Browsing by Subject "osteoarthritis"

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    An Objective Computational Method to Quantify Ankle Osteoarthritis From Low-Dose Weightbearing Computed Tomography.
    (Foot & ankle orthopaedics, 2022-07) Tazegul, Tutku E; Anderson, Donald D; Barbachan Mansur, Nacime S; Kajimura Chinelati, Rogerio Marcio; Iehl, Caleb; VandeLune, Christian; Ahrenholz, Samuel; Lalevee, Matthieu; de Cesar Netto, Cesar

    Background

    The treatment of ankle osteoarthritis (OA) varies depending on the severity and distribution of the associated joint degeneration. Disease staging is typically based on subjective grading of appearance on conventional plain radiographs, with reported subpar reproducibility and reliability. The purpose of this study was to develop and describe computational methods to objectively quantify radiographic changes associated with ankle OA apparent on low-dose weightbearing CT (WBCT).

    Methods

    Two patients with ankle OA and 1 healthy control who had all undergone WBCT of the foot and ankle were analyzed. The severity of OA in the ankle of each patient was scored using the Kellgren-Lawrence (KL) classification using plain radiographs. For each ankle, a volume of interest (VOI) was centered on the tibiotalar joint. Initial computation analysis used WBCT image intensity (Hounsfield units [HU]) profiles along lines perpendicular to the subchondral bone/cartilage interface of the distal tibia extending across the entire VOI. Graphical plots of the HU distributions were generated and recorded for each line. These plots were then used to calculate the joint space width (JSW) and HU contrast.

    Results

    The average JSW was 3.89 mm for the control ankle, 3.06 mm for mild arthritis (KL 2), and 1.57 mm for severe arthritis (KL 4). The average HU contrast was 72.31 for control, 62.69 for mild arthritis, and 33.98 for severe arthritis. The use of 4 projections at different locations throughout the joint allowed us to visualize specifically which quadrants have reduced joint space width and contrast.

    Conclusion

    In this technique report, we describe a novel methodology for objective quantitative assessment of OA using JSW and HU contrast.

