Stem Cell Therapy for Hip Pain: A Patient's Complete Guide

Hip pain is the indication where we see the most diagnostic confusion. The hip joint is deep, the symptoms often refer in unexpected ways, and several conditions in and around the hip can present similarly. Pain that feels like hip pain often isn't from the hip joint at all.

This guide walks through how we evaluate and treat hip-related pain at Apex. It covers the joint itself (osteoarthritis, AVN), the surrounding soft tissue (tendinopathies, bursitis), and the conditions commonly mistaken for hip pain (back, SI joint, abdomen). It also covers the most clinically distinctive indication in our hip practice: early-stage avascular necrosis, where cellular therapy has emerging support that's specific to this condition.

If you're trying to figure out what's actually wrong with your hip and what to do about it, the long version of the conversation lives here.

What's actually wrong with your hip?

Pain around the hip can come from:

Hip osteoarthritis. Wear of the cartilage on the femoral head and the acetabulum. Common in middle-aged and older adults.

Avascular necrosis (AVN, osteonecrosis) of the femoral head. A specific condition where the blood supply to part of the femoral head is compromised, leading to bone death and eventual collapse. Can occur in younger patients (40s, 50s) and is often unilateral.

Labral tears. Cartilaginous rim around the hip socket. Tears can be traumatic or related to FAI.

Femoroacetabular impingement (FAI). A structural problem where the femoral head or the acetabular rim creates abnormal contact with each other during certain motions. Sub-types include cam (femoral side), pincer (acetabular side), and mixed.

Greater trochanteric pain syndrome (GTPS). Pain on the outside of the hip, often related to gluteal tendinopathy and/or trochanteric bursitis.

Gluteal tendinopathy. Degenerative changes in the gluteus medius and minimus tendons at their insertion on the greater trochanter. Common cause of lateral hip pain.

Hamstring tendinopathy. Pain at the ischial tuberosity (sit bone), at the proximal hamstring origin.

Iliopsoas tendinopathy or bursitis. Pain at the front of the hip from the iliopsoas tendon or its associated bursa.

Snapping hip syndrome. A clicking or snapping sensation, internal (iliopsoas over the femoral head) or external (IT band over the greater trochanter).

Referred pain. Lumbar spine, SI joint, abdomen, pelvis. The "hip pain" patient with a low back source is one we see frequently.

The pattern of pain often suggests which structure is involved. Anterior groin pain usually points to the joint itself or to iliopsoas pathology. Lateral hip pain points to greater trochanteric structures. Posterior buttock pain points to gluteal or hamstring origin or to lumbar/SI sources. The exam usually narrows it further.

The workup

For hip pain at Apex, the workup includes:

History. When the pain started, where it hurts, what makes it better or worse, what positions or activities provoke it, your activity level, your goals. Specific patterns are highly suggestive.

Targeted exam. Range of motion, both passive and active, in flexion, extension, abduction, adduction, and rotation. Provocation maneuvers: FABER (flexion-abduction-external rotation, sensitive for hip joint pathology and SI joint), FADIR (flexion-adduction-internal rotation, sensitive for FAI and labral pathology), Stinchfield (resisted hip flexion in supine, suggestive of intra-articular pathology), Ober's test (IT band), Trendelenburg sign, gait analysis. Palpation of specific structures: trochanteric region, ischial tuberosity, anterior hip. Neurologic and back screen.

Imaging review. Plain X-rays for joint space, alignment, and bony detail. MRI for soft tissue, labrum, cartilage, bone marrow edema, and AVN evaluation. MR arthrography (MRI with intra-articular contrast) sometimes for clearer labral evaluation.

Targeted diagnostic injection if needed. An image-guided intra-articular hip injection with local anesthetic can confirm whether the joint itself is the source of pain. This is particularly useful in cases where the imaging is ambiguous or where multiple potential sources exist.

A good workup separates the most common patterns within an hour. The most common diagnostic mistake we see: patients treated for "hip pain" that's actually from their lumbar spine, SI joint, or gluteal soft tissue, without anyone confirming the source.

