Revista de Osteoporosis y Metabolismo Mineral

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Author: Romm

Osteonecrosis of the jaw: lights and shadows in the knowledge of its pathophysiology

Osteonecrosis of the jaw (ONJ) was described by Marx et al.[1] in 2005. In the following years, both isolated cases and series of patients were published which, over the years, was decreasing, on the one hand, due to the saturation of the journals and the low interest that the description of new cases may cause. Furthermore, knowledge of this disease has lead to the development of preventive measures that may have diminished its incidence.
Regarding ONJ, a whole range of “fears, risks and dangers” have been developed that are largely unjustified. ONJ was indicated as a complication of prolonged bisphosphonate treatment and in this sense it was equalized to the diaphyseal fractures[2], when both processes most certainly have different etiopathogenic mechanisms[3]. Fears concerning ONJ or diaphyseal fractures developed a whole doctrine about the need to suspend treatment with bisphosphonates or denosumab, the so-called “therapeutic vacations” that in reality what it was about was simply to suspend the antiresorptive treatment, before that the possible complications of its use appear[4-6]. This is especially common in the field of dentists, who, in many cases, concerned about the possible development of an ONJ do not perform virtually any dental intervention in patients receiving bisphosphonates or denosumab. With this, what has been observed is an increase in the abandonment of treatment with antiresorptive drugs which produces an increased risk of fragility fractures after discontinuation of bisphosphonate therapy, a risk that has an extreme severity in the case of suspension of denosumab treatment, with the appearance of multiple vertebral fractures[7-11].

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The Wnt/β-catenin pathway decreases the amount of osteoclasts in the bone and promotes its apoptosis

The accumulated evidence over the past few years has established that the Wnt/β-catenin pathway is crucial for bone formation and the maintenance of skeletal homeostasis [1,2]. Wnt proteins exert their cellular functions by activating different signaling pathways, commonly called canonical pathway and non-canonical pathways [3]. The former acts by controlling the amount of β-catenin not associated with cadherin, while the other routes do not require the presence of β-catenin [4]. At present, the signaling pathway mediated by β-catenin is the best studied and understood. Activation of the Wnt/β-catenin pathway begins at the cell membrane with the binding of certain Wnt ligands, such as Wnt3a, to the transmembrane receptors of the Frizzled family. This binding recruits the LRP5/6 co-receptor (low-density-lipoprotein receptor-related protein 5/6), to form a ternary complex that destabilizes a cytoplasmic conglomerate of proteins that would otherwise phosphorylate the β-catenin of the cytoplasm for its destruction in the proteasome [5-7]. So, after ligand binding to the receptor, β-catenin is not phosphorylated or destroyed, and, therefore, can accumulate in the cytoplasm, from where it will be transferred to the nucleus. There it joins the transcription factor TCF/LEF (T-cell factor/lymphoid enhancer factor) and induces target gene expression [8].

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A novel therapeutic target for osteoarthritis: control of cellular plasticity and senescence using connexin43

Osteoarthritis (OA) is a chronic disease that is characterized by a progressive degradation of the articular cartilage that covers the surface of the synovial joints, which allow the movement of the skeleton without causing pain. Chondrocytes from patients with osteoarthritis undergo changes in the phenotype associated with an increase in catabolic and inflammatory activity [1,2], along with an increase in cellular senescence and senescence-associated secretory phenotype (SASP) [2,3]. Our research group has previously shown that chondrocytes in the articular cartilage have long cytoplasmic projections that cross the extracellular matrix (ECM) [4], which form connections and gap junctions (GJs) through connexin-43 channels (Cx43) [4,5]. In 2013, our research group published relevant results associated with alterations in the activity of Cx43 in osteoarthritis, indicating that from the disease’s early stages there is an increase and changes in the localization of the protein in the cartilage of patients with arthrosis [6]. Subsequently, using animal models, we observed that the C-terminal domain of Cx43 plays a fundamental role in the structure and composition of articular cartilage [7].

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Qualitative and quantitative status of general bone in osteonecrosis of the jaws. Effect of bisphosphonates

Osteonecrosis of the jaw (ONJ) is a disease described fairly recently. After the reported findings by Marx [1], bisphosphonates were considered the etiological agent responsible for the disease, even being called osteonecrosis due to bisphosphonates [2-5], which is wrong since many factors in addition to these drugs may be implicated in the etiopathogenesis of ONJ [1,6,7].
One of the hypothesis about ONJ’s development would be the existence of an excess suppression of bone remodeling, which can be produced by bisphosphonates or by other potent anti-resorptives, such as denosumab, a drug that is also involved in ONJ [8,9]. Since these drugs act on the entire skeleton, if there is such an excess of oversupression of bone remodelling, one could expect the existence of alterations in both the amount of BMD and bone quality in other locations. Although there are many descriptions of isolated cases or series of this disease in the literature, outlining its clinical characteristics and possible association with different diseases and risk factors [1,3-7,10], we have not found publications that analyze the possible quantitative alterations and/or qualitative bone in patients with ONJ.

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Osteogenic cells affected by soluble tumor factors contribute to bone pre-metastatic niche formation

The appearance of metastatic disease seriously threatens the survival rate of patients who develop a tumor. Certain types of tumors have been found to present a high tendency to colonize specific organs. From the hypothesis formulated by Paget (“seed-and-soil”) [1], few studies have deciphered the regulatory mechanisms of metastatic organotropism. Initial studies focused on the function of the intrinsic properties of the tumor cell, such as gene expression and colonization regulation pathways, in the direction of organotropism [2-4].
Bone is an organ frequently infiltrated by the metastatic spread of solid tumors [5,6]. The appearance of metastatic disease is a serious threat in the survival rate of patients who develop a tumor. From 65-80% of subjects with prostate cancer or metastatic breast present skeletal complications [5]. The study of bone metastases has mainly focused on the interaction of the tumor cell with the bone, once the metastasis has been established, ignoring the subclinical stages of the process that occurs previously. The establishment of tumor cells in the bone microenvironment alters the balance of the bone remodeling process between bone formation, induced by osteoblasts, and osteoclast-mediated resorption. Consequently, the survival and proliferation pathways of tumor cells are favored, inducing the formation of “a vicious cycle of bone metastases” [7].
Though not exclusive, tumors cause two different types of skeletal lesions. The most common form, represented by breast cancer is the osteolytic lesion associated with an alteration of bone remodeling with an increase in osteoclastic activity and subsequent osteolysis [8-11].

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Clinical Notes
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Original Articles
Osteology images
Poster Communications
Presentation
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