Tendons are connective tissue structures of paramount importance to human ability of locomotion. The understanding of their physiology and pathology is gaining importance as advances in regenerative medicine are being made today. So far, very few studies were conducted to extend the knowledge about pathology, healing response and management of tendon lesions. In this paper we summarize actual knowledge on structure, process of healing and ageing of the tendons. The structure of tendon is optimized for the best performance of the tissue. Despite the simplicity of the healing response, numerous studies showed, that the problems with full recovery are common and much more significant than we thought, that is why we discussed the issue of immobilization and mechanical stimulation during healing process. The phenomenon of tendons' ageing is poorly understood, although it seems to be a natural and painless process, it is completely different to degeneration in tendinopathy. Recent studies of biological treatment reported faster and optimal healing of the tendons when augmented by growth factors and stem cells. Despite advances in biology of tendons, management of their injuries is still a challenge for physicians, therefore further studies are required to improve treatment outcomes. Tendons are connective tissue structures of paramount importance to human ability of locomotion. The understanding of their physiology and pathology is gaining importance as advances in regenerative medicine are being made today. So far, very few studies were conducted to extend the knowledge about pathology, healing response and management of tendon lesions. In this paper we summarize actual knowledge on structure, process of healing and ageing of the tendons. The structure of tendon is optimized for the best performance of the tissue. Despite the simplicity of the healing response, numerous studies showed, that the problems with full recovery are common and much more significant than we thought, that is why we discussed the issue of immobilization and mechanical stimulation during healing process. The phenomenon of tendons' ageing is poorly understood, although it seems to be a natural and painless process, it is completely different to degeneration in tendinopathy. Recent studies of biological treatment reported faster and optimal healing of the tendons when augmented by growth factors and stem cells. Despite advances in biology of tendons, management of their injuries is still a challenge for physicians, therefore further studies are required to improve treatment outcomes.

Tendinopathy of the long head of the biceps tendon is a difficult medical issue. Its pathogenesis and etiology is multifactorial and unclear. Tendinopathy is thought to be primarily degenerative in nature, as tendons are characterized by impaired regeneration and healing. Thirty–five patients with preoperatively diagnosed tendinopathy of long head of the biceps tendon were referred to the Orthopedics Department. All patients underwent an arthroscopic–assisted biceps tenodesis or tenotomy. The intra-articular portion of the long head of the biceps tendon was obtained from each of the patients who underwent arthroscopy. A macroscopic and microscopic evaluation of biceps tendon samples revealed degeneration among all specimens. This study demonstrates the prevalence of the degeneration process and the presence of marginal inflammation process in tendinopathy of the long head of biceps tendon. The role, that inflammation process plays in tendinopathy is important in the early phase and gradually becomes secondary to the developing degeneration. The inflammatory cells, occasionally seen in pathological tendons, could be an evidence of re–injury and recent healing response.

Background and purpose — Severe backside wear, observed in older generations of total knee replacements (TKRs), led to redesign of locking mechanisms to reduce micromotions between tibial tray and inlay. Since little is known about whether this effectively reduces backside wear in modern designs, we examined backside damage in retrievals of various contemporary fixed-bearing TKRs. Patients and methods — A consecutive series of 102 inlays with a peripheral (Stryker Triathlon, Stryker Scorpio, DePuy PFC Sigma, Aesculap Search Evolution) or dovetail locking mechanism (Zimmer NexGen, Smith and Nephew Genesis II) was examined. Articular and backside surface damage was evaluated using the semiquantitative Hood scale. Inlays were examined using scanning electron microscopy (SEM) to determine backside wear mechanisms. Results — Mean Hood scores for articular (A) and backside (B) surfaces were similar in most implants—Triathlon (A: 46, B: 22), Genesis II (A: 55, B: 24), Scorpio (A: 57, B: 24), PFC (A: 52, B: 20); Search (A: 56, B: 24)—except the NexGen knee (A: 57, B: 60), which had statistically significantly higher backside wear scores. SEM studies showed backside damage caused by abrasion related to micromotion in designs with dovetail locking mechanisms, especially in the unpolished NexGen trays. In implants with peripheral liner locking mechanism, there were no signs of micromotion or abrasion. Instead, “tray transfer” of polyethylene and flattening of machining was observed. Interpretation — Although this retrieval study may not represent well-functioning TKRs, we found that a smooth surface finish and a peripheral locking mechanism reduce backside wear in vivo, but further studies are required to determine whether this actually leads to reduced osteolysis and lower failure rates.

Background: The ultrastructural alterations related to tendinopathy have not been well described. Most studies on this subject have been conducted many years ago and focused on material from the Achilles tendon. It was demonstrated that various comorbidities can affect ultrastructural alterations in the advanced tendinopathy, however there is very little data on ultrastructural morphology in tendinopathies related to mechanical overload as in case of the long head of the biceps brachii tendon (LHBT). The aim was to determine intermediate ultrastructural alterations in middle to severe grade the LHBT tendinopathy and to establish if they are different than those reported in the literature for other anatomical locations. Materials and methods: In this study we examined the ultrastructure of a series of the LHBT fragments arthroscopically removed due to tendinopathy and investigated the morphology of tenocytes and collagen fibers in cases of the LHBT tendinopathy. Results: In pathological samples tenocytes were randomly scattered, their shape was round and the shape of nuclei was also disrupted. The presence of apoptotic-like features in tenocytes' nuclei was noted. All samples showed replacement of collagen fibrils by non-collagen ECM and diffuse collagen disorganization. Conclusions: It was demonstrated at ultrastructural level that the LHBT tendinopathy is not simply a wear and tear phenomenon, since chronic degeneration of the extracellular matrix and tenocytes were present, similarly as in tendinopathies, in other anatomical locations. Background: The ultrastructural alterations related to tendinopathy have not been well described. Most studies on this subject have been conducted many years ago and focused on material from the Achilles tendon. It was demonstrated that various comorbidities can affect ultrastructural alterations in the advanced tendinopathy, however there is very little data on ultrastructural morphology in tendinopathies related to mechanical overload as in case of the long head of the biceps brachii tendon (LHBT). The aim was to determine intermediate ultrastructural alterations in middle to severe grade the LHBT tendinopathy and to establish if they are different than those reported in the literature for other anatomical locations. Materials and methods: In this study we examined the ultrastructure of a series of the LHBT fragments arthroscopically removed due to tendinopathy and investigated the morphology of tenocytes and collagen fibers in cases of the LHBT tendinopathy. Results: In pathological samples tenocytes were randomly scattered, their shape was round and the shape of nuclei was also disrupted. The presence of apoptotic-like features in tenocytes' nuclei was noted. All samples showed replacement of collagen fibrils by non-collagen ECM and diffuse collagen disorganization. Conclusions: It was demonstrated at ultrastructural level that the LHBT tendinopathy is not simply a wear and tear phenomenon, since chronic degeneration of the extracellular matrix and tenocytes were present, similarly as in tendinopathies, in other anatomical locations.