Hip osteoarthritis

Wear of the hip joint cartilage, often progressing over years to decades.

Typical presentation. Groin or anterior thigh pain, worse with weight-bearing, prolonged walking, or specific motions (like getting in and out of a car). Morning stiffness. Range of motion loss, particularly internal rotation. Patients often describe difficulty with shoes, socks, and getting up from low chairs.

Mild to moderate disease. Cellular therapy is a reasonable option. The evidence base for hip is smaller than for knee but the principles align. Image-guided intra-articular injection of allogeneic MSCs and exosomes. Expected response: 50 to 65 percent of patients show meaningful improvement at 12 months, with effect lasting 12 to 24 months in responders.

Severe disease. Total hip arthroplasty (THA) is typically the right answer. Hip replacement is one of the most successful procedures in orthopedic surgery, with high satisfaction rates and excellent functional outcomes. Cellular therapy isn't a substitute for it.

Why hip has a smaller cellular therapy evidence base than knee. Two reasons: the joint is deeper and harder to access, and hip replacement is so successful and well-tolerated that fewer patients have driven research demand for an alternative. The biology is similar to knee; the clinical literature is just smaller.

Decision considerations. Patient age, activity level, severity of disease, response to conservative care, willingness to consider surgery, and goals over the next decade all factor in. We walk through these specifically during consultation.

Avascular necrosis (AVN)

A specific condition where the blood supply to part of the femoral head is interrupted, leading to bone death. Can be caused by:

Trauma. Femoral neck fracture, hip dislocation.

Steroid use. High-dose or long-term corticosteroid therapy, including for medical conditions like asthma, autoimmune disease, or organ transplant.

Alcohol use. Heavy chronic alcohol consumption.

Coagulopathies. Certain blood-clotting disorders.

Idiopathic. A meaningful percentage of cases have no clear cause.

Other risk factors. Sickle cell disease, lupus, certain cancers and chemotherapies, decompression sickness.

Classification. The Ficat-Arlet system stages AVN based on imaging:

• Stage 0: pre-radiographic, asymptomatic
• Stage I: positive MRI, normal X-ray
• Stage II: X-ray changes (sclerosis, cysts), no collapse
• Stage III: subchondral fracture or femoral head collapse
• Stage IV: end-stage joint destruction

Why this matters. Stages 0 to II are pre-collapse. Stage III is the inflection point. After collapse, the structural problem progresses rapidly toward joint destruction, and hip replacement becomes the next answer.

The regenerative case for early-stage AVN. Hernigou and colleagues have published long-term follow-up of bone marrow concentrate injection (with or without core decompression surgery) in pre-collapse AVN, showing meaningful rates of avoiding hip replacement in treated patients. Other groups have published similar findings with various cellular protocols.

The window of opportunity is real but narrow. Cellular therapy for AVN is most effective when delivered before collapse. Patients with Ficat I or early Ficat II disease who undergo cellular therapy may avoid or significantly delay the progression that leads to replacement. The data are encouraging though still maturing.

Our approach. We see meaningful numbers of AVN patients at Apex, often referred by orthopedic surgeons who recognize that conservative management of early AVN is unsatisfying and cellular therapy is worth offering before the disease progresses. We coordinate closely with surgical colleagues for patients who may need surgical intervention (core decompression, sometimes with cellular augmentation) as part of the protocol.

What we don't promise. AVN that has already progressed to collapse won't be reversed by cellular therapy. Bilateral disease may not respond equally on both sides. Some patients progress despite optimal treatment.

Why this indication may be one of the most interesting for cellular therapy. Because there's a clear structural endpoint we're trying to prevent (femoral head collapse), a measurable disease stage (Ficat), and a meaningful unmet need (early AVN has no truly effective standard treatment besides core decompression with mixed results). The biology of MSCs (immune modulation, paracrine repair, anti-inflammatory effect, potential support of bone-supporting cellular activity) aligns reasonably well with what's wrong in early AVN.

Labral tears and FAI

The hip labrum is a cartilaginous rim around the acetabulum (hip socket) that contributes to joint stability and suction.

