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AbstractWe describe a new simple reconstruction for neglected chronic ruptures of patellar tendon using ipsilateral hamstrings tendon autograft. This has been validated in thirteen patients with mean follow up six years resulting in favorable outcome. Thirteen patients with mean age 58.2 years (range 30–64 years) presented with chronic patellar tendon rupture. They all underwent patellar tendon reconstruction using ipsilateral hamstrings tendon autograft. The average time from injury was 10 months (range 3–20 months). The cause of rupture was fall from height or after TKA and the preoperative Lysholm score was 65 (range 50–80). Postoperatively with a mean follow up of six years (range 5–7 years), all patients had a stable knee with mean flexion of 123°, extension lag 0°, and Insall-Salvati index 1.2. Quadriceps power was regained in 8 cases to 5/5 and in 5 cases to 4/5. No complications were inspected. The postoperative Lysholm score was 93 (range 89–95). Patellar tendon reconstruction using ipsilateral hamstrings as free autograft, consists an effective treatment option for chronic neglected patellar tendon ruptures. Our technique has favorable clinical outcome, complications are not expected, and consist a simple and anatomic reconstruction with a powerful graft, without the requirement for allograft or implants.

The classic technique of microfracture does not promote hyaline cartilage restoration. Subchondral bone perforations lead to the formation of a clot containing pluripotent progenitor cells and finally the cartilage defect is filled by fibrocartilage tissue. Researchers have focused on enhancing the quality of the newly formed tissue in cartilage defects after microfracture arthroscopic surgery. Adjuvant treatments are categorized in four main groups: scaffolds, pharmaceutical agents, growth factors and combinations of the aforementioned. Several experimental studies utilize pharmaceutical or biological agents in combination with microfracture, to improve the quality of the regenerated cartilage. The mechanism of action of the agents used is either to exert a chondroprotective effect on the newly formed fibrocartilage tissue, or to induce the recruitment of mesenchymal stem cells towards chondrogenesis instead of osteogenesis during microfracture repair. Additionally, scaffolds have been used for both release of the biological agents and mechanical support of the newly formed blood clot. This review highlights current data regarding the combination of microfracture technique with adjuvant treatments in order to ameliorate the final outcome.

IntroductionMicrofracture does not lead to complete healing of full-thickness cartilage defects. The aim of this study was to evaluate the effect of modifying Wnt/β-catenin signaling following microfracture, on the restoration of a full-thickness cartilage defect in a rabbit model. The modification of the canonical Wnt pathway was achieved through per os administration of lithium carbonate, which is an intracellular inhibitor of glycogen synthase kinase 3-β (Gsk3-β) and therefore induces Wnt/β-catenin signaling.Materials and methodsFull-thickness cartilage defects of 4 mm in diameter were created in the patellar groove of the right femurs of 18 male New Zealand white rabbits. The rabbits were divided into three groups of six (n = 6) based on post-surgery treatment differences, as follows: microfracture only (group 1), microfracture plus lithium carbonate 7 mM in the drinking water for 1 week (group 2), microfracture plus lithium carbonate 7 mM in the drinking water for 4 weeks (group 3). All animals were sacrificed 9 weeks after surgery. The outcome was assessed histologically, by using the International Cartilage Repair Society (ICRS) visual histological scale. Immunohistochemistry for type II collagen was also conducted.ResultsStatistical analysis of the histological ICRS scores showed that group 3 was significantly superior to group 1 in four out of six ICRS categories, while group 2 was superior to 1 in only two out of six.ConclusionThe combination of microfracture and systematic administration of lithium carbonate 7 mM for 4 weeks shows statistically significant superiority in four out of six ICRS categories compared with microfracture only for the treatment of full-thickness cartilage defects in a rabbit experimental model.

Canonical Wnt signaling regulation is essential for controlling stemness and differentiation of mesenchymal stem cells (MSCs). However, the mechanism through which canonical Wnt-dependent MSC lineage commitment leads to chondrogenesis is controversial. Some studies hypothesize that inhibition of canonical Wnt signaling induces MSC chondrogenic differentiation, while others support that the pathway should be activated to achieve MSC chondrogenesis. The purpose of the present review is to analyze data from recent studies to elucidate parameters regarding the role of canonical Wnt signaling in MSC chondrogenic differentiation.

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