The Catabolic Fate of Hyaluronic Acid

Laurent, Torvard C.; Dahl, Inger Marie S.; Dahl, Lauritz Bredrup; Engström‐Laurent, Anna; Eriksson, Sigbritt; Fraser, J. R. E.; Granath, Kirsti; Laurent, Claude; Laurent, Ulla B.G.; Lilja, Karin; Pertoft, Håkan; Smedsrød, Bård; Tengblad, Anders; Wik, Ove

doi:10.3109/03008208609001971

Cited by 65 publications

(28 citation statements)

References 37 publications

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“…Changes in the rate of clearance of these markers from the blood circulation also are unlikely to have played a major role since HA molecules are cleared from the blood mostly by the liver (33), antigenic KS by both the liver and the kidneys (34), and the crosslinks by the kidneys (14).…”

Section: Discussionmentioning

confidence: 99%

Treatment with calcitonin suppresses the responses of bone, cartilage, and synovium in the early stages of canine experimental osteoarthritis and significantly reduces the severity of the cartilage lesions

Manicourt

Altman

Williams

et al. 1999

Arthritis & Rheumatism

115

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Bone, synovium, and articular cartilage all appear to be involved in the state of hypermetabolism that develops in unstable joints. Furthermore, the rate of bone resorption increases markedly in the early stages of this OA model and is likely to contribute to cartilage breakdown. Since calcitonin reduced the severity of OA changes, this form of therapy may have benefits for humans who have recently experienced a traumatic knee injury.

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Section: Discussionmentioning

confidence: 99%

Treatment with calcitonin suppresses the responses of bone, cartilage, and synovium in the early stages of canine experimental osteoarthritis and significantly reduces the severity of the cartilage lesions

Manicourt

Altman

Williams

et al. 1999

Arthritis & Rheumatism

115

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“…The major portion of HA released from the tissues is taken up and degraded in lymphatic system. [20][21][22] The degraded HA enters the blood and is transported to the liver, where it is catabolized. Circulating HA is efficiently sequestered by the receptor-mediated endocytosis of liver endothelial cells.…”

Section: Introductionmentioning

confidence: 99%

Control of the molecular degradation of hyaluronic acid hydrogels for tissue augmentation

Kang

Kim

et al. 2007

J Biomedical Materials Res

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A novel protocol to control the molecular degradation of hyaluronic acid (HA) hydrogels was successfully developed for tissue augmentation applications. HA has a different conformational structure in water and organic solvent, and the carboxyl group of HA is known to be the recognition site of hyaluronidase and HA receptors. Based on these findings, HA was chemically modified by grafting adipic acid dihydrazide (ADH) to the carboxyl group of HA in the water to prepare HA-ADH(WATER) and in the mixed solvent of water and ethanol to prepare degradation-controlled HA-ADH(WATER/ETHANOL). Three kinds of HA hydrogels were prepared by the crosslinking of HA-ADH(WATER) or HA-ADH(WATER/ETHANOL) with bis(sulfosuccinimidyl) suberate, and by the crosslinking of HA-OH with divinyl sulfone (DVS). In vitro and in vivo degradation tests showed that HA-DVS hydrogels were degraded most rapidly, followed by HA-ADH(WATER) hydrogels and HA-ADH(WATER/ETHANOL) hydrogels. There was no adverse effect during and after in vivo degradation tests. All of the HA hydrogel samples appeared to be biocompatible, according to the histological analysis with hematoxylin-eosin and Alcian blue.

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“…Hyaluronan is an important structural component of the extracellular matrix in skin and is of importance for the control of fluid balance of the tissues [1], During recent years it has been shown that the hyaluronan con centration in lymph from skin, lung, and intestine is between 5 and 50 pg/ml [2][3][4][5][6], Following entrance into the bloodstream hyaluronan is rapidly degraded by the liver endothelial cells [7][8][9], and the concentration of hyaluronan in plasma is normally less than 100ng/ml [10]. We have previously shown that the hyaluronan con centration in prenodal lymph from canine paw is about 10 pg/ml and that stepwise increase in lymph flow up to five times above control resulted in only a small decrease in lymph hyaluronan concentration [4], This observation implies that the flux of hyaluronan from the tissue via lymphatic drainage is determined primarily by interstitial fluid flux.…”

Section: Introductionmentioning

confidence: 99%

Lymphatic Hyaluronan Flux from Skin Increases during Increased Lymph Flow Induced by Intravenous Saline Loading

et al. 1994

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Hyaluronan is a structural component of the interstitial matrix in skin and is catabolized locally in skin as well as by lymphatic removal and subsequent degradation in lymph nodes and liver. The present experiments were designed to evaluate the role of interstitial fluid flux in turnover of hyaluronan in skin by measuring the maximal lymphatic flux of hyaluronan. Lymph flow, total protein concentration, hyaluronan concentration, and flux were measured every 15 min in prenodal lymph from the hind paw in 12 pentobarbital-anesthetized mongrel dogs at normal and increased interstitial fluid flux. An intravenous saline load (15% of body weight during the course of 30 min) was followed by a one-step increase in local venous pressure 30 min later (to a maximum of 50 mm Hg) and maintained at this level for the next 240 min. Lymph flow and hyaluronan concentration during the control period averaged 25.6 ± (SD) 23.2 (range 4.7-61.9) μl/min and 8.6 ± 2.8 (range 2.0-11.6) μg/ml, respectively. The hyaluronan concentration fell by 30% during the experimental period, while the lymph flow increased up to ten times above control. Total tissue water increased from 1.73 ± 0.11 ml/g dry weight during the control period to 1.91 ± 0.12 ml/g dry weight at the end of the experiment (p < 0.01). The corresponding tissue contents of hyaluronan averaged 3.5 ± 0.9 and 3.6 ± 0.6 mg/g dry weight, respectively (p > 0.05). The average lymphatic hyaluronan flux was 8.4 ± 5.4μg/h during the control period, peaked at about 60 μg/h, and averaged 33.6 ± 13.9 μg/h during the last hour of the experimental period. The total amount of hyaluronan drained from the paw during the 5-hour experimental period averaged 182 ± 137 (range 39-525) μg and corresponds to the normal daily lymphatic output of hyaluronan. Thus, the hyaluronan flux in lymph increases with increasing lymph flow and is maintained over a period of several hours, affecting hyaluronan turnover in skin.

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The Catabolic Fate of Hyaluronic Acid

Cited by 65 publications

References 37 publications

Treatment with calcitonin suppresses the responses of bone, cartilage, and synovium in the early stages of canine experimental osteoarthritis and significantly reduces the severity of the cartilage lesions

Treatment with calcitonin suppresses the responses of bone, cartilage, and synovium in the early stages of canine experimental osteoarthritis and significantly reduces the severity of the cartilage lesions

Control of the molecular degradation of hyaluronic acid hydrogels for tissue augmentation

Lymphatic Hyaluronan Flux from Skin Increases during Increased Lymph Flow Induced by Intravenous Saline Loading

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