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Case 1.11
Published in Monica Fawzy, Plastic Surgery Vivas for the FRCS(Plast), 2023
What is the blood supply of tendons, and how do they heal?There are two sources of blood supply:the first is via diffusion through synovial sheaths, which is the more important source distal to the MCP joint, andthe second is via direct vascular perfusion by the vincular system.Tendon healing occurs via two pathways:an intrinsic pathway – involving epitenon and endotenon tenocytes, andan extrinsic pathway – by invasion of inflammatory and synovial cells from the surrounding sheath and synovium, which contributes to adhesions and scarring.As with all tissue healing, it occurs via an inflammatory, proliferative, and remodelling phase.
Achilles tendon rupture
Published in Maneesh Bhatia, Essentials of Foot and Ankle Surgery, 2021
Manuel Monteagudo, Pilar Martínez de Albornoz
The Achilles tendon works under considerable stress in all phases of gait. This is because evolution placed the foot in a biomechanically disadvantaged position due to the leveraged forces placed upon it by ground reaction forces. The cause of rupture is multifactorial. The potential combination of different mechanisms may explain most acute ruptures. Coalescent tendinous fibres of the gastrocnemius originating from the distal femur, and of the soleus originating from the proximal tibia, form the tendon that twists around 90° internally upon descending towards its calcaneal insertion. The twisting of the tendon allows for the accumulation and release of energy when walking or running. The midsection receives a relatively poor blood supply, which might make it more vulnerable to degeneration and rupture. The blood supply decreases with increasing age and might be another factor that would facilitate rupture when exposed to minor trauma. A torsional ischaemic effect, with the transient vasoconstriction of the intratendinous vessels may cause hyperthermia that damages tenocytes. The Achilles tendon may be susceptible to the effects of this temperature increase in its relatively avascular area, where most ruptures occur.
Hands
Published in Tor Wo Chiu, Stone’s Plastic Surgery Facts, 2018
Tendons contain few cells: tenocytes, fibroblasts and synovial cells. The paucity of cells and the presence of avascular zones within the synovial areas led to the impression that tendons would not heal well intrinsically and needed extrinsic cells; however, whilst the collagen bundles are dense, tendons are still metabolically active. Theories on the mechanism(s) of healing are as follows: Extrinsic – it was initially thought that healing comes from fibroblasts producing peritendinous adhesions that act as pathways for cell migration and revascularisation, and this theory was the basis for the immobilisation regimes of the past. By this mechanism, the tendon heals ‘typically’ with inflammation, proliferation and remodelling.Intrinsic – tendons bathed in synovial fluid were found to heal well with minimal inflammation; collagen is produced by tenocytes (in epitenon) that act like fibroblasts and can bridge a tendon gap. This type of healing is increased by tendon motion.
Cell-based therapy in soft tissue sports injuries of the knee: a systematic review
Published in Expert Opinion on Biological Therapy, 2021
Nardeen Kader, Vipin Asopa, Kwaku Baryeh, David Sochart, Nicola Maffulli, Deiary Kader
Clarke et al. [29] examined the use of autologous skin-derived tenocyte-like-cells performing an RCT in patients with patellar ‘tendonitis,’ comparing a treatment group (n = 33) and a control group (n = 27) injected with plasma alone. They tracked the Victorian Institute of Sports Assessment Patellar Tendon (VISA-P) scores between groups, with statistically significant improvements in both. The treatment group had a higher follow-up VISA-P score by an average of 8.1 points (P = 0.0006). Both groups also showed improvements in the following ultrasonographic variables: thickness, hypoechogenicity, tear-size, and neovascularity. However, there was no significant difference between the two arms of the study with respect to this. Of note, one patient in the treatment group subsequently had a traumatic rupture of their patellar tendon playing soccer, which required surgical repair. At this point, a histological specimen was taken, which showed ‘almost-normal-appearing tenocyte-like cells in the area of rupture.’ Both studies reported no significant complications as a result of treatment. It is unclear what this finding implies, as previous studies have shown that torn tendons present profound histological changes [30].
Application of amniotic membrane in reconstructive urology; the promising biomaterial worth further investigation
Published in Expert Opinion on Biological Therapy, 2019
Jan Adamowicz, Shane Van Breda, Dominik Tyloch, Marta Pokrywczynska, Tomasz Drewa
The immune system plays a central role in tissue regeneration due to its integrative coordination tasks during the response to tissue injury. Modifying the immune response via biomaterials is an attractive approach in regenerative medicine. AM allows for the generation of a low inflammatory environment corresponding to the fetal one by active tempering of the proinflammatory signal after implantation in adult tissue [42]. Hortensius et al. demonstrated that the enrichment of a collagen scaffold with AM decreased expression of inflammatory response genes in tenocytes governing tendon healing [43]. A proposed strategy for the use of AM as an immunomodulatory agent should become an incentive for urological tissue engineering which is currently in stagnation due to the inability to overcome fibrotic reactions within urinary tracts. The capacity of AM to modify the adult immune response is mediated by a wide array of cytokines, many of which are also involved in tissue regeneration.
Essential role of Mohawk for tenogenic tissue homeostasis including spinal disc and periodontal ligament
Published in Modern Rheumatology, 2018
Ryo Nakamichi, Kensuke Kataoka, Hiroshi Asahara
In the previous study, the repair system of tendon and ligament is reported that it is divided three phases [17–22]: an inflammatory phase, a cell proliferative phase, and a remodeling phase. The inflammatory phase occurs immediately after injury to several days thereafter. Blood vessels present in the tendon sheath cause hematoma, which contains fibrin, platelets, various growth factors, and cytokines. These attract neutrophils and macrophages to the injured site, and angiogenic factors are also released at this time. The cell proliferation phase begins from Day 3 and lasts for several weeks after injury. This phase is classified into two categories: exogenous repair and endogenous repair. In exogenous repair, fibroblasts migrate to the injured site via macrophages because of lactic acid produced by ischemia tissue [23]. Fibroblasts produce irregular extracellular matrix mainly composed of type III collagen, which forms mechanically weak and non-gliding tissue. In endogenous repair, tenocytes migrate from the inner and outer tendon sheath and form a structure imitating collagen fibrils [24]. Both repair systems work at the injured site, but exogenous repair works slightly earlier than endogenous repair. In addition, the balance between the two repair systems depends on the distance between the stump ends of the injured tendons, the injury range, and post-therapy. The remodeling phase occurs 6–8 weeks after injury, and type III collagen is slowly replaced with type I collagen. Type I collagen is rearranged in the axial direction of the tendon, and its mechanical strength increases (Figure 3).