Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2006-9-18
pubmed:abstractText
Osteoarthritis (OA) is a joint disease that involves degeneration of articular cartilage, limited intraarticular inflammation manifested by synovitis and changes in the subchondral bone. The aetiology of OA is largely unknown, but since it may involve multiple factors, including mechanical, biochemical and genetic factors, it has been difficult to identify unique targets for therapy. Chondrocytes, which are the unique cellular component of adult articular cartilage, are capable of responding to structural changes in the surrounding cartilage matrix. Since the initial stages of OA involve increased cell proliferation and synthesis of matrix proteins, proteinases and cytokines in the cartilage, laboratory investigations have focused on the chondrocyte as a target for therapeutic intervention. The capacity of the adult articular chondrocyte to regenerate the normal cartilage matrix architecture is limited, however, and the damage becomes irreversible unless the destructive process is interrupted. Current pharmacological interventions that address chronic pain are insufficient and no proven disease-modifying therapy is available. Identification of methods for early diagnosis is of key importance, since therapeutic interventions aimed at blocking or reversing structural damage will be more effective when there is the possibility of preserving normal homeostasis. At later stages, cartilage tissue engineering with or without gene therapy with anabolic factors will also require therapy to inhibit inflammation and block damage to newly repaired cartilage. This review will focus on experimental approaches currently under study that may lead to elucidation of effective strategies for therapy in OA, with emphasis on mediators that affect the function of chondrocytes and interactions with surrounding tissues.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1521-6942
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1003-25
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Update on the biology of the chondrocyte and new approaches to treating cartilage diseases.
pubmed:affiliation
Department of Medicine, Division of Rheumatology, Beth Israel Deaconess Medical Center, New England Baptist Bone and Joint Institute and Harvard Medical School, Boston, MA 02115, USA. mgoldrin@bidmc.harvard.edu
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural