Objectives. Inflammation of the
Insertional Achilles tendonitis is an inflammatory disorder affecting mainly active young patients. The etiology is multifactorial and include the combination of anatomical and biomechanical characteristics. One fifth of the tendon injuries in athletes are insertional complaints which includes bursitis and insertion tendinitis.The complex of the insertion of the Achilles tendon includes three main components of fibrocartilage sesamoid, periosteum and enthesis. A conservative regime is recommended as the first line of treatment. In case of failure a surgical decompression of the posterior margin of the calcaneum is indicated. Nine cadaveric legs were used for the experiment. The leg was mounted on an MTS machine and was axially loaded 360 N. The foot was attached to a plate which enabled dorsal and plantar flexion. The Achilles was sutured twice in an Ethibond No. 5 using the Krakow technique in order to anchor the tendon to an actuator. A thin pressure sensor plate (Teckscan) was inserted into the
Introduction:. The insertion footprint of the different muscles tendon fascicles of the Achilles Tendon on the calcanium tuberosity has not been described before. Method:. Twelve fresh frozen leg specimens were dissected to identify the different Achilles Tendon fascicles insertion footprint on the calcaneum in relation to their corresponding muscles. Further ten embalmed cadaveric leg specimens were examined to confirm an observation on the
Introduction. Kager's fat pad (KFP) is located in Kager's triangle between the Achilles tendon (AT), the superior cortex of the calcaneus and Flexor Hallucis Longus (FHL) muscle & tendon. Although the biomechanical functions of KFP are not yet fully understood, a number of studies suggested that KFP performs important biomechanical roles including assisting in the dynamic lubrication of the AT subtendinous area, protection of AT vascular supply, and load and stress distribution within the
Introduction: Since 2004 we chose the arthroscopic method of therapy by the
The Achilles tendon is commonly operated on, but has associated wound complications, ranging from 7–14% in previously reported series larger than 100 cases. We report a retrospective review of one surgeon’s practice conducted to assess the prevalence of wound complications associated with acute and chronic rupture repair, peritenolysis, tenodesis, debridement,
Background: The Achilles tendon is commonly operated on, but has associated wound complications, ranging from 7–14% in previously reported series larger than 100 cases. Methods: A retrospective review of one surgeon’s practice was conducted to assess the prevalence of wound complications associated with acute and chronic rupture repair, peritenolysis, tenodesis, debridement,
Eighty-one patients treated surgically for non-insertional Achilles’ tendinopathy between 1987 and 1999 by one surgeon were reviewed by a comprehensive postal questionnaire. Fifty-six patients (73 tendons) returned a questionnaire at an average of 58.7 months after surgery. The duration of preoperative symptoms averaged 24.6 months. In all cases, conservative treatment was first attempted but failed to alleviate symptoms. Twenty (35.7%) of these patients were involved in competitive or serious recreational sport. There were 34 men and 22 women with a mean age of 42.5 years (range: 23 to 66). All patients who had insertional tendinopathy or
Tendon is a bradytrophic and hypovascular tissue, hence, healing remains a major challenge. The molecular key events involved in successful repair have to be unravelled to develop novel strategies that reduce the risk of unfavourable outcomes such as non-healing, adhesion formation, and scarring. This review will consider the diverse pathophysiological features of tendon-derived cells that lead to failed healing, including misrouted differentiation (e.g. de- or transdifferentiation) and premature cell senescence, as well as the loss of functional progenitors. Many of these features can be attributed to disturbed cell-extracellular matrix (ECM) or unbalanced soluble mediators involving not only resident tendon cells, but also the cross-talk with immigrating immune cell populations. Unrestrained post-traumatic inflammation could hinder successful healing. Pro-angiogenic mediators trigger hypervascularization and lead to persistence of an immature repair tissue, which does not provide sufficient mechano-competence. Tendon repair tissue needs to achieve an ECM composition, structure, strength, and stiffness that resembles the undamaged highly hierarchically ordered tendon ECM. Adequate mechano-sensation and -transduction by tendon cells orchestrate ECM synthesis, stabilization by cross-linking, and remodelling as a prerequisite for the adaptation to the increased mechanical challenges during healing. Lastly, this review will discuss, from the cell biological point of view, possible optimization strategies for augmenting Achilles tendon (AT) healing outcomes, including adapted mechanostimulation and novel approaches by restraining neoangiogenesis, modifying stem cell niche parameters, tissue engineering, the modulation of the inflammatory cells, and the application of stimulatory factors. Cite this article:
The June 2012 Foot &
Ankle Roundup360 looks at: the Achilles tendon Total Rupture Score (ATRS); endoscopic treatment of Haglund’s syndrome; whether it is worth removing metalwork; hyaluronic acid injection; thromboembolic events after fracture fixation in the ankle; whether surgeons are as good as CT scans for OCD of the talus; proximal fractures of the fifth metatarsal; nerve blocks for hallux valgus surgery; chronic osteomyelitis in the non-diabetic patient; Charcot arthropathy.
The August 2012 Foot &
Ankle Roundup360 looks at: calcaneocuboid distraction arthrodesis with allograft for acquired flatfoot; direct repair of the plantar plate; thromboembolism after fixation of the fractured ankle; weight loss after ankle surgery; Haglund’s syndrome and three-portal endoscopic surgery; Keller’s procedure; arthroscopy of the first MTPJ; and Doppler spectra in Charcot arthropathy.