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Early diagnosis, intervention key to managing particulate damage
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The longer an orthopedic surgeon is in practice, the more likely he or she will encounter a problem related to particulates in a patient.
Many studies have addressed the significance of particulate wear and debris. For this month’s interview, I turned to Joshua J. Jacobs, MD, of Chicago, one of the experts in this field, to answer four basic questions. Dr. Jacobs, who heads the Basic Science & Research section on the Orthopedic Today Editorial Board, provides succinct answers that I find are helpful in following and interpreting what is going on in our patients.
Douglas W. Jackson, MD: What is the definition of “biologically active particles,“ and what damage do they do?
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Joshua J. Jacobs, MD: Wear and corrosion are inevitable consequences of the implantation of orthopedic implants manufactured from contemporary materials. As a result of these degradative processes, particulate and ionic debris are generated, which are released into the periprosthetic environment and can be associated with a series of cellular responses. In a sense, all debris is biologically active; however, the intensity of the biological response will determine whether or not clinical symptoms and/or device failure ensues.
Over the past decade, we have learned that the intensity of the biological response is dictated by the rate of release (ie, the dose) of the particles, the particle size (ie, debris less than 10 µm in size are phagocytosable by the surrounding cells and elicit a greater response than debris that is too large to be phagocytosed), and the particle composition (ie, metal, ceramic or polyethylene).
While it is clear that numerous other factors may play a role in the biological response to particulate debris, including surface roughness, shape, composition of adsorbed proteins, and individual variation, this has yet to be fully elucidated.
Jackson: What should the clinician understand concerning particulate size and the phagocyte? What happens when a phagocyte ingests a particle?
Jacobs: Phagocytosable particles generally smaller than 10 micrometers in size typically initiate a cascade of intracellular signaling events in macrophages, fibroblasts and osteoblasts, which often lead to an upregulation of the expression and synthesis of various inflammatory mediators, including cytokines such as interleukin-1, interleukin-6 and tumor necrosis factor alpha. They may also lead to matrix-degrading enzymes — matrix metalloproteinases, collagenase and stromelysin — and activators of osteoclastogenesis, such as the receptor activator of nuclear factor kappa B ligand (RANKL).
Phagocytosis of particulate wear and corrosion debris may also cause inhibition of certain cellular functions, such as collagen expression and synthesis in osteoblasts. The net effect of this local cellular response is often progressive periprosthetic bone loss (ie, osteolysis) and aseptic loosening.
Jackson: What do we know clinically about the newer and harder surfaces, such as metal and ceramics with less wear debris and their potential for local and systemic problems?
Jacobs: To a great extent, the potential for local and systemic response is dictated by the quantity of debris that is generated at the bearing surfaces and elsewhere in the reconstruction. Given that hard-on-hard bearings and highly crosslinked polyethylene bearings have been shown to have lower volumetric wear rates compared to metal-on-conventional polyethylene bearing couples, there is an expectation that the local response to particulate debris (ie, chronic inflammation leading to osteolysis and aseptic loosening) will be lessened, leading to longer implant survivorship.
However, the physical characteristics (size, shape, surface roughness) of the debris from these newer bearings may be different than conventional polyethylene debris. For example, highly crosslinked polyethylene debris tends to be smaller than conventional polyethylene debris. In addition, particulate debris from metal-on-metal bearings is approximately 10 times smaller than debris from conventional polyethylene.
Thus, even though the volumetric wear rate for metal-on-metal bearings is less than for metal-on-polyethylene, the number of particles generated from metal-on-metal bearing couples is greater, due to their minute size. The local and systemic biological implications of these differences in size within the phagocytosable size range are not known and are currently under investigation.
Jackson: What are the early clinical signs a patient may be developing a problem related to wear debris?
Jacobs: Wear-related problems are typically asymptomatic until they reach a relatively advanced stage. In some cases, patients may present with pain secondary to a debris-induced synovitis or with a periprosthetic fracture through an osteolytic lesion. More commonly, the earliest clinical signs are noted on radiographs that demonstrate periprosthetic bone resorption (osteolysis) in the absence of clinical symptoms. It is for this reason that many joint replacement surgeons strongly recommend continued radiographic surveillance of patients with joint replacement devices throughout the lifetime of the device.
If debris-induced osteolysis can be detected at an earlier phase, prior to the development of clinical symptomatology, early intervention with articular surface exchange — or possibly drug intervention in the future — may avoid a situation with massive bone loss with or without a catastrophic failure.