Shoulder arthroplasty - macrophage response to wear particles

MIXED IMPLANT DEBRIS CAUSES A STRONG MACROPHAGE RESPONSE IN ANATOMIC AND REVERSE TOTAL SHOULDER ARTHROPLASTIES


These authors examined retrieved anatomic (aTSAs n=11) and reverse ( rTSAs n=12) shoulder arthroplasties to determine the extent of implant damage and to characterize the nature of the responses of the periprosthetic tissues.

The polyethylene bearing surfaces of aTSAs were dominated by three body wear and plastic deformation, whereas the rTSA PE components exhibited mainly polishing and scratching. 

In both groups the primary nature of the inflammatory response was a moderate to marked macrophage response to wear particles (78% of cases). The particle-laden macrophages tended to occur in broad sheets and contained metal, PE, bone cement and suture debris. 

The extent of macrophage and foreign body giant cell responses was greater in the aTSA group.

Metal particles were seen in 63% of aTSAs and 83% of rTSAs. 

In the aTSA group, bone cement was seen in all cases and suture was observed in 9 cases,

A mild lymphocyte response and chromium-phosphate debris was present within the tissue of a aTSA case with marked corrosion, which may be indicative of an early stage adverse local tissue reaction.

Comment: This work demonstrates that shoulder arthroplasties shed debris: PE, metal, bone cement and suture and that this debris can stimulate a substantial macrophage response. We surely need to learn more about particulate disease in the shoulder, not only with respect to its role in implant failure, but also its role in shoulders that are unexpectedly symptomatic post arthroplasty.

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What if aseptic loosening is not aseptic?

Emperor's new clothes: Is particle disease really infected particle disease?

These authors point out that loosening remains the most significant (70%) long-term complication of total hip replacement and that inflammatory response to wear particles is thought to be its main trigger. The clinical presentation includes pain and osteolysis. The diagnosis of 'aseptic' is based on the absence of evidence of infection. But as the authors state, 'the absence of evidence is not evidence of absence'.

Recently, there have been increasing numbers of positive bacterial isolates and other evidence of bacterial presence reported among patients with clinically absent infection.  Such evidence can be missed for many reasons, including failure to submit multiple specimens for culture, failure to submit tissue specimens of sufficient size, failure to sonicate or vortex retrieved implants, reliance on cultures of joint fluid (that will not reveal sessile bacteria in a biofilm), failure to observe cultures for sufficiently long, failure to culture specimens on aerobic and anaerobic media, bacterial fastidiousness or dormancy, presence of prophylactic antibiotics, attribution of positive culture results to 'contamination',  use of complex and arbitrary definitions for 'infection', failure to use non-culture methods for bacterial identification and others.

These authors also point out that bacterial presence may alter the response to micro particles of cement, polyethylene, and bone as well as the ability of bone to maintain itself and integrate with a prosthesis.

Comment: In the shoulder world, we've learned that while some periprosthetic infections are obvious, it is common for revision surgeries for shoulders presenting as pain, stiffness or loosening to yield multiple positive cultures. 

We suggest that a meaningful way to present the culture results from a revision surgery is to indicate the number and sources of the specimens submitted for culture, the culture protocol, and the number of cultures that are positive for each organism. This approach frees us from trying to decide if the joint is 'aseptic' or not, or if it meets someones definition of 'infection'. With these data we may be able to resolve the role that positive cultures play in the presentation and management of failed arthroplasties.

We all remember the time when ulcers were 'caused by acid' before the importance of H. Pylori was recognized.

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