Labral tears. Common, often associated with FAI or trauma. Many labral tears are asymptomatic and incidental on imaging. Some cause clicking, catching, or anterior groin pain, particularly with certain motions.

Femoroacetabular impingement (FAI). Structural mismatch between the femoral head and the acetabular rim. Cam impingement (femoral head/neck shape abnormality) is more common in younger active males. Pincer impingement (acetabular over-coverage) is more common in females. Mixed patterns are also common.

Conservative care. PT focused on hip mechanics, activity modification, addressing compensatory patterns. Many FAI and labral tear patients respond well to structured rehab without needing intervention.

Regenerative approach. PRP or cellular therapy can address some of the inflammation and irritation associated with labral tears and FAI symptoms, without addressing the structural problem directly. For some patients, this provides meaningful symptom relief and avoids the need for surgery. For others, the underlying mechanical issue eventually drives them to consider arthroscopic hip preservation surgery.

Surgical alternatives. Hip arthroscopy with labral repair, debridement, or labral reconstruction. Femoral or acetabular osteoplasty to address the impingement. The surgical literature on hip arthroscopy has matured substantially in the last decade, with reasonable outcomes for the right patients.

Decision considerations. Patient age, severity of mechanical symptoms, progression of cartilage damage, response to conservative care, and goals all matter. We coordinate with surgical colleagues for patients considering hip arthroscopy.

Greater trochanteric pain syndrome and gluteal tendinopathy

Lateral hip pain is one of the most common hip-area complaints we see. It's often misdiagnosed as "bursitis" when the actual primary problem is gluteal tendinopathy.

Typical presentation. Pain on the outside of the hip, often worse when lying on the affected side, with prolonged walking, with stairs, or with crossing the legs. Tenderness over the greater trochanter on exam.

The bursitis vs tendinopathy distinction. Historically called "trochanteric bursitis," the contemporary understanding is that the underlying problem is usually gluteus medius and minimus tendinopathy, with secondary bursal involvement. The terminology shifted to "greater trochanteric pain syndrome" (GTPS) to reflect this.

Conservative care. PT focused on hip abductor strengthening, activity modification, addressing gait or biomechanical contributors. NSAIDs for short-term symptom control.

Regenerative approach. PRP injection into the gluteal tendons (and adjacent bursa if there's significant bursal component) under ultrasound guidance. Strong evidence base for chronic gluteal tendinopathy. Often combined with shockwave for chronic refractory cases.

Steroid injection caution. Trochanteric bursal injection with corticosteroid is widely used for short-term relief but has a documented negative effect on tendon quality with repeated use, similar to other tendinopathies. We typically prefer PRP for any patient considering more than one or two steroid injections.

Surgical alternatives. Endoscopic or open repair of significant gluteal tendon tears in cases that have failed conservative and regenerative care.

Expected response. 60 to 75 percent of patients show meaningful improvement at 12 to 16 weeks. Durability 9 to 18 months typical.

Hamstring tendinopathy and other less common indications

Proximal hamstring tendinopathy. Pain at the ischial tuberosity (the sit bone), often in runners and other athletes. PRP plus eccentric loading is the typical protocol. Surgical management for severe refractory cases.

Iliopsoas tendinopathy or bursitis. Pain at the anterior hip, often with hip flexion. PRP under ultrasound guidance for refractory cases.

Pubic symphysis pain. Common in athletes (the "athletic pubalgia" or "sports hernia" pattern). Often requires a careful workup; the regenerative role is limited but specific.

Snapping hip syndrome. Often a mechanical problem that responds to PT and biomechanical work. Cellular therapy is rarely the primary intervention.

What hip regenerative procedures look like

For most hip procedures at Apex:

Intra-articular cellular injection (for OA or AVN). 75 to 105 minutes total. Image-guided injection via ultrasound. The hip joint is deeper than the knee, so accurate placement requires more setup. Some patients tolerate a brief sedation or anxiolytic for comfort.

