop Relat Res, 2003(417): p. 112-20.

14.       Clohisy, J.C., et al., Radiographic structural abnormalities associated with premature, natural hip-joint failure. J Bone Joint Surg Am, 2011. 93 Suppl 2: p. 3-9.

15.       Lung, R., et al., The prevalence of radiographic femoroacetabular impingement in younger individuals undergoing total hip replacement for osteoarthritis. Clin Rheumatol, 2012. 31(8): p. 1239-42.

16.       Ecker, T.M., et al., Pathomorphologic alterations predict presence or absence of hip osteoarthrosis. Clin Orthop Relat Res, 2007. 465: p. 46-52.

17.       Johnston, T.L., et al., Relationship between offset angle alpha and hip chondral injury in femoroacetabular impingement. Arthroscopy, 2008. 24(6): p. 669-75.

18.       Pollard, T.C., et al., The hereditary predisposition to hip osteoarthritis and its association with abnormal joint morphology. Osteoarthritis Cartilage, 2013. 21(2): p. 314-21.

19.       Zilkens, C., et al., Symptomatic femoroacetabular impingement: does the offset decrease correlate with cartilage damage? A pilot study. Clin Orthop Relat Res, 2013. 471(7): p. 2173-82.

20.       Kumar, D., et al., Association of cartilage defects, and other MRI findings with pain and function in individuals with mild-moderate radiographic hip osteoarthritis and controls. Osteoarthritis Cartilage, 2013. 21(11): p. 1685-92.

21.       Frank, J.M., et al., Prevalence of Femoroacetabular Impingement Imaging Findings in Asymptomatic Volunteers: A Systematic Review. Arthroscopy, 2015. 31(6): p. 1199-204.

22.       Brunner, R., et al., Prevalence and Functional Consequences of Femoroacetabular Impingement in Young Male Ice Hockey Players. Am J Sports Med, 2016. 44(1): p. 46-53.

23.       Johnson, A.C., M.A. Shaman, and T.G. Ryan, Femoroacetabular impingement in former high-level youth soccer players. Am J Sports Med, 2012. 40(6): p. 1342-6.

24.       Kapron, A.L., et al., In-vivo hip arthrokinematics during supine clinical exams: Application to the study of femoroacetabular impingement. J Biomech, 2015. 48(11): p. 2879-86.

25.       Jung, K.A., et al., The prevalence of cam-type femoroacetabular deformity in asymptomatic adults. J Bone Joint Surg Br, 2011. 93(10): p. 1303-7.

26.       Reichenbach, S., et al., Prevalence of cam-type deformity on hip magnetic resonance imaging in young males: a cross-sectional study. Arthritis Care Res (Hoboken), 2010. 62(9): p. 1319-27.

27.       Reichenbach, S., et al., Association between cam-type deformities and magnetic resonance imaging-detected structural hip damage: a cross-sectional study in young men. Arthritis Rheum, 2011. 63(12): p. 4023-30.

28.       Agricola, R. and H. Weinans, Femoroacetabular impingement: what is its link with osteoarthritis? Br J Sports Med, 2016. 50(16): p. 957-8.

29.       Nicholls, A.S., et al., The association between hip morphology parameters and nineteen-year risk of end-stage osteoarthritis of the hip: a nested case-control study. Arthritis Rheum, 2011. 63(11): p. 3392-400.

30.       Lohan, D.G., et al., Cam-type femoral-acetabular impingement: is the alpha angle the best MR arthrography has to offer? Skeletal Radiol, 2009. 38(9): p. 855-62.

31.       Fabricant, P.D., et al., The effect of femoral and acetabular version on clinical outcomes after arthroscopic femoroacetabular impingement surgery. J Bone Joint Surg Am, 2015. 97(7): p. 537-43.


1.         Fehring, T.K., et al., The obesity epidemic: its effect on total joint arthroplasty. J Arthroplasty, 2007. 22(6 Suppl 2): p. 71-6.

2.         Chmell, M.J. and R.D. Scott, Total knee arthroplasty in patients with rheumatoid arthritis. An overview. Clin Orthop Relat Res, 1999(366): p. 54-60.

3.         Lee, J.K. and C.H. Choi, Total knee arthroplasty in rheumatoid arthritis. Knee Surg Relat Res, 2012. 24(1): p. 1-6.

4.         Jacoby, R.K., M.I. Jayson, and J.A. Cosh, Onset, early stages, and prognosis of rheumatoid arthritis: a clinical study of 100 patients with 11-year follow-up. Br Med J, 1973. 2(5858): p. 96-100.

5.         Makela, K.T., et al., Cemented versus cementless total hip replacements in patients fifty-five years of age or older with rheumatoid arthritis. J Bone Joint Surg Am, 2011. 93(2): p. 178-86.

