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Outer Hip Pain: Why it Exists and How to Fix it

hip pain self treatment video Sep 16, 2022
 

 

Have you ever had persistent pain that occurred on the outside of the hip? It is especially tender at night when you’re trying to go to bed, maybe even the side that you’re laying on. Most commonly, these ailments are always chalked up to be “hip bursitis”, which is actually untrue. This comes to a relief, as well, because we’ve been identifying the incorrect structures that are provoking pain.. Historically, this musculoskeletal condition is very difficult to treat, but we’ve also been using treatment methods that are more aligned with that of bursitis (inflammation to the bursa sac). These treatments can be described as attacking inflammatory mediators with interventions like corticosteroid injections, NSAID’s, or surgery. Recent radiographic evidence may suggest that these “hip bursitis” cases are actually a result of a gluteal tendinopathy. This is why most clinicians and researchers are now referring to this condition as Greater Trochanter Pain Syndrome (GTPS), instead of strictly bursitis. This systematic literature review (looking at all papers published on GTPS and hip bursitis) stated that within all of the studies they sifted through, radiographic evidence suggested 4-46% were present with inflammation of the bursa and 18-50% presented with gluteal tendinopathy (1). 

GTPS affects about 2-6 per 1,000 people. Most commonly this affects women from the ages of 40-60. What’s also interesting is that 2/3rds of people who have GTPS also have accompanying low back pain or hip osteoarthritis. Research has stated that the cause of GTPS has a wide spectrum of mechanisms, such as, repetitive compression and friction between the iliotibial band (IT) and the greater trochanter causing microtrauma to the gluteal tendons, which is most commonly caused by a wider pelvic width compared to whole body width, and congenital anomalies occurring at the femur neck (1). 

A study conducted had MRI’s completed on symptomatic and asymptomatic hip joints in 40 people that presented with one sided hip pain, to look at potential mechanisms of pain. The results obtained from the MRI’s were sent to 3 independent radiologists to be read. What they found is that even though there is bursa inflammation present, it failed to correlate with pain the patient was experiencing. What they continued to discover is that on the symptomatic side of the patients, gluteal tendinopathy of the gluteus medius and atrophy (wasting away) of the gluteus minimus (figure 1) was almost exclusively on the side of symptoms (2). This was consistent with other research that has been presented. And so, Gluteus Medius Tendinopathy has been identified as a major player in the cause of GTPS. Tendinopathy, as described by one of the leading researchers in tendon pathology, is tendinopathy will present with these cardinal signs: hypercelluarity (increase in cell production), increase in protein production, disorganization of collagen fibers, neovascularization, but NO INFLAMMATION (figure 2) (1). Instead, what they’re hypothesizing is the pain associated with persistent hip pain is actually due to substance p (pain mediating chemical), and “sprouting” of new nerves, which is more than likely accompanying the neovascularization (1). This all means “there was something that disrupted the tendon collagen fibers, the body recognizes this and increases the reparative process with increased cellular and protein activity; this requires more blood flow for tissue being laid down and we also need more innervation (nerves) in the area. 

Figure 1: Gluteus minimus (inner highlighted muscle) and gluteus medius (outer highlight muscle) and iliotibial band (faded out)

Figure 2: Comparing a healthy tendon to a tendon that has undergone some kind of structural damage

A systematic review looked at all of the interventions for GTPS and what they found is that conservative care is the gold standard, having a 90% success rate (1). What they deemed conservative care is NSAID’s, corticosteroid injection, shockwave therapy, and physiotherapy (corrective exercise). I would like to address some of these interventions, because they might have been successful at decreasing pain, but could be causing more damage to the tendon. NSAID’s have been found to impair tendon repair and disrupt osteoblast activity and therefore bone remodeling (5,6). Corticosteroids injections are shown to weaken tendons, shifting type 1 collagen production to type 3 (4). Remember when I mentioned disorganization in the collagen fibers? That’s because type 3 collagen is what is laid down after an injury and is then converted to type 1 collagen with appropriate stress introduced to the tendon. Corticosteroid injections inhibit this conversion, which leads to a weakened tendon.

Here is a study that compared interventions that looked at the difference between a corticosteroid injection, low energy shock wave, and a home training program. What they found is that at a 15 month follow up with the groups, 80% of the home training program participants reported pain reduction, 75% of the shockwave therapy group reported pain reduction, while the corticosteroid group reported 48% pain reduction (3). What this study highlights is going after the underlying problem (tendon loading or function issue) and not the symptoms (inflammation or pain) is what solves this neuromusculoskeletal condition. So when you’re seeking out a provider for hip pain, think conservative care physicians that go after tendon function! 

References:

  1. Reid, Diane. “The Management of Greater Trochanteric Pain Syndrome: A Systematic Literature Review.” Journal of Orthopaedics, vol. 13, no. 1, 2016, pp. 15–28., doi:10.1016/j.jor.2015.12.006. 
  2. Woodley S, Nicholson H, Livingstone V, et al. Lateral hip pain: findings from magnetic resonance imaging and clinical examination. J Orthop Sports Phys Ther. 2008;38:313.
  3. Rompe J, Segal N, Cachio A, et al. Home training, local corticosteroid injection, or radio shock wave therapy for greater trochanteric pain syndrome. Am J Sports Med. 2009;37:1981
  4. Hugate R, Pennypacker J, Saunders M, Juliano P. The effects of intratendinous injections of corticosteroid on the biomechanical properties of rabbit Achilles tendons. JBJS (American). 2004;86:794-801.
  5. Simon AM, Manigrasso MB, O’Connor JP, COX-2 function is essential for bone fracture healing. J Bone Miner Res. 2002;17:963–976.
  6. Cohen D, Kawamura S, Ehteshami J, Rodeo S. Indomethacin and Celecoxib impair rotator cuff tendon-to-bone healing. Am J Sports Med. 2006;34:362-369.
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