Osteoporosis and Alveolar Bone Health in Periodontitis Niche: A Predisposing Factors-Centered Review

Abstract

Periodontitis is a periodontal inflammatory condition that results from disrupted periodontal host-microbe homeostasis, manifested by the destruction of tooth-supporting structures, especially inflammatory alveolar bone loss. Osteoporosis is characterized by systemic deterioration of bone mass and microarchitecture. The roles of many systemic factors have been identified in the pathogenesis of osteoporosis, including endocrine change, metabolic disorders, health-impaired behaviors and mental stress. The prevalence rate of osteoporotic fracture is in sustained elevation in the past decades. Recent studies suggest that individuals with concomitant osteoporosis are more vulnerable to periodontal impairment. Current reviews of worse periodontal status in the context of osteoporosis are limited, mainly centering on the impacts of menopausal and diabetic osteoporosis on periodontitis. Herein, this review article makes an effort to provide a comprehensive view of the relationship between osteoporosis and periodontitis, with a focus on clarifying how those risk factors in osteoporotic populations modify the alveolar bone homeostasis in the periodontitis niche.

Keywords: hormones; lifestyle; metabolic disorders; osteoporosis; periodontitis; psychological stress.

Figure 1

Shared predisposing factors for osteoporosis and periodontitis. Some predisposing factors might be the potential link between osteoporosis and periodontitis, including four categories: hormones, metabolic disorders of energy substrates, lifestyle and psychological stress.

Figure 2

Impacts of hormones on periodontal status. There are multiple hormones that play a role in periodontal homeostasis, and their effects vary with hormone nature and circulating level. Androgen excess, estrogen deficiency, FSH, continuous PTH, GCs, TH, and GH deficiency are evident harmful factors, contributing to periodontitis. Moreover, continuous PTH is a potentially harmful factor. On the contrary, androgen and estrogen at a physiological level, progesterone, vitamin D, iPTH, calcitonin, melatonin, and GH excess are evident protective factors for periodontal health. Direct evidence for the impacts of progesterone and continuous PTH on periodontal tissues is still lacking yet. FSH follicle stimulating hormone; PTH, parathyroid hormone; GCs, glucocorticoids; TH, thyroid hormone; GH, growth hormone.

Figure 3

Impacts of metabolic disorders of energy substrates on periodontal status. Hyperglycemia, dyslipidemia and abnormal AAs profile are common manifestations of disordered metabolism of energy substrates. They display comprehensive actions on periodontal components, including PDL cells, osteoblasts, osteoclasts, osteocytes and bacteria. The symbol “+” indicates promoting effect, and symbol “−” indicates adverse effect. FAs, fatty acids; SFA, saturated fatty acid; UFA, unsaturated fatty acids; AAs, amino acids; PDL, periodontal ligament.

Figure 4

Impacts of lifestyle on periodontal status. Smoking and excessive alcohol consumption are typical unhealthy lifestyles. They inhibit the osteogenic differentiation of PDL cells and osteoblastic bone formation and promote osteoclastic bone resorption. Furthermore, they also aggravate the bacterial infection. PDL, periodontal ligament.

Figure 5

Impacts of psychological stress on periodontal status. Psychological stress affects periodontitis via three pathways, including lifestyle change, endocrine change and neurogenic pathway. Health-impairing lifestyles, such as smoking and alcohol consumption, exacerbate periodontitis-associated alveolar bone loss. Endocrine change mainly manifests as altered levels of stress hormones, such as GCs and catecholamine. GCs and catecholamine modulate bone remodeling and immuno-inflammatory response, adding to periodontal deterioration. Neuropeptides are the major effectors in the neurogenic pathway. Current evidence indicates the presence of both protective and harmful factors among neuropeptides. GCs, glucocorticoids.