6.         Zwartele, R.E., et al., Cementless total hip arthroplasty in rheumatoid arthritis: a systematic review of the literature. Arch Orthop Trauma Surg, 2012. 132(4): p. 535-46.

7.         Cooke, T.D., et al., Localization of antigen-antibody complexes in intraarticular collagenous tissues. Ann N Y Acad Sci, 1975. 256: p. 10-24.

8.         Howe, C.R., G.C. Gardner, and N.J. Kadel, Perioperative medication management for the patient with rheumatoid arthritis. J Am Acad Orthop Surg, 2006. 14(9): p. 544-51.

9.         Samama, C.M., et al., Antiplatelet agents in the perioperative period: expert recommendations of the French Society of Anesthesiology and Intensive Care (SFAR) 2001--summary statement. Can J Anaesth, 2002. 49(6): p. S26-35.

10.       Shaw, M. and B.F. Mandell, Perioperative management of selected problems in patients with rheumatic diseases. Rheum Dis Clin North Am, 1999. 25(3): p. 623-38, ix.

11.       Luessenhop, C.P., et al., Multiple prosthetic infections after total joint arthroplasty. Risk factor analysis. J Arthroplasty, 1996. 11(7): p. 862-8.

12.       Hayashi, M., et al., Effect of total arthroplasty combined with anti-tumor necrosis factor agents in attenuating systemic disease activity in patients with rheumatoid arthritis. Mod Rheumatol, 2012. 22(3): p. 363-9.

13.       Grennan, D.M., et al., Methotrexate and early postoperative complications in patients with rheumatoid arthritis undergoing elective orthopaedic surgery. Ann Rheum Dis, 2001. 60(3): p. 214-7.

14.       Gill, G.S., K.C. Chan, and D.M. Mills, 5- to 18-year follow-up study of cemented total knee arthroplasty for patients 55 years old or younger. J Arthroplasty, 1997. 12(1): p. 49-54.

15.       Zalavras, C.G. and J.R. Lieberman, Osteonecrosis of the femoral head: evaluation and treatment. J Am Acad Orthop Surg, 2014. 22(7): p. 455-64.

16.       Lieberman, J.R., A.A. Scaduto, and E. Wellmeyer, Symptomatic osteonecrosis of the hip after orthotopic liver transplantation. J Arthroplasty, 2000. 15(6): p. 767-71.

17.       Ha, Y.C., et al., Prediction of collapse in femoral head osteonecrosis: a modified Kerboul method with use of magnetic resonance images. J Bone Joint Surg Am, 2006. 88 Suppl 3: p. 35-40.

18.       Nishii, T., et al., Progression and cessation of collapse in osteonecrosis of the femoral head. Clin Orthop Relat Res, 2002(400): p. 149-57.

19.       Ito, H., T. Matsuno, and A. Minami, Relationship between bone marrow edema and development of symptoms in patients with osteonecrosis of the femoral head. AJR Am J Roentgenol, 2006. 186(6): p. 1761-70.

20.       Hernigou, P., et al., Fate of very small asymptomatic stage-I osteonecrotic lesions of the hip. J Bone Joint Surg Am, 2004. 86-A(12): p. 2589-93.

21.       Nam, K.W., et al., Fate of untreated asymptomatic osteonecrosis of the femoral head. J Bone Joint Surg Am, 2008. 90(3): p. 477-84.

22.       Marker, D.R., et al., Do modern techniques improve core decompression outcomes for hip osteonecrosis? Clin Orthop Relat Res, 2008. 466(5): p. 1093-103.

23.       Israelite, C., et al., Bilateral core decompression for osteonecrosis of the femoral head. Clin Orthop Relat Res, 2005. 441: p. 285-90.

24.       Hernigou, P. and F. Beaujean, Treatment of osteonecrosis with autologous bone marrow grafting. Clin Orthop Relat Res, 2002(405): p. 14-23.

25.       Lieberman, J.R., A. Conduah, and M.R. Urist, Treatment of osteonecrosis of the femoral head with core decompression and human bone morphogenetic protein. Clin Orthop Relat Res, 2004(429): p. 139-45.

26.       Plakseychuk, A.Y., et al., Vascularized compared with nonvascularized fibular grafting for the treatment of osteonecrosis of the femoral head. J Bone Joint Surg Am, 2003. 85-A(4): p. 589-96.

27.       Soucacos, P.N., et al., Treatment of avascular necrosis of the femoral head with vascularized fibular transplant. Clin Orthop Relat Res, 2001(386): p. 120-30.

28.       Ortiguera, C.J., I.T. Pulliam, and M.E. Cabanela, Total hip arthroplasty for osteonecrosis: matched-pair analysis of 188 hips with long-term follow-up. J Arthroplasty, 1999. 14(1): p. 21-8.

29.       Kim, S.M., et al., Cementless modular total hip arthroplasty in patients younger than fifty with femoral head osteonecrosis: minimum fifteen-year follow-up. J Arthroplasty, 2013. 28(3): p. 504-9.

