The disruption of these pathways underlies several diseases: osteoporosis (elevated RANKL or reduced OPG) [68]; sclerosteosis and Van Buchem disease (SOST mutations and sclerostin deficiency, leading to excessive bone formation) [67]; and inflammatory bone loss in conditions such as rheumatoid arthritis, where TNF-α and IL-6 enhance osteoclastogenesis. This evidence concerns the gene SOST and hyperostosis corticalis generalisata.