While this article concerns the use of methylene blue to indicate the presence of bacterial biofilms on implant surfaces, it also provides a useful review of the role of biofilms in periprosthetic infections (PJI). With respect to the shoulder it is recognized that the organism most commonly causing PJI, Cutibacterium, avidly forms biofilms on the most commonly used implant material, titanium alloy. See this link and this link.
The term 'biofilm' refers to bacteria embedded in an extracellular slime layer consisting of polysaccharides, extracellular DNA, proteins and lipids. Biofilms can develop channels allowing for diffusion of nutrients to the embedded bacteria. Because of the limited ability of oxygen to enter, the biofilm provides a range of environments from aerobic on the surface to anaerobic at the depth. Spatial separation of metabolic environments allows for niches for different types of bacteria. Bacteria in biofilms behave differently from those in the free-floating (planktonic) form.
Biofilms can form on all orthopaedic implants, including metal, plastic, and cement. They can be found in fibrous membranes surrounding implants. Because they are viscoelastic liquids, they can resist detachment and can flow across surfaces.
Biofilms protect bacteria from host defenses (1) forming conglomerates too large for phagocytosis by inflammatory cells and (2) blocking antibodies from diffusing in to reach the bacteria. They also protect the bacteria from antibiotics such that the levels a 1000 times greater concentration is required to kill bacteria in biofilms in comparison to planktonic bacteria.
Biofilms make bacteria difficult to recover. Even though a prosthesis has a bacteria-ladened biofilm, joint fluid aspiration may well be negative because the bacteria are not present in the fluid. Bacteria in biofilms are not easily recovered because conventional culturing methods may not dislodge the biofilm. Even if the biofilm is recovered, host factors such as endonucleases may prevent the bacteria from growing. Bacteria in biofilms may enter a dormant or slow growing phenotype that grows slowly or not at all in cultures.
Essentially all periprosthetic infections involve biofilms. These can progress very slowly and may be non-symptomatic for years. Biofilm infections may exert their pathological effects by triggering insidious tissue damage (such as bone resorption) rather than by creating the usual signs of inflammation. Thus it may be very difficult to differentiate prosthetic loosening from the chronic effects of a biofilm from 'aseptic' mechanical loosening. These infections do not resolve spontaneously and usually require surgical debridement and antibiotics.
Biofilms may serve as sources of more obvious planktonic infection if the biofilm is stimulated or if the host is weakened.
These observations regarding biofilms have informed our current approach to failed shoulder arthroplasty.
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