    Clinical relevance

    Objective, software-based measurements are generally more reliable than subjective qualitative evaluations. This method may offer a starting point for the development of a more robust OA classification system or deeper understanding of the pathogenesis and response to ankle OA treatment.
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    Ankle Osteoarthritis.
    (Revista brasileira de ortopedia, 2021-12) Godoy-Santos, Alexandre Leme; Fonseca, Lucas Furtado; de Cesar Netto, Cesar; Giordano, Vincenzo; Valderrabano, Victor; Rammelt, Stefan
    Osteoarthritis (OA) is characterized by a chronic, progressive and irreversible degradation of the joint surface associated with joint inflammation. The main etiology of ankle OA is post-traumatic and its prevalence is higher among young and obese people. Despite advances in the treatment of fractures around the ankle, the overall risk of developing post-traumatic ankle OA after 20 years is almost 40%, especially in Weber type B and C bimalleolar fractures and in fractures involving the posterior tibial border. In talus fractures, this prevalence approaches 100%, depending on the severity of the lesion and the time of follow-up. In this context, the current understanding of the molecular signaling pathways involved in senescence and chondrocyte apoptosis is fundamental. The treatment of ankle OA is staged and guided by the classification systems and local and patient conditions. The main problems are the limited ability to regenerate articular cartilage, low blood supply, and a shortage of progenitor stem cells. The present update summarizes recent scientific evidence of post-traumatic ankle OA with a major focus on changes of the synovia, cartilage and synovial fluid; as well as the epidemiology, pathophysiology, clinical implications, treatment options and potential targets for therapeutic agents.
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    Collagen biomarkers for arthritis applications.
    (Biomark Insights, 2007-02-07) Birmingham, James D; Vilim, Vladimir; Kraus, Virginia B
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    Inflammatory signaling sensitizes Piezo1 mechanotransduction in articular chondrocytes as a pathogenic feed-forward mechanism in osteoarthritis.
    (Proceedings of the National Academy of Sciences of the United States of America, 2021-03) Lee, Whasil; Nims, Robert J; Savadipour, Alireza; Zhang, Qiaojuan; Leddy, Holly A; Liu, Fang; McNulty, Amy L; Chen, Yong; Guilak, Farshid; Liedtke, Wolfgang B
    Osteoarthritis (OA) is a painful and debilitating condition of synovial joints without any disease-modifying therapies [A. M. Valdes, T. D. Spector, Nat. Rev. Rheumatol. 7, 23-32 (2011)]. We previously identified mechanosensitive PIEZO channels, PIEZO1 and PIEZO2, both expressed in articular cartilage, to function in chondrocyte mechanotransduction in response to injury [W. Lee et al., Proc. Natl. Acad. Sci. U.S.A. 111, E5114-E5122 (2014); W. Lee, F. Guilak, W. Liedtke, Curr. Top. Membr. 79, 263-273 (2017)]. We therefore asked whether interleukin-1-mediated inflammatory signaling, as occurs in OA, influences Piezo gene expression and channel function, thus indicative of maladaptive reprogramming that can be rationally targeted. Primary porcine chondrocyte culture and human osteoarthritic cartilage tissue were studied. We found that interleukin-1α (IL-1α) up-regulated Piezo1 in porcine chondrocytes. Piezo1 expression was significantly increased in human osteoarthritic cartilage. Increased Piezo1 expression in chondrocytes resulted in a feed-forward pathomechanism whereby increased function of Piezo1 induced excess intracellular Ca2+ at baseline and in response to mechanical deformation. Elevated resting state Ca2+ in turn rarefied the F-actin cytoskeleton and amplified mechanically induced deformation microtrauma. As intracellular substrates of this OA-related inflammatory pathomechanism, in porcine articular chondrocytes exposed to IL-1α, we discovered that enhanced Piezo1 expression depended on p38 MAP-kinase and transcription factors HNF4 and ATF2/CREBP1. CREBP1 directly bound to the proximal PIEZO1 gene promoter. Taken together, these signaling and genetic reprogramming events represent a detrimental Ca2+-driven feed-forward mechanism that can be rationally targeted to stem the progression of OA.
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    Patellar skin surface temperature by thermography reflects knee osteoarthritis severity.
    (Clin Med Insights Arthritis Musculoskelet Disord, 2010-10-15) Denoble, Anna E; Hall, Norine; Pieper, Carl F; Kraus, Virginia B
    BACKGROUND: Digital infrared thermal imaging is a means of measuring the heat radiated from the skin surface. Our goal was to develop and assess the reproducibility of serial infrared measurements of the knee and to assess the association of knee temperature by region of interest with radiographic severity of knee Osteoarthritis (rOA). METHODS: A total of 30 women (15 Cases with symptomatic knee OA and 15 age-matched Controls without knee pain or knee OA) participated in this study. Infrared imaging was performed with a Meditherm Med2000™ Pro infrared camera. The reproducibility of infrared imaging of the knee was evaluated through determination of intraclass correlation coefficients (ICCs) for temperature measurements from two images performed 6 months apart in Controls whose knee status was not expected to change. The average cutaneous temperature for each of five knee regions of interest was extracted using WinTes software. Knee x-rays were scored for severity of rOA based on the global Kellgren-Lawrence grading scale. RESULTS: The knee infrared thermal imaging procedure used here demonstrated long-term reproducibility with high ICCs (0.50-0.72 for the various regions of interest) in Controls. Cutaneous temperature of the patella (knee cap) yielded a significant correlation with severity of knee rOA (R = 0.594, P = 0.02). CONCLUSION: The skin temperature of the patellar region correlated with x-ray severity of knee OA. This method of infrared knee imaging is reliable and as an objective measure of a sign of inflammation, temperature, indicates an interrelationship of inflammation and structural knee rOA damage.
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    Serum C-Reactive Protein (CRP), Target for Therapy or Trouble?
    (Biomark Insights, 2007-02-07) Kraus, Virginia B; Jordan, Joanne M
    High sensitivity serum C-reactive protein (hs-CRP) has come into clinical use as a marker of risk for cardiovascular disease (CVD). In addition to a role as a marker of disease, CRP has also been implicated in the pathogenesis of CVD. Specific small-molecule inhibitors of CRP have recently been developed with the intent of mitigating cardiac damage during acute myocardial infarction. However, the use of CRP, both as a risk marker and a disease target are controversial for several reasons. Serum hs-CRP concentrations can be elevated on the basis of genetics, female gender, and non-Caucasian ethnicity. It is not clear, in these contexts, that elevations of hs-CRP have any pathological significance. As a non-specific indicator of inflammation, CRP is also not a specific indicator of a single disease state such as cardiovascular disease but elevated concentrations can be seen in association with other comorbidities including obesity and pulmonary disease. In sharp contrast to the proposed inhibition of CRP for cardiovascular disease treatment, the infusion of CRP has been shown to have profound therapeutic benefits for autoimmune disease and septic shock. The balance between the risks and benefits of these competing views of the role of CRP in disease and disease therapy is reminiscent of the ongoing controversy regarding the use of non-steroidal anti-inflammatory drugs (NSAIDs) for musculoskeletal disease and their cardiovascular side effects. Soon, NSAIDs may not be the only agents about which Rheumatologists and Cardiologists may spar.