Pathogenesis (disease development)
In Paget’s disease, there is overactivity of osteoclasts (“bone-degrading cells”). The resulting excessive bone resorption, mainly subcortical (“lying beneath the bone cortex”), is compensated by excessive new bone formation by osteoblasts (“bone-building cells”) during the course of the disease. As a result, bone is distended and thickened by subperiosteal (“lying below the periosteum (periosteum)”) bone accretions, leading to poorer bone structure. This in turn causes fractures and deformities.
The etiology is unknown. Currently, a slow virus infection (infectious disease of the central nervous system (CNS) characterized by an extremely long incubation period (time between the entry of a pathogen into the body and the appearance of the first symptoms) is suspected in sporadic cases.
Etiology (causes)
Biographic causes
- Genetic burden from parents, grandparents – risk is increased seven- to tenfold if first-degree relatives are affected
