Intra-Tendinous Arterial Supply of the Gluteus Medius and Minimus Muscles

Abstract

Gluteal tendinopathy is the most prevalent of all lower limb tendinopathies, and includes a spectrum of injury from inflammation to rupture/tear. The exact pathophysiology of tendinopathy is not understood with three theories currently being postulated. The vascular theory suggests that injury occurs at areas of hypovascularity within the tendon but a greater understanding of the intra-tendinous arterial supply of the gluteus medius and minimus muscles is important to examining the veracity of this theory. The aim was of this thesis was to describe and define the vascular supply of the gluteus medius and minimus tendons in the context of their macro- and micro-vasculature. A further aim was to examine the validity of using micro-computed tomography (CT) to visualise intra-tendinous arterial anatomy. First, sixteen embalmed Wistar rats were used to investigate the accuracy of two contrast media (barium sulfate and lead oxide) to visualise and measure the extent of contrast penetration and diameter of blood vessels using micro-CT. There was no difference (mean difference [MD] 0.05; MD 95% confidence interval [CI] -0.83 to 0.93) between the number of branching generations for either filled vessels. The mean difference between the contrast medium and true cannula diameter was greater for lead oxide (0.11 mm) than barium sulfate (0.03 mm) when the cannulae were scanned at high resolution. Therefore, barium sulphate was used for the embalmed human cadaveric investigation. Second, ten human cadaveric specimens were used to compare micro-CT angiography with three-dimensional (3-D) images and histological investigations (Haematoxylin and Eosin stain) of the intra-tendinous arterial supply of the gluteus medius and minimus muscle and tendons. Prior to micro-CT all specimens were injected with contrast into blood vessels proximal to the tendon and scanned using CT. No intra-tendinous arteries were seen on the micro-CT images or histological slides. However, capillaries were visualised within the tendon enthesis, two mm from the tidemark, likely resulting from neovascularisation secondary to tendinopathic changes. These changes occurred at the common sites of gluteal tendon tears. The contrast filled to the ascending branch of the LCFA proximal to the greater trochanteric attachment of the gluteal tendons in only 30% of specimens; and in only 40% of the transverse branch. All LCFAs originated from the profunda femoris artery (PFA) compared to 50% of MCFAs. The remaining MCFAs arose from the femoral artery (40%) and a common trunk with the PFA (10%). The modified Bonar scores, which quantified the extent of tendon degeneration ranged from 4 – 10 out of a possible 15 (worst). An incidental finding of muscle fat infiltrate was found distally in all specimens and proximally in only 50%. These results suggest that micro-CT may not be a good method for assessing intra-tendinous arterial supply. However, penetration of the contrast may have been inhibited by using embalmed cadaveric specimens. There were no intra-tendinous vessels detected except for signs of neovascularisation secondary to tendon degeneration potentially supporting the vascular theory of tendon degeneration. Future studies would benefit from using fresh and younger specimens or in vivo techniques.