30.       Stoen, R.O., et al., Randomized trial of hemiarthroplasty versus internal fixation for femoral neck fractures: no differences at 6 years. Clin Orthop Relat Res, 2014. 472(1): p. 360-7.

31.       Rogmark, C., CORR Insights (R): Randomized trial of hemiarthroplasty versus internal fixation for femoral neck fractures: no differences at 6 years. Clin Orthop Relat Res, 2014. 472(1): p. 368-9.

32.       Rogmark, C. and O. Johnell, Primary arthroplasty is better than internal fixation of displaced femoral neck fractures: a meta-analysis of 14 randomized studies with 2,289 patients. Acta Orthop, 2006. 77(3): p. 359-67.

33.       Blomfeldt, R., et al., A randomised controlled trial comparing bipolar hemiarthroplasty with total hip replacement for displaced intracapsular fractures of the femoral neck in elderly patients. J Bone Joint Surg Br, 2007. 89(2): p. 160-5.

34.       Blomfeldt, R., et al., Comparison of internal fixation with total hip replacement for displaced femoral neck fractures. Randomized, controlled trial performed at four years. J Bone Joint Surg Am, 2005. 87(8): p. 1680-8.

35.       Hedbeck, C.J., et al., Comparison of bipolar hemiarthroplasty with total hip arthroplasty for displaced femoral neck fractures: a concise four-year follow-up of a randomized trial. J Bone Joint Surg Am, 2011. 93(5): p. 445-50.

36.       Baker, R.P., et al., Total hip arthroplasty and hemiarthroplasty in mobile, independent patients with a displaced intracapsular fracture of the femoral neck. A randomized, controlled trial. J Bone Joint Surg Am, 2006. 88(12): p. 2583-9.

37.       Macaulay, W., et al., Displaced femoral neck fractures in the elderly: hemiarthroplasty versus total hip arthroplasty. J Am Acad Orthop Surg, 2006. 14(5): p. 287-93.

38.       Macaulay, W., et al., Prospective randomized clinical trial comparing hemiarthroplasty to total hip arthroplasty in the treatment of displaced femoral neck fractures: winner of the Dorr Award. J Arthroplasty, 2008. 23(6 Suppl 1): p. 2-8.

39.       Skoldenberg, O., et al., Reduced dislocation rate after hip arthroplasty for femoral neck fractures when changing from posterolateral to anterolateral approach. Acta Orthop, 2010. 81(5): p. 583-7.

40.       Mehlhoff, T., G.C. Landon, and H.S. Tullos, Total hip arthroplasty following failed internal fixation of hip fractures. Clin Orthop Relat Res, 1991(269): p. 32-7.

41.       Mabry, T.M., et al., Long-term results of total hip arthroplasty for femoral neck fracture nonunion. J Bone Joint Surg Am, 2004. 86-A(10): p. 2263-7.

42.       Haidukewych, G.J. and D.J. Berry, Hip arthroplasty for salvage of failed treatment of intertrochanteric hip fractures. J Bone Joint Surg Am, 2003. 85-A(5): p. 899-904.

43.       Ganz, R., et al., The etiology of osteoarthritis of the hip: an integrated mechanical concept. Clin Orthop Relat Res, 2008. 466(2): p. 264-72.

44.       Ganz, R., et al., Femoroacetabular impingement: a cause for osteoarthritis of the hip. Clin Orthop Relat Res, 2003(417): p. 112-20.

45.       Parvizi, J. and R. Ganz, Hip osteoarthritis. Orthopedics, 2003. 26(11): p. 1099, 1109.

46.       Steppacher, S.D., et al., Mean 20-year followup of Bernese periacetabular osteotomy. Clin Orthop Relat Res, 2008. 466(7): p. 1633-44.

47.       Crowe, J.F., V.J. Mani, and C.S. Ranawat, Total hip replacement in congenital dislocation and dysplasia of the hip. J Bone Joint Surg Am, 1979. 61(1): p. 15-23.

48.       Erdemli, B., et al., Total hip arthroplasty in developmental high dislocation of the hip. J Arthroplasty, 2005. 20(8): p. 1021-8.

49.       Parvizi, J., et al., Arthroscopy for labral tears in patients with developmental dysplasia of the hip: a cautionary note. J Arthroplasty, 2009. 24(6 Suppl): p. 110-3.

50.       Domb, B.G., et al., Arthroscopic labral reconstruction is superior to segmental resection for irreparable labral tears in the hip: a matched-pair controlled study with minimum 2-year follow-up. Am J Sports Med, 2014. 42(1): p. 122-30.

51.       Konan, S., S.J. Rhee, and F.S. Haddad, Hip arthroscopy: analysis of a single surgeon's learning experience. J Bone Joint Surg Am, 2011. 93 Suppl 2: p. 52-6.