{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/20557"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/20557","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Joint motion studies of the normal and cranial cruciate ligament deficient stifle in large breed dogs","abstract":"Joint motion was measured for the intact and cranial cruciate (CCL) deficient stifle in five large breed dogs. A combined method using an instrumented spatial linkage (ISL) and radiophotogrammetry provided a sensitive method of measuring the three dimensional motion of the stifle over time. It was possible to attach the linkage directly to the bones using modified bone plates without severely impairing the dog's gait. Motion data was presented in terms of a clinical coordinate system which included flexion, abduction, external rotation, lateral, cranial and distraction displacements. The kinematic data was highly reproducible for a given dog. For normal stifle kinematics, the swing phase of motion included flexion, internal rotation and abduction while the stance phase included only flexion motion. Loss of the CCL altered joint kinematic over the entire gait cycle but the changes were most severe for the stance phase. At the swing to stance transition, the CCL deficient stifle demonstrated an abrupt cranial subluxation of the tibia which was sustained throughout stance. Internal rotation and abduction were also noted during stance. The transition to the swing phase was characterized by an abrupt return of the joint to its normal, baseline cranial displacement, i.e., the orientation of the femoral and tibial joint surfaces was returned to normal. The dog's stifle was thus shown to be CCL-dependent during stance. The dog compensated for CCL loss by dramatically reducing the external load on the limb and by carrying the limb in greater flexion throughout the gait cycle. Despite these changes, the dogs were not able to prevent joint subluxation during stance. These results clearly demonstrate that abnormal kinematics accompanies CCL loss in dogs. It is this continuous repetitive joint subluxation which is presumably responsible for joint degeneration.","abstract_html":"Joint motion was measured for the intact and cranial cruciate (CCL) deficient stifle in five large breed dogs. A combined method using an instrumented spatial linkage (ISL) and radiophotogrammetry provided a sensitive method of measuring the three dimensional motion of the stifle over time. It was possible to attach the linkage directly to the bones using modified bone plates without severely impairing the dog's gait. Motion data was presented in terms of a clinical coordinate system which included flexion, abduction, external rotation, lateral, cranial and distraction displacements. The kinematic data was highly reproducible for a given dog. For normal stifle kinematics, the swing phase of motion included flexion, internal rotation and abduction while the stance phase included only flexion motion. Loss of the CCL altered joint kinematic over the entire gait cycle but the changes were most severe for the stance phase. At the swing to stance transition, the CCL deficient stifle demonstrated an abrupt cranial subluxation of the tibia which was sustained throughout stance. Internal rotation and abduction were also noted during stance. The transition to the swing phase was characterized by an abrupt return of the joint to its normal, baseline cranial displacement, i.e., the orientation of the femoral and tibial joint surfaces was returned to normal. The dog's stifle was thus shown to be CCL-dependent during stance. The dog compensated for CCL loss by dramatically reducing the external load on the limb and by carrying the limb in greater flexion throughout the gait cycle. Despite these changes, the dogs were not able to prevent joint subluxation during stance. These results clearly demonstrate that abnormal kinematics accompanies CCL loss in dogs. It is this continuous repetitive joint subluxation which is presumably responsible for joint degeneration.","abstract_has_math":false,"creators":["Korvick, Donna Lee"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Engineering, Biomedical","degree_department":null,"school":null,"contributors":["Pijanowski, Gerald J."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2011,"date_issued":"2011-05-07T12:42:40Z","date_published":"2011-05-07T12:42:40Z","updated_at":"2026-07-22T22:25:16Z","subjects":["Engineering, Biomedical","Biology, Veterinary Science"],"languages":["eng"],"rights":["Copyright 1991 Korvick, Donna Lee"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["AAI9136641","(UMI)AAI9136641"],"render_values":[{"text":"AAI9136641","href":null,"code":true},{"text":"(UMI)AAI9136641","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/20557","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Pijanowski, Gerald J."]},{"key":"dc:creator","label":"Author","values":["Korvick, Donna Lee"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2011-05-07T12:42:40Z","10000-01-01","1991"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Engineering, Biomedical","Biology, Veterinary Science"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Engineering, Biomedical","Biology, Veterinary Science"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]},{"key":"dc:rights","label":"Dc Rights","values":["Copyright 1991 Korvick, Donna Lee"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["AAI9136641","(UMI)AAI9136641","http://hdl.handle.net/2142/20557"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Joint motion was measured for the intact and cranial cruciate (CCL) deficient stifle in five large breed dogs. A combined method using an instrumented spatial linkage (ISL) and radiophotogrammetry provided a sensitive method of measuring the three dimensional motion of the stifle over time. It was possible to attach the linkage directly to the bones using modified bone plates without severely impairing the dog's gait. Motion data was presented in terms of a clinical coordinate system which included flexion, abduction, external rotation, lateral, cranial and distraction displacements. The kinematic data was highly reproducible for a given dog. For normal stifle kinematics, the swing phase of motion included flexion, internal rotation and abduction while the stance phase included only flexion motion. Loss of the CCL altered joint kinematic over the entire gait cycle but the changes were most severe for the stance phase. At the swing to stance transition, the CCL deficient stifle demonstrated an abrupt cranial subluxation of the tibia which was sustained throughout stance. Internal rotation and abduction were also noted during stance. The transition to the swing phase was characterized by an abrupt return of the joint to its normal, baseline cranial displacement, i.e., the orientation of the femoral and tibial joint surfaces was returned to normal. The dog's stifle was thus shown to be CCL-dependent during stance. The dog compensated for CCL loss by dramatically reducing the external load on the limb and by carrying the limb in greater flexion throughout the gait cycle. Despite these changes, the dogs were not able to prevent joint subluxation during stance. These results clearly demonstrate that abnormal kinematics accompanies CCL loss in dogs. It is this continuous repetitive joint subluxation which is presumably responsible for joint degeneration.","Made available in DSpace on 2011-05-07T12:42:40Z (GMT). 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A combined method using an instrumented spatial linkage (ISL) and radiophotogrammetry provided a sensitive method of measuring the three dimensional motion of the stifle over time. It was possible to attach the linkage directly to the bones using modified bone plates without severely impairing the dog's gait. Motion data was presented in terms of a clinical coordinate system which included flexion, abduction, external rotation, lateral, cranial and distraction displacements. The kinematic data was highly reproducible for a given dog. For normal stifle kinematics, the swing phase of motion included flexion, internal rotation and abduction while the stance phase included only flexion motion. Loss of the CCL altered joint kinematic over the entire gait cycle but the changes were most severe for the stance phase. At the swing to stance transition, the CCL deficient stifle demonstrated an abrupt cranial subluxation of the tibia which was sustained throughout stance. Internal rotation and abduction were also noted during stance. The transition to the swing phase was characterized by an abrupt return of the joint to its normal, baseline cranial displacement, i.e., the orientation of the femoral and tibial joint surfaces was returned to normal. The dog's stifle was thus shown to be CCL-dependent during stance. The dog compensated for CCL loss by dramatically reducing the external load on the limb and by carrying the limb in greater flexion throughout the gait cycle. Despite these changes, the dogs were not able to prevent joint subluxation during stance. These results clearly demonstrate that abnormal kinematics accompanies CCL loss in dogs. It is this continuous repetitive joint subluxation which is presumably responsible for joint degeneration.","Made available in DSpace on 2011-05-07T12:42:40Z (GMT). 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