In developed nations Charcot arthropathy is most commonly caused by diabetes mellitus. Worldwide, leprosy remains the primary cause. All evidence points to a relationship between neurologic loss, continued loading activities and the development of unrecognized bone fragmentation. In type 2 diabetes, dysregulation of leptin biology causes bone loss and may be an important factor in precipitating Charcot events. Bone density studies show massive loss of bone in patients with ankle and hindfoot Charcot problems, but not midfoot problems. This suggests a different mechanism for collapse. Stable collapse with ulcer development in the midfoot can be treated with exostectomy. Realignment and fusion remain the mainstays of treatment for diabetic Charcot neuropathy, especially in the ankle and hindfoot. Bone mineralization deficiencies require special consideration of fixation techniques. Thin wire external fixation – either as primary fixation or to reinforce/neutralize other methods can be very helpful. Large bridging screws and carefully selected bridging plates are frequently also valuable to consider. Excessive immobilization periods (often double the normal amount of time) are generally required. The goal may be limited to a braceable, plantigrade foot

Osteoarthritis (OA) is a disease of the joints stemming from a variety of factors, including joint injuries and abnormally high mechanical loading. Although the traditional treatment alternatives for end-stage OA are arthroplasty in the case of the hip and knee, and arthroplasty or arthrodesis in the case of the ankle, these options are not ideal for younger, more active patients. For these patients, joint prostheses would be expected to fail relatively quickly, and ankle fusion is not amenable to maintaining their active lifestyles. In these cases, joint distraction has attracted investigative attention as a conservative OA treatment for younger patients. 9-14. . Based on the principle that decreasing the mechanical load on cartilage stimulates its regeneration. 15. , distraction treatment calls for reduced loading of the joint during a period of typically 3 months, during which time the load customarily passing through the joint is taken up by an external fixator spanning the joint . By mounting the fixator components to the bone on each side of the joint, and then lengthening the rods connecting the proximal and distal portions of the fixator, the joint is distracted. Assuming the fixation is appropriately stiff, any load passes through the fixator instead of the joint, and the two articular surfaces will not be allowed to contact each other under physiologic loading. The exact mechanisms leading to cartilage regeneration during distraction are not yet understood. A possible negative consequence of joint fixation is cartilage degeneration due to immobilization during the treatment. It has been shown by Haapala et al. and others that long-term immobilization can be detrimental to articular cartilage. 16-18. . Conversely, joint motion during fixation (even passive motion) is thought to stimulate or encourage cartilage regeneration. 19-22. Toward this end, considerable effort has been invested in the application of hinges to external fixation for joints Joint motion has also been suggested as a potentially beneficial factor in distraction treatment, as well. 10. This is borne out by data from an RCT comparing the use of a rigid vs motion external fixator. Change in joint biology due to resorption of cysts may be responsible for reversal of symptoms

Aims

The traditional transosseus flexor hallucis longus (FHL) tendon transfer for patients with Achilles tendinopathy requires two incisions to harvest a long tendon graft. The use of a bio-tenodesis screw enables a short graft to be used and is less invasive, but lacks supporting evidence about its biomechanical behaviour. We aimed, in this study, to compare the strength of the traditional transosseus tendon-to-tendon fixation with tendon-to-bone fixation using a tenodesis screw, in cyclical loading and ultimate load testing.

The incidence of acute and chronic conditions of the tendo Achillis appear to be increasing. Causation is multifactorial but the role of inherited genetic elements and the influence of environmental factors altering gene expression are increasingly being recognised. Certain individuals’ tendons carry specific variations of genetic sequence that may make them more susceptible to injury. Alterations in the structure or relative amounts of the components of tendon and fine control of activity within the extracellular matrix affect the response of the tendon to loading with failure in certain cases.

This review summarises present knowledge of the influence of genetic patterns on the pathology of the tendo Achillis, with a focus on the possible biological mechanisms by which genetic factors are involved in the aetiology of tendon pathology. Finally, we assess potential future developments with both the opportunities and risks that they may carry.

Cite this article: Bone Joint J 2013;95-B:305–13.