Viral infection and lipopolysaccharide: Pathological axis “lung–joints” as a potential cause of osteonecrosis

The article concerns the effects of viral infections, e.g., SARS-CoV-2, and bacterial lipopolysaccharide (LPS), a component of the cell wall of Gram-negative microbes, on the development of osteonecrosis via the pathological lung–joint axis. Viral infection causes damage to lung cells and vascular endothelium, and leads to inflammatory and blood clotting disorders, increasing the risk of bone ischemia. LPS, by interacting with TLR4 receptors, enhances the inflammatory response and disrupts the blood supply to bones, thus stimulating resorption and preventing bone formation. In addition, the article highlights the role of lung dysbiosis caused by viral infection, which enhances inflammation and increases permeability of tissue barriers for endotoxins. Appropriate information was searched for the keywords “osteonecrosis and lipopolysaccharide”, “COVID-19 virus and lipopolysaccharide-binding protein”, “viremia and osteonecrosis”, “lung microflora and LPS” in foreign and domestic scientometric databases such as PubMed and eLIBRARY. The presented data suggest that the combined effect of imbalanced LPS-binding systems, impaired pulmonary barrier, viral infection and LPS exposure is an important aggravating pro-inflammatory factor. This combination may propote a predisposal for the full-scale osteonecrosis. This concept seems to be promising for clinical research of potential tools influencing these conditions, either single factors or their combined effects. This study focuses on the variety of effects exerted by viral infections and bacterial LPS upon the bone tissue. Current research shows that influencing these mechanisms may open up new ways for the development of therapeutic strategies. The prospects of using targeted therapies to mitigate the negative effects of these interactions are also being considered. These data emphasize a need for integrated approach in the study and treatment of osteonecrosis, with respect to both infectious and inflammatory components of this disorder.