Biomaterial Database

Heterotopic bone formation after total hip arthroplasty. 1992

B J Thomas

University of California, Los Angeles School of Medicine.

Formation of heterotopic bone can cause pain and limit motion, thus ruin what would otherwise have been an excellent result after total hip arthroplasty. The cause of bone formation remains controversial, and diphosphonates have been ineffective in its prevention. Radiotherapy and nonsteroidal anti-inflammatory drugs, however, are effective preventative agents. Once the bone is formed, however, surgical excision is the only effective treatment.

UI	MeSH Term	Description	Entries
D009999	Ossification, Heterotopic	The development of bony substance in normally soft structures.	Ossification, Pathologic,Ectopic Ossification,Heterotopic Ossification,Ossification, Ectopic,Ossification, Pathological,Pathologic Ossification,Pathological Ossification
D011183	Postoperative Complications	Pathologic processes that affect patients after a surgical procedure. They may or may not be related to the disease for which the surgery was done, and they may or may not be direct results of the surgery.	Complication, Postoperative,Complications, Postoperative,Postoperative Complication
D004164	Diphosphonates	Organic compounds which contain P-C-P bonds, where P stands for phosphonates or phosphonic acids. These compounds affect calcium metabolism. They inhibit ectopic calcification and slow down bone resorption and bone turnover. Technetium complexes of diphosphonates have been used successfully as bone scanning agents.	Bisphosphonate,Bisphosphonates
D006622	Hip Prosthesis	Replacement for a hip joint.	Femoral Head Prosthesis,Femoral Head Prostheses,Hip Prostheses,Prostheses, Femoral Head,Prostheses, Hip,Prosthesis, Femoral Head,Prosthesis, Hip
D006801	Humans	Members of the species Homo sapiens.	Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000894	Anti-Inflammatory Agents, Non-Steroidal	Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions. They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects.	Analgesics, Anti-Inflammatory,Aspirin-Like Agent,Aspirin-Like Agents,NSAID,Non-Steroidal Anti-Inflammatory Agent,Non-Steroidal Anti-Inflammatory Agents,Nonsteroidal Anti-Inflammatory Agent,Anti Inflammatory Agents, Nonsteroidal,Antiinflammatory Agents, Non Steroidal,Antiinflammatory Agents, Nonsteroidal,NSAIDs,Nonsteroidal Anti-Inflammatory Agents,Agent, Aspirin-Like,Agent, Non-Steroidal Anti-Inflammatory,Agent, Nonsteroidal Anti-Inflammatory,Anti-Inflammatory Agent, Non-Steroidal,Anti-Inflammatory Agent, Nonsteroidal,Anti-Inflammatory Analgesics,Aspirin Like Agent,Aspirin Like Agents,Non Steroidal Anti Inflammatory Agent,Non Steroidal Anti Inflammatory Agents,Nonsteroidal Anti Inflammatory Agent,Nonsteroidal Anti Inflammatory Agents,Nonsteroidal Antiinflammatory Agents