Greater trochanteric region PRP (for GTPS/gluteal tendinopathy). 60 minutes total. Ultrasound-guided injection into the affected tendons. Local anesthetic for comfort. Patient drives home.

Other peri-articular injections (iliopsoas, ischial tuberosity, etc.). Similar setup, similar recovery.

Recovery for hip regenerative procedures:

Days 1 to 3. Mild to moderate local soreness, sometimes more pronounced for the deeper intra-articular injections. Acetaminophen and ice. No NSAIDs for 5 days.

Days 4 to 7. Most patients are back to normal walking and light activity. We restrict high-impact loading and aggressive stretching for the first week.

Weeks 2 to 4. Progressive return to normal activity. Continued restriction on running, jumping, and high-load gym work.

Weeks 4 to 8. Symptomatic improvement typically becomes noticeable.

Weeks 8 to 12. Improvement deepens. Formal re-evaluation at 12 weeks.

Months 4 to 6. Continued improvement. Peak effect typically in this window for intra-articular protocols.

When hip replacement is the right answer

A few patterns where surgical consultation should be the next step:

Severe hip OA with bone-on-bone disease and significant functional impairment.

Advanced AVN with femoral head collapse.

Significant FAI with progressive cartilage damage and failed conservative/regenerative care, in a patient appropriate for hip arthroscopy.

Hip fracture (acute trauma).

Hip dislocation with significant structural compromise.

If your case fits one of these, we'll tell you and coordinate with orthopedic surgeons we trust. Hip replacement, in particular, is a procedure that genuinely transforms quality of life for the right patient. We don't try to talk anyone out of it when they need it.

Specific patient profiles

The 55-year-old with moderate left hip OA, working full-time, active. Cellular therapy candidate. Realistic goal: 18 to 24 months of substantial improvement, delaying replacement.

The 42-year-old with recently diagnosed Ficat II AVN, no collapse. Important regenerative candidate. Time-sensitive. Discuss cellular therapy, possibly with surgical core decompression depending on lesion size and progression risk.

The 68-year-old with severe bilateral hip OA, marked functional limitation. Bilateral hip replacement conversation. Not a cellular therapy case.

The 58-year-old with lateral hip pain that's worse at night. Likely GTPS/gluteal tendinopathy. PRP plus PT plus possibly shockwave. Not an intra-articular case.

The 35-year-old athlete with anterior hip pain, FADIR-positive exam, imaging showing cam FAI and labral fraying. Workup carefully. Some patients respond to PT-focused conservative care. Some respond to PRP or cellular adjunct. Some progress to hip arthroscopy. The decision depends on imaging severity, symptoms, and activity goals.

The 50-year-old with vague "hip pain" that turns out to be lumbar radiculopathy. Different protocol. We screen for back contribution on every hip patient.

The 72-year-old with hip pain after months of high-dose steroid therapy for autoimmune disease. Imaging-confirmed AVN is on the differential. If confirmed, time-sensitive workup and treatment discussion.

How to book

To request a consultation about your hip, request a consultation or call (972) 768-2328. We're at 2111 Kirkwood Blvd, Suite 110b, Southlake, TX 76092.

If you've been told you need hip replacement and want a second opinion, bring the imaging. Most patients we see in this category turn out to need the replacement eventually, but for some, cellular therapy buys meaningful additional time. The honest answer requires looking at your imaging.

If you've been diagnosed with AVN, particularly early-stage, reach out sooner rather than later. The window for cellular therapy in pre-collapse AVN is real but doesn't last forever.

A short note from Dr. Abdullah

The hip is the joint where I'm most often surprised by what the workup turns up. Patients arrive thinking they have hip OA who actually have severe lumbar radiculopathy. Patients arrive thinking they have "bursitis" who actually have gluteal tendinopathy. Patients arrive thinking they have a benign mechanical issue who actually have early AVN that desperately needs attention. The diagnostic synthesis matters more here than for any other joint. When the picture is clear and the indication fits, cellular therapy delivers excellent results, particularly for early AVN, where the alternative is watching a destructive disease progress without an effective intervention. That subset of patients is some of the most rewarding work we do.