I maging of the lymphatic vessels is an essential tool for diagnostic assessment of lymphedema. Lymphoscintigraphy is the current reference standard for lymphatic imaging (1-3). SPECT (4), indocyanine green (ICG) fluorescent lymphography (5-7), and MR lymphography (8) are emerging techniques. Lymphatic imaging of the lower limb requires intradermal or subcutaneous injection of tracer or contrast material in the foot to demonstrate the lymphatic vessels. No standard protocol exists, and single or multiple injections are applied at different sites.Each lymphatic vessel has an independent origin in the foot. The lymphatic vessel often branches and converges throughout its course, but it is uncommon to have interconnections with adjacent lymphatic vessels to produce a network. These characteristics allow us to categorize the lymphatic pathways in the lower limb into groups. Conventionally, the lymphatic pathways are divided into two groups: an anteromedial group connecting to the superficial inguinal lymph nodes and a posterolateral group connecting to the popliteal lymph nodes (9,10).Few anatomic studies have addressed the lymphatic vessels because of technical difficulties with their identification. Kinmonth and Eustace (11) developed lymphangiography and found that leg lymphedema is caused by deterioration of lymphatic vessels, lymph nodes, or both and that the pathologic process arose first in the lymph node. However, current lymphatic imaging protocols may miss information because of the lack of anatomic knowledge regarding the relationship between lymphatic vessels and their regional lymph nodes (12). Investigators of a previous study of ICG fluorescent lymphography in cadavers ( 13) classified lymphatic pathways into four distinct groups in the lower limb: anteromedial, anterolateral, posteromedial, and posterolateral. Origins of the lymphatic vessels in the foot may be defined in relationship to these four lymphatic groups, which could be selectively visualized with ICG lymphography.A limitation of previous studies was that the relationship between a lymphatic group and its regional lymph nodes could not be determined with ICG lymphography

Hyaluronan (HA) is an extracellular matrix (ECM) component of articular cartilage and has been used to treat patients with osteoarthritis (OA). A disintegrin and metalloproteinases with thrombospondin motifs (ADAMTSs) play an important role in cartilage degradation in OA. We have previously reported that ADAMTS4 and ADAMTS9 were induced by cytokine stimulation. However, the effect of HA on the cytokine-inducible ADAMTS9 has never been investigated. Moreover, it is unclear whether HA protects cartilage by suppressing aggrecan degradation. Here, we examined the effects of HA on ADAMTS expression in vitro and on cartilage degradation in vivo. ADAMTS9 expression was higher than that of the other aggrecanases (ADAMTS4 and 5) in human chondrocytes, chondrocytic cells, and rat cartilage. ADAMTS4 and 9 mRNA levels were upregulated in cytokine-stimulated chondrocytes and chondrocytic cells. Pre-incubation with HA significantly inhibited ADAMTS9 mRNA expression in cytokine-stimulated cells. In a rat OA model, Adamts5 and 9 mRNA levels were transiently increased after surgery; intra-articular HA injections attenuated the induction of Adamts5 and 9 mRNA. HA also blocked aggrecan cleavage by aggrecanase in OA rats in a molecular size-dependent manner. These results demonstrate that HA attenuates induced aggrecanases expression in OA and thereby protects articular cartilage degradation by this enzyme. Our findings provide insight into the molecular basis for the beneficial effects of HA in OA. © 2018 The Authors. Journal of Orthopaedic Research® Published by Wiley Periodicals, Inc. on behalf of Orthopaedic Research Society. J Orthop Res 9999:1-9, 2018.

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