Willert and Semlitsch examined how the tissue around artificial joints reacts to prosthetic wear particles and what that reaction means for long‑term implant function.
Histopathologic series of capsule and cement‑bone tissue from 123 reoperated joint prostheses, mostly hips, with infected cases excluded.
Methods
Design
Histopathologic case series of reoperation tissue
Infected cases excluded
Patients
123 reoperated joint prostheses
Mostly hip, some knee, elbow and finger
Revised for malposition, loosening, fracture, calcification or unexplained complaints
Treatment
Metal almost exclusively Co‑Cr‑Mo cast alloy
High‑density polyethylene or polyester plastic
Palacos or CMW bone cement
Outcomes
Histology with light, polarized and electron microscopy
Particle analysis by spectral methods and microprobe
Key Findings
Capsular tissue from failed replacements held plastic, metal and cement wear particles that provoked foreign‑body granulation tissue with macrophages and giant cells.
Mononuclear histiocytes usually engulfed small particles, while giant cells gathered around larger ones.
Small debris loads were cleared along perivascular lymph spaces, but when wear exceeded that capacity the particles accumulated and the reaction could spread through the periarticular tissues.
The authors believed that granulation tissue resorbing the trabeculae of the implant bed caused loosening, particularly of prostheses with Teflon or polyester components.
A balance between wear and tissue reaction was seen most often with cast Co‑Cr‑Mo metal‑on‑metal and metal‑on‑polyethylene bearings, which the authors considered optimal while wear cannot be eliminated.
Cement particles drew both giant cells and histiocytes with little fibrosis, and their numbers rose rapidly when loosening shattered the cement.
Board pearl
Willert proposed that once debris overwhelms clearance, the foreign‑body membrane lining the cement can erode the adjacent bone anchorage and loosen cemented components.
Authors' conclusion
Where this transport system is insufficient to handle the volume, however, the foreign-body response may extend to the whole environment surrounding the joint. In such cases, there may be loosening of the cemented prosthetic parts because of deterioration of contiguous bone anchors by the tissue membrane lining the bone cement.
Willert and Semlitsch examined how the tissue around artificial joints reacts to prosthetic wear particles and what that reaction means for long‑term implant function.
Histopathologic series of capsule and cement‑bone tissue from 123 reoperated joint prostheses, mostly hips, with infected cases excluded.
Methods
Design
Histopathologic case series of reoperation tissue
Infected cases excluded
Patients
123 reoperated joint prostheses
Mostly hip, some knee, elbow and finger
Revised for malposition, loosening, fracture, calcification or unexplained complaints
Treatment
Metal almost exclusively Co‑Cr‑Mo cast alloy
High‑density polyethylene or polyester plastic
Palacos or CMW bone cement
Outcomes
Histology with light, polarized and electron microscopy
Particle analysis by spectral methods and microprobe
Key Findings
Capsular tissue from failed replacements held plastic, metal and cement wear particles that provoked foreign‑body granulation tissue with macrophages and giant cells.
Mononuclear histiocytes usually engulfed small particles, while giant cells gathered around larger ones.
Small debris loads were cleared along perivascular lymph spaces, but when wear exceeded that capacity the particles accumulated and the reaction could spread through the periarticular tissues.
The authors believed that granulation tissue resorbing the trabeculae of the implant bed caused loosening, particularly of prostheses with Teflon or polyester components.
A balance between wear and tissue reaction was seen most often with cast Co‑Cr‑Mo metal‑on‑metal and metal‑on‑polyethylene bearings, which the authors considered optimal while wear cannot be eliminated.
Cement particles drew both giant cells and histiocytes with little fibrosis, and their numbers rose rapidly when loosening shattered the cement.
Board pearl
Willert proposed that once debris overwhelms clearance, the foreign‑body membrane lining the cement can erode the adjacent bone anchorage and loosen cemented components.
Authors' conclusion
Where this transport system is insufficient to handle the volume, however, the foreign-body response may extend to the whole environment surrounding the joint. In such cases, there may be loosening of the cemented prosthetic parts because of deterioration of contiguous bone anchors by the tissue membrane lining the bone cement.