Pathophysiology and pharmacologic control of osseous mandibular condylar resorption.
OBJECTIVE
When osseous mandibular condylar resorption occurs there can be many different diagnoses: inflammatory arthritis, TMJ compression, trauma, hormone imbalances, and others. While each diagnosis has its own original inciting event, the pathophysiological pathway for articular bone loss is the same. The aim of this article is to review the relevant literature on condylar resorption and the use of pharmacotherapy to control arthritic erosions and resorption.


METHODS
The literature search was performed using PubMed database with various combinations of related keywords. Preference was given to clinical trials when reviewing articles.


RESULTS
The literature reveals that common cellular level events associated with articular resorption include the activation of osteoblasts by cytokines, free radicals, hormone imbalances and/or potent phospholipid catabolites. The osteoblast then activates the recruitment of osteoclasts and promotes the release of matrix degrading enzymes from the osteoclast. Research into articular erosions has focused on elucidating the important steps in the bone destructive pathways and interfering with them by pharmacological means. The use of antioxidants, tetracyclines, omega-3 fatty acids, non-steroidal anti-inflammatories and inflammatory cytokine inhibitors to aid in preventing and controlling articular bone loss including osseous mandibular condylar resorption has been successful.


CONCLUSIONS
By understanding the known pathways that lead to condylar resorption and the individual patient's susceptibilities, targeted pharmacotherapy might be able to disturb these pathways and prevent further condylar resorption. Basic clinical investigations and randomized clinical trials are still required, but the present science is encouraging.
Arnett and Gunson Facial Reconstruction, Santa Barbara, CA 93101, USA. gunson@arnettgunson.com
Michael J
MJ
Gunson
G William
GW
Arnett
Stephen B
SB
Milam
D001168:Arthritis / Q000503:physiopathology / Q000517:prevention & control; D050071:Bone Density Conservation Agents / Q000627:therapeutic use*; D001862:Bone Resorption / Q000503:physiopathology / Q000517:prevention & control*; D004198:Disease Susceptibility / Q000503:physiopathology; D006801:Humans; D008335:Mandibular Condyle / Q000187:drug effects* / Q000503:physiopathology; D010006:Osteoblasts / Q000502:physiology; D010010:Osteoclasts / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology; D013705:Temporomandibular Joint Disorders / Q000503:physiopathology / Q000517:prevention & control*
D050071:Bone Density Conservation Agents