{"id":{"repo_id":"mit","oai_identifier":"oai:dspace.mit.edu:1721.1/28279"},"canonical_url":"https://search.dev.ndltd.org/etd/mit/oai:dspace.mit.edu:1721.1/28279","repository":{"repo_id":"mit","name":"MIT","base_url":"https://dspace.mit.edu/oai/request"},"display":{"title":"In vitro models for injurious compression of bovine and human articular cartilage","abstract":"Patients who have sustained a traumatic joint injury, such as a ligament rupture or cartilage fracture, are known to have an increased risk for the development of osteoarthritis (OA) in that joint. This has motivated the use of in vitro models of mechanical cartilage injury in order to identify processes that could lead to cartilage degradation. The overall aims of the work presented here has been to focus on further identification of the effects of in vitro injurious mechanical compression of cartilage on cell-mediated processes and to develop models for injurious compression of the cartilage that seek to incorporate interactions with other joint tissues, such as inflammatory mediators elaborated from the joint capsule tissue. Major results are that i) injurious compression of newborn bovine cartilage can result in cell death predominantly by an apoptotic mechanism; ii) incubation of mechanically injured bovine and human cartilage with exogenous cytokines produces a synergistic increase in proteoglycan loss from the cartilage; and iii) coincubation of cartilage with joint capsule tissue profoundly inhibits cartilage biosynthetic activity through an IL-1-independent pathway. We also characterize the activity and activation of ADAMTS-4 (aggrecanase-1) in the cartilage tissue, one of the major enzymes responsible for proteoglycan degradation. These results may help to identify some of the interactions between mechanical stimuli, joint tissue damage, and chondrocyte behavior which lead to unbalanced cartilage degradation and arthritis.","abstract_html":"Patients who have sustained a traumatic joint injury, such as a ligament rupture or cartilage fracture, are known to have an increased risk for the development of osteoarthritis (OA) in that joint. This has motivated the use of in vitro models of mechanical cartilage injury in order to identify processes that could lead to cartilage degradation. The overall aims of the work presented here has been to focus on further identification of the effects of in vitro injurious mechanical compression of cartilage on cell-mediated processes and to develop models for injurious compression of the cartilage that seek to incorporate interactions with other joint tissues, such as inflammatory mediators elaborated from the joint capsule tissue. Major results are that i) injurious compression of newborn bovine cartilage can result in cell death predominantly by an apoptotic mechanism; ii) incubation of mechanically injured bovine and human cartilage with exogenous cytokines produces a synergistic increase in proteoglycan loss from the cartilage; and iii) coincubation of cartilage with joint capsule tissue profoundly inhibits cartilage biosynthetic activity through an IL-1-independent pathway. We also characterize the activity and activation of ADAMTS-4 (aggrecanase-1) in the cartilage tissue, one of the major enzymes responsible for proteoglycan degradation. These results may help to identify some of the interactions between mechanical stimuli, joint tissue damage, and chondrocyte behavior which lead to unbalanced cartilage degradation and arthritis.","abstract_has_math":false,"creators":["Patwari, Parth, 1972-"],"institution":"Massachusetts Institute of Technology","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":"Massachusetts Institute of Technology. Dept. of Electrical Engineering and Computer Science.","school":null,"contributors":[],"advisors":["Alan J. Grodzinsky."],"committee_chairs":[],"committee_members":[],"year":2003,"date_issued":"2003","date_published":"2003","updated_at":"2026-07-22T22:21:01Z","subjects":["Electrical Engineering and Computer Science."],"languages":["en_US"],"rights":["M.I.T. theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. See provided URL for inquiries about permission."],"rights_urls":["http://dspace.mit.edu/handle/1721.1/7582"],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/1721.1/28279","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Alan J. Grodzinsky."]},{"key":"dc:contributor.department","label":"Department","values":["Massachusetts Institute of Technology. Dept. of Electrical Engineering and Computer Science."]},{"key":"dc:contributor.other","label":"Dc Contributor Other","values":["Massachusetts Institute of Technology. Dept. of Electrical Engineering and Computer Science."]},{"key":"dc:creator","label":"Author","values":["Patwari, Parth, 1972-"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2005-09-26T19:32:11Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2005-09-26T19:32:11Z"]},{"key":"dc:date.issued","label":"Date","values":["2003"]},{"key":"dc:publisher","label":"Institution","values":["Massachusetts Institute of Technology"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Electrical Engineering and Computer Science."]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en_US"]},{"key":"dc:rights","label":"Dc Rights","values":["M.I.T. theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. See provided URL for inquiries about permission."]},{"key":"dc:rights.uri","label":"Rights URI","values":["http://dspace.mit.edu/handle/1721.1/7582"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/1721.1/28279"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Thesis (Sc. D.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2003.","Includes bibliographical references (leaves 150-159)."]},{"key":"dc:description.abstract","label":"Abstract","values":["Patients who have sustained a traumatic joint injury, such as a ligament rupture or cartilage fracture, are known to have an increased risk for the development of osteoarthritis (OA) in that joint. This has motivated the use of in vitro models of mechanical cartilage injury in order to identify processes that could lead to cartilage degradation. The overall aims of the work presented here has been to focus on further identification of the effects of in vitro injurious mechanical compression of cartilage on cell-mediated processes and to develop models for injurious compression of the cartilage that seek to incorporate interactions with other joint tissues, such as inflammatory mediators elaborated from the joint capsule tissue. Major results are that i) injurious compression of newborn bovine cartilage can result in cell death predominantly by an apoptotic mechanism; ii) incubation of mechanically injured bovine and human cartilage with exogenous cytokines produces a synergistic increase in proteoglycan loss from the cartilage; and iii) coincubation of cartilage with joint capsule tissue profoundly inhibits cartilage biosynthetic activity through an IL-1-independent pathway. We also characterize the activity and activation of ADAMTS-4 (aggrecanase-1) in the cartilage tissue, one of the major enzymes responsible for proteoglycan degradation. These results may help to identify some of the interactions between mechanical stimuli, joint tissue damage, and chondrocyte behavior which lead to unbalanced cartilage degradation and arthritis."]},{"key":"dc:description.degree","label":"Dc Description Degree","values":["Sc.D."]},{"key":"dc:format.mimetype","label":"Dc Format Mimetype","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["In vitro models for injurious compression of bovine and human articular cartilage"]}]}],"canonical_facts":{"dc:contributor.advisor":["Alan J. Grodzinsky."],"dc:contributor.department":["Massachusetts Institute of Technology. Dept. of Electrical Engineering and Computer Science."],"dc:contributor.other":["Massachusetts Institute of Technology. Dept. of Electrical Engineering and Computer Science."],"dc:creator":["Patwari, Parth, 1972-"],"dc:date.accessioned":["2005-09-26T19:32:11Z"],"dc:date.available":["2005-09-26T19:32:11Z"],"dc:date.issued":["2003"],"dc:description":["Thesis (Sc. D.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2003.","Includes bibliographical references (leaves 150-159)."],"dc:description.abstract":["Patients who have sustained a traumatic joint injury, such as a ligament rupture or cartilage fracture, are known to have an increased risk for the development of osteoarthritis (OA) in that joint. This has motivated the use of in vitro models of mechanical cartilage injury in order to identify processes that could lead to cartilage degradation. The overall aims of the work presented here has been to focus on further identification of the effects of in vitro injurious mechanical compression of cartilage on cell-mediated processes and to develop models for injurious compression of the cartilage that seek to incorporate interactions with other joint tissues, such as inflammatory mediators elaborated from the joint capsule tissue. Major results are that i) injurious compression of newborn bovine cartilage can result in cell death predominantly by an apoptotic mechanism; ii) incubation of mechanically injured bovine and human cartilage with exogenous cytokines produces a synergistic increase in proteoglycan loss from the cartilage; and iii) coincubation of cartilage with joint capsule tissue profoundly inhibits cartilage biosynthetic activity through an IL-1-independent pathway. We also characterize the activity and activation of ADAMTS-4 (aggrecanase-1) in the cartilage tissue, one of the major enzymes responsible for proteoglycan degradation. These results may help to identify some of the interactions between mechanical stimuli, joint tissue damage, and chondrocyte behavior which lead to unbalanced cartilage degradation and arthritis."],"dc:description.degree":["Sc.D."],"dc:format.mimetype":["application/pdf"],"dc:identifier.uri":["http://hdl.handle.net/1721.1/28279"],"dc:language.iso":["en_US"],"dc:publisher":["Massachusetts Institute of Technology"],"dc:rights":["M.I.T. theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. See provided URL for inquiries about permission."],"dc:rights.uri":["http://dspace.mit.edu/handle/1721.1/7582"],"dc:subject":["Electrical Engineering and Computer Science."],"dc:title":["In vitro models for injurious compression of bovine and human articular cartilage"],"dc:type":["Thesis"]},"updated_at":"2026-07-22T22:21:01Z"}