Abstract
Objective: There are two monocyte populations in human blood: CD14+CD16- classical monocytes and CD14+CD16+ inflammatory monocytes. CD14+CD16+ inflammatory monocytes, account for approximately 10% of the total monocytes, may be expanded in various types of inflammatory conditions. The purpose of this study was to investigate whether the expansion of the CD14+CD16+ monocyte population represents a risk factor of aseptic loosening (AL). Methods: Peripheral monocytes subsets were measured in revision patients with AL (n = 35) and in patients with stable implants (SI, n = 56). The gene profiles of TNFα, IL-1β, CD16, CD68 and TRAP5B from collected loosening periprosthetic tissues were analyzed. Results: There were no significant differences in the CD14+CD16+ monocyte populations between the SI and AL patients. The CD14+CD16+ monocytes were marginally higher in revision patients with osteolysis (n = 30), compared to patients without osteolysis (n = 5) though no statistically difference was found. There was an association between the CD14+CD16+ monocyte subpopulation and the tissue gene profiles, including IL-1β (p = 0.063), CD68 (p = 0.036), and TRAP5B (p = 0.073). Conclusion: It was demonstrated that the expansion of CD14+CD16+ monocytes reflects, to some extent, the inflammatory status of the loosening periprosthetic tissues. It is unclear if some of those SI patients (no pain and negative radiograph) who have a higher frequency of CD14+CD16+ monocytes may be at the early stage of AL. Further evaluation of CD14+CD16+ monocyte population, independently or combined with other factors, will be useful to design a risk profile for AL incidence and progression.
Highlights
More than 500,000 total joint arthroplasty (TJA) operations are performed annually in the USA [1] [2]
Analysis of loosening periprosthetic membranes has demonstrated an abundance of macrophages and multinucleated giant cells that comprise 60% - 80% of the entire cellular population [24] [43]
Activated macrophages play a critical role in the pathology of aseptic loosening (AL) [25] through a multitude of biologic functions, including production of proinflammatory cytokines (TNFα, IL-1β, tartrate-resistant acid phosphatase (TRAP), etc.) [26]-[31] and differentiation into bone resorbing cells [24] [32] [44]
Summary
More than 500,000 total joint arthroplasty (TJA) operations are performed annually in the USA [1] [2]. Activated macrophages secrete pro-inflammatory cytokines that stimulate periprosthetic tissue inflammation and osteolysis [5] [8]. It is unclear why some patients develop AL/osteolysis while others do not. The development of biomarkers that could predict or assess the risk of early implant failure and bone loss is clinically important [11]. This is especially true since all patients have some periprosthetic inflammatory changes after surgery
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