The Effect of Hypothyroidism on Bone Loss at Dental Implants

Hypothyroidism (HT) is an endocrine disorder characterized by abnormally reduced thyroid gland activity, and is most commonly of autoimmune etiology. HT is associated with alterations in bone metabolism, and HT patients typically experience decreased bone resorption. The objective of this study was to use dental implants as standardized reference markers to compare the extent of alveolar bone loss in implant patients with and without HT. We examined medical and dental history records, and radiographic data, from 635 patients receiving 1480 implants during 2000-2017. The rate of bone loss was calculated from differences in radiographic bone levels over time, corrected for radiographic distortion. Peri-implant bone loss from patients with HT was significantly lower than for those without HT (t 1252 = -3.42; 95% confidence interval= 0.47-1.73; P<0.001; M= 0.53 mm/yr and 1.63 mm/yr, respectively. A similar relationship persisted after excluding smokers and diabetics, and after additionally excluding those on systemic steroids, hormone replacement therapy, hormone medications, or autoimmune diseases other than HT. Our data suggest that patients with HT have a decreased rate of bone loss around dental implants and may not be at increased risk for dental implant failure. The decreased bone metabolic rate among patients with HT might contribute to those findings.

Osteoporosis and fragility fracture

Osteoporosis is defined as a systemic bone disease with reduction in both bone density and microarchitectural integrity, resulting in an increase in fragility fracture risk. It is a multifactorial disease which, through effects on bone formation and resorption, reduces the peak bone mass achieved during early adulthood and increases the rate of bone loss in later adulthood. Osteoporosis is clinically silent until a fragility fracture occurs. There are 3 million patients with osteoporosis in the UK, with over 200 000 fractures per year and 80 000 hip fractures. This chapter addresses the causes, clinical features, diagnosis, and management of osteoporosis.

FSH, Bone Mass, Body Fat, and Biological Aging

The Study of Women’s Health Across the Nation has taught us that impending ovarian failure during late perimenopause is associated with a sharp rise in serum FSH, which coincides with the most rapid rate of bone loss and the onset of visceral adiposity. At this time in a woman’s life, serum estrogen levels are largely unaltered, so the hypothesis that hypoestrogenemia is the sole cause of bone loss and visceral obesity does not offer a full explanation. An alternative explanation, arising from animal models and human data, is that both physiologic aberrations, obesity and osteoporosis, arise at least in part from rising FSH levels. Here, we discuss recent findings on the mechanism through which FSH exerts biological actions on bone and fat and review clinical data that support a role for FSH in causing osteoporosis and obesity. We will also provide a conceptual framework for using a single anti-FSH agent to prevent and treat both osteoporosis and obesity in women across the menopausal transition.