Effect of Oxidative Stress on Bone Remodeling in Periprosthetic Osteolysis

The success of implant performance and arthroplasty is based on several factors, including oxidative stress-induced osteolysis. Oxidative stress is a key factor of the inflammatory response. Implant biomaterials can release wear particles which may elicit adverse reactions in patients, such as local inflammatory response leading to tissue damage, which eventually results in loosening of the implant. Wear debris undergo phagocytosis by macrophages, inducing a low-grade chronic inflammation and reactive oxygen species (ROS) production. In addition, ROS can also be directly produced by prosthetic biomaterial oxidation. Overall, ROS amplify the inflammatory response and stimulate both RANKL-induced osteoclastogenesis and osteoblast apoptosis, resulting in bone resorption, leading to periprosthetic osteolysis. Therefore, a growing understanding of the mechanism of oxidative stress-induced periprosthetic osteolysis and anti-oxidant strategies of implant design as well as the addition of anti-oxidant agents will help to improve implants’ performances and therapeutic approaches.

Towards a Standard Approach to Assess Tibial Bone Loss Following Total Knee Arthroplasty

Long-term implant failure in the form of aseptic loosening and periprosthetic fracture is the most common cause of revision procedures in total knee arthroplasty (TKA). While early loosening can often be attributed to failure of primary fixation, late implant failure could be associated with loss of fixation secondary to bone resorption, as a result of stress shielding in the proximal tibia. This current review study was performed to identify the clinical effects of different implant-, patient-, and surgery-related biomechanical factors on TKA-related tibial bone loss in clinical reality. Implant-related factors considered were the fixation method, and the implant type, geometry, and stiffness. In terms of patient characteristics, the effects of age, sex, knee alignment, bone density, body weight, and activity level were analyzed. The clinical literature on these topics mostly concerned longitudinal radiographic studies investigating the effect of a single factor on changes in the proximal tibia over time using bone densitometry. Implant stiffness, implant geometry and knee alignment were the only factors consistently found to affect regional bone density changes over time. Each clinical study used its own specific study design, with different definitions used for the baseline density, time points of baseline and follow-up measurements, and regions of interest. Due to the differences in study design, direct comparison between the clinical impact of different biomechanical factors was not possible. Based on the findings over the densitometry studies, a standardized guideline was proposed to allow reliable comparison between consistently reported outcome of future radiographic TKA studies.

Adipokines and Chronic Rheumatic Diseases: from Inflammation to Bone Involvement

Besides its well-known role as energy storage tissue, adipose tissue is a biologically active tissue that can also be considered as an endocrine organ, as it is able to secrete adipokines. These bioactive factors, similar in structure to cytokines, are involved in several physiological and pathological conditions, such as glucose homeostasis, angiogenesis, blood pressure regulation, control of food intake, and also inflammation and bone homeostasis via endocrine, paracrine, and autocrine mechanisms. Given their pleiotropic functions, the role of adipokines has been evaluated in chronic rheumatic osteoarticular inflammatory diseases, particularly focusing on their effects on inflammatory and immune response and on bone alterations. Indeed, these diseases are characterized by different bone complications, such as local and systemic bone loss and new bone formation. The aim of this review is to summarize the role of adipokines in rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, osteoarthritis, and osteoporosis, especially considering their role in the pathogenesis of bone complications typical of these conditions.