Browsing by Subject "RANKL"

Now showing 1 - 3 of 3
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    Expression of TRAIL and its receptors DR5 and DcR2 in orthodontic tooth movement
    (F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2013) Cardile, V.; Musumeci, G.; Sicurezza, E.; Caggia, S.; Rusu, M.C.; Leonardi, R.; Loreto, C.
    Background. TRAIL is a transmembrane protein that induces apoptosis in various tissues including alveolar bone. Its in vitro expression can be activated by several methods, such as RANKL administration and cell scraping. Expression of TRAIL and its receptors DR5 and DcR2 was examined in osteoclast-like cells to analyze their effects on cell lifespan and to explore their role in orthodontic tooth movement. Materials and Methods. Osteoclast-like cells were differentiated from a mouse hematopoietic cell line by stimulation with RANKL for 24 h (T1), 72 h (T2) or 5 days (T3); some cultures were then scraped. Immunostaining for TRAIL, DR5 and DcR2 was evaluated by immunocytochemistry and Western blot analysis in control and treated cells. Results. Significantly greater TRAIL expression was found in treated osteoclast-like cells at T1 and T3 both on immunocytochemistry and Western blotting. TRAIL expression peaked at T1 and T3 in correspondence with DcR2 and DR5 maxima, respectively. Conclusions. These data may contribute to a better understanding of the mechanisms regulating tooth movement and to improve the accuracy of orthodontic treatments.
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    PlGF/Flt-1/MMP-1 axis in gingival carcinoma bone invasion
    (Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Nguyen Phuong Thao; Miyauchi Mutsumi; Subarnbhesaj Ajiravudh; Ogawa Ikuko; Chea Chanbora; Takata Takashi; Biología Celular e Histología
    Background. Gingival squamous cell carcinoma (SCC) frequently invades adjacent bone tissue, leading to significant morbidity and mortality. Understanding the molecular mechanisms driving bone invasion is crucial for developing targeted therapies. We investigated the role of placental growth factor (PlGF) in this process, focusing on its interaction with RANKL and MMP-1. Methods. We examined the role of PlGF in bone invasion of gingival SCC through analysis of patient samples (n=55) and various in-vitro assays, including an in-vitro bone-cell coculture system. We investigated the molecular mechanisms underlying PlGF-mediated bone invasion and its relationship with RANKL and MMP-1 expression. Results. Our findings demonstrate that gingival SCC-secreted PlGF promotes local bone invasion through two possible ways: 1) direct induction of RANKL expression, activating osteoclast formation and bone resorption, and 2) indirect upregulation of RANKL via MMP-1 signaling. PlGF secretion by tumor cells triggered RANKL and MMP-1 production and significantly stimulated migration and osteoclastogenesis (p<0.05). Furthermore, PlGF is highly expressed in gingival SCC and significantly correlated with bone invasion. Finally, we also confirmed the significantly positive correlation between expression levels of MMP-1 with PlGF and Flt-1 expression. Conclusion. This study identifies PlGF as a key regulator of osteoclastogenesis in gingival SCC through both direct and MMP-1-mediated pathways. Therefore, targeting PlGF activity may represent a potential therapeutic strategy for inhibiting bone invasion in gingival SCC
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    The histogenesis of giant cell tumour of bone: a model of interaction between neoplastic cells and osteoclasts
    (Murcia : F. Hernández, 2001) Zheng, M.H.; Robbins, P.; Xu, J.; Huang, Liping; Wood, D.J.; Papadimitriou, J.M.
    Giant cell tumour of bone (GCT) is a benign primary neoplasm of a bone characterised by distinctive clinical, radiological and pathological features. Females are slightly more often affected than males, and the majority of patients present between the ages of 20 and 50. GCT is locally aggressive and produces expansive and lytic lesions, most commonly in the epiphyses of long tubular bones. Histologically, it is composed of oval and spindle mononuclear cells, uniformly distributed amongst which are large multinucleated osteoclast-like giant cells. Although the term "Giant Cell Tumour" (and the erroneous historical term 'osteoclastoma') may imply that it is the multinucleated giant cells which are responsible for the proliferative capacity of the tumour, there is evidence that the stromal-like cells, the major component of the mononuclear celi population, represent the true neoplastic component of the neoplasm. The diagnosis and management of conventional GCT are often challenging and there is considerable current interest in its pathobiology. The precise histogenesis of GCT and the nature of its varying cellular constituents have remained a matter of some controversy. Factors influencing the clinical course and biological aggression of GCT are also unclear. In this selective review, the clinicopathological characteristics of GCT are summarised and current areas of interest in the study of the neoplasm are presented and discussed. Lastly, a hypothetical model of the mechanism of histogenesis and the biological behaviour of GCT is presented.