The cells in the core of embryonic tendon are connected via adherens junctions that function to organise the cells and influence the parallelism of the tendon matrix. In adult tendon the cells are connected via gap junctions that are involved in intercellular communication in response to mechanical stress. We showed here that the cells at the surface of embryonic tendon are connected by tight junctions, which in other tissues function as a selective permeability barrier, to maintain apicobasal polarity, and regulate cell behaviour. Staining for tight junction components in embryonic tendon and keratin 1 and 10 in postnatal tendon was a convenient method of visualising the tendon epithelium. Analysis showed that the Tiotropium Bromide hydrate epithelium in embryonic tendon consisted of several layers of cells whereas in the adult it was a single cell thick. We hypothesise that the epithelium is important for tendon formation during embryogenesis and has a major role postnatally to protect the tendon from adhesion formation. Our findings of a BM at the tendon surface prompted us to investigate the requirement of collagen IV in tendon development. ENU-induced mutations in mice had generated the Svc mouse that is small and has vacuolar cataracts resulting from a missense mutation in the Kaempferol-3-O-rutinoside Col4a1 gene that encodes collagen IV. Mice that are heterozygous for the mutation are viable facilitating the examination of flexor tendons of postnatal mice. Examination of 3 month-old Col4a1+/Svc mice showed that tendons had developed but the BM was interrupted leading to spontaneous formation of adhesions. Immunolocalisation studies of tail and flexor tendon showed that the deposition of laminin and collagen IV was patchy, resulting in regions where the tendon was devoid of BM. Studies of mice deficient for Col4a1 and Col4a2 has shown that collagen IV is required for mechanical stability of postnatal BMs but is dispensable for BM development. Our results confirm that a structural defect in collagen IV can lead to the loss of BM, which is probably most apparent in tissues such as tendon that are under considerable mechanical wear-and-tear. However, the results also show that in the absence of an intact BM, the tendon is susceptible to spontaneous adhesions formation. How the adhesions are formed is unclear, and further studies are needed to investigate the disease mechanism.