Introduction: A Rose calcaneal osteotomy and Cobb procedure for treatment of acquired pes planus is gaining in popularity as a result of the advantages of anatomical reconstruction and reduced graft site morbidity. Although, its ability to provide long term dynamic function and effect on patient’s symptoms remains to be seen.

Materials and Methods: Twenty-two patients with stage two and three Posterior tibialis tendon dysfunction underwent surgical reconstruction with a Cobb procedure and Rose calcaneal osteotomy between 2003 and 2008. The average age was 59 years (range: 20–80 years). There were 18 females and four males.

Results: We evaluated the dynamic function of the Tibialis posterior muscle tendon function by ultra-sonograms postoperatively at mean follow-up time of 36 months. Eighty three per cent of patients achieved a single heel raise. Seventy-three percent of the patients showed an intact and mobile tibialis posterior tendon on supination and pronation movements. There was no difference in the satisfaction of patients with a tenodesis or non tenodesis.

Conclusion: Our results suggest that Cobb procedure does provide dynamic Tibialis posterior function in majority of patients.

Elastic energy-storing tendons including the equine superficial digital flexor tendon (SDFT) and human Achilles tendon significantly increase locomotor efficiency, but suffer high injury rates and experience increased core temperatures during exercise. Tenocytes are linked by gap junctions (GJ) comprised of connexin (Cx) proteins that mediate intercellular communication and are necessary for strain-induced collagen synthesis. The effects of hyperthermia on gap junction intercellular communication (GJIC) are unknown. We investigated the hypothesis that there is a down regulation in GJIC and Cx protein by tenocytes in response to hyperthermic episodes similar to those experienced in the SDFT of galloping horses.

Monolayers of equine SDFT-derived cells were heated to 45°C for 10 minutes. GJIC, Cx43 and Cx32 protein expression and cell viability were measured by fluorescence recovery after photobleaching (FRAP) and immunofluorescent labelling respectively.

There was a marked reduction in GJIC (p=< 0.0001) compared with controls (37oC) at 30min and 1h post-heating, with significant recovery by 2h (p=< 0.0001). The number of Cx43 plaques/cell also decreased significantly at 30mins (p=< 0.05), 1h (p=< 0.0001) and 2h (p=< 0.0001). There was however a 3-fold increase in the number of Cx32 plaques/cell at 1h (p=< 0.0001) that returned to normal by 2h. There was little change in cell viability up to 2h, however by 24h post-heating there was an 80% decrease in cell number indicating significant levels of cell death (p=< 0.0001).

Reductions in GJIC following exercise-induced hyperthermia may inhibit tenocyte collagen synthesis. Connexin isotypes may differentially modulate tenocyte collagen synthesis, therefore the dissimilar alterations in Cx43 and Cx32 following heating could have functional importance. The return of GJIC a few hours post-heating might facilitate spread of apoptotic death signals, killing neighbouring cells which would have otherwise escaped death. Understanding the responses of GJ to increased temperature, and the effects of this on viability and collagen synthetic capacity is likely to increase our knowledge of how exercise-induced SDFT core degeneration accumulates.