A 3-portal approach for arthroscopic subtalar arthrodesis

We present a 3-portal approach for arthroscopic subtalar arthrodesis with the patient in the prone position. The prone position allows the use of the two standard posterior portals and it allows for accurate control of hindfoot alignment during surgery. Furthermore, the introduction of talocalcaneal lag screws is easy with the patient in this position. In addition to the standard posterior portals, an accessory third portal is created at the level of the sinus tarsi for introduction of a large diameter blunt trocar to open up the subtalar joint. Due to the curved geometry of the posterior subtalar joint, removal of the anterior articular cartilage is impossible by means of the posterior portals only. An advantage of the 3-portal approach is that ring curettes can be introduced through the accessory sinus tarsi portal to remove the articular cartilage of the anterior part of the posterior talocalcaneal joint. Arthroscopic subtalar arthrodesis in patients with a talocalcaneal coalition presents a technical challenge as the subtalar joint space is limited. The 3-portal technique was successfully used in three subsequent patients with a talocalcaneal coalition; bony union of the subtalar arthrodesis occurred at 6 weeks following surgery. With the 3-portal technique, a safe and time-efficient arthroscopic subtalar arthrodesis can be performed even in cases with limited subtalar joint space such as in symptomatic talocalcaneal coalition

Retro-trochanteric sciatica-like pain: current concept

The aim of this manuscript is to review the current knowledge in terms of retro-trochanteric pain syndrome, make recommendations for diagnosis and differential diagnosis and offer suggestions for treatment options. The terminology in the literature is confusing and these symptoms can be referred to as ‘greater trochanteric pain syndrome’, ‘trochanteric bursitis’ and ‘trochanteritis’, among other denominations. The authors focus on a special type of sciatica, i.e. retro-trochanteric pain radiating down to the lower extremity. The impact of different radiographic assessments is discussed. The authors recommend excluding pathology in the spine and pelvic area before following their suggested treatment algorithm for sciatica-like retro-trochanteric pain. Level of evidence II

Recruitment of the mitotic exit network to yeast centrosomes couples septin displacement to actomyosin constriction

The Mitotic Exit Network (MEN) promotes mitotic exit and cytokinesis but if and how MEN independently controls these two processes is unclear. Here, the authors report that MEN displaces septins from the cell division site to promote actomyosin ring constriction, independently of MEN control of mitotic exit

Deciphering the pathogenesis of tendinopathy: a three-stages process

Our understanding of the pathogenesis of "tendinopathy" is based on fragmented evidences like pieces of a jigsaw puzzle. We propose a "failed healing theory" to knit these fragments together, which can explain previous observations. We also propose that albeit "overuse injury" and other insidious "micro trauma" may well be primary triggers of the process, "tendinopathy" is not an "overuse injury" per se. The typical clinical, histological and biochemical presentation relates to a localized chronic pain condition which may lead to tendon rupture, the latter attributed to mechanical weakness. Characterization of pathological "tendinotic" tissues revealed coexistence of collagenolytic injuries and an active healing process, focal hypervascularity and tissue metaplasia. These observations suggest a failed healing process as response to a triggering injury. The pathogenesis of tendinopathy can be described as a three stage process: injury, failed healing and clinical presentation. It is likely that some of these "initial injuries" heal well and we speculate that predisposing intrinsic or extrinsic factors may be involved. The injury stage involves a progressive collagenolytic tendon injury. The failed healing stage mainly refers to prolonged activation and failed resolution of the normal healing process. Finally, the matrix disturbances, increased focal vascularity and abnormal cytokine profiles contribute to the clinical presentations of chronic tendon pain or rupture. With this integrative pathogenesis theory, we can relate the known manifestations of tendinopathy and point to the "missing links". This model may guide future research on tendinopathy, until we could ultimately decipher the complete pathogenesis process and provide better treatments