Mental health and periodontal and peri-implant diseases

Abstract

Mental health disorders, particularly depression and anxiety, affect a significant number of the global population. Several pathophysiological pathways for these disorders have been identified, including the hypothalamic-pituitary-adrenal axis, autonomic nervous system, and the immune system. In addition, life events, environmental factors, and lifestyle affect the onset, progression, and recurrence of mental health disorders. These may all overlap with periodontal and/or peri-implant disease. Mental health disorders are associated with more severe periodontal disease and, in some cases, poorer healing outcomes to nonsurgical periodontal therapy. They can result in behavior modification, such as poor oral hygiene practices, tobacco smoking, and alcohol abuse, which are also risk factors for periodontal disease and, therefore, may have a contributory effect. Stress has immunomodulatory effects regulating immune cell numbers and function, as well as proinflammatory cytokine production. Stress markers such as cortisol and catecholamines may modulate periodontal bacterial growth and the expression of virulence factors. Stress and some mental health disorders are accompanied by a low-grade chronic inflammation that may be involved in their relationship with periodontal disease and vice versa. Although the gut microbiome interacting with the central nervous system (gut-brain axis) is thought to play a significant role in mental illness, less is understood about the role of the oral microbiome. The evidence for mental health disorders on implant outcomes is lacking, but may mainly be through behaviourial changes. Through lack of compliance withoral hygiene and maintenance visits, peri-implant health can be affected. Increased smoking and risk of periodontal disease may also affect implant outcomes. Selective serotonin reuptake inhibitors have been linked with higher implant failure. They have an anabolic effect on bone, reducing turnover, which could account for the increased loss.

Keywords: Alzheimer disease; anxiety disorder; bipolar; depression; gut-brain axis; mental health; microbiome; mood (affective) disorder; peri-implant disease; periodontal disease; schizophrenia; stress; substance use disorder.

FIGURE 1

Pathogen host defense hypothesis (redrawn from Miller and Raison, ³² ). Early human evolution required an active immunity for survival that was held in check by the immunomodulatory microbiome. Modern society lacks the same exposure to an immunomodulatory microbiome, resulting in the onset of a “sickness” with depression‐like behavior

FIGURE 2

Inflammasome model of neuroinflammation (Miller and Raison ³² ). Inflammasome formation in monocytes results in the production of proinflammatory cytokines, increasing the levels of neuroinflammation through humoral, neural, and cellular routes. ATP, adenosine triphosphate; DAMPs, damage‐associated molecular patterns; HSP, heat shock protein; IL: interleukin; MAMPs, microbial‐associated molecular patterns; NA, noradrenaline; SNS, sympathetic nervous system; UA, uric acid

FIGURE 3

Effect of stress on the hypothalamic‐pituitary‐adrenal (HPA) axis. Activation of the hypothalamic‐pituitary‐adrenal stimulates the pituitary gland. Adrenocorticotropic hormone (ACTH) release results in increased cortisol from the adrenal glands, which then affects the autonomic nervous system. AVP, arginine vasopressin; CRF, corticotropin‐releasing factor; NA, noradrenaline

FIGURE 4

Possible mechanism how periodontal disease may affect Alzheimer disease through increased chronic inflammation and infection of the brain by oral bacteria

FIGURE 5

Oral‐brain axis (redrawn from Martínez et al, ²⁰¹ ). (1) Bacteremia of the periodontal pathogens can reach the brain directly through the bloodstream and damaged blood‐brain barrier. (2) Activation of endothelial cells by proinflammatory cytokines can indirectly affect the central nervous system. (3) Expression of tumor necrosis factor alpha (TNF‐α) and interleukin‐1 (IL‐1) endothelial receptors activates microglia that results in inflammation. (4) Increased permeability of the periodontal vasculature results in “leaking” of lipopolysaccharide (LPS). (5) Lipopolysaccharide can activate the hypothalamic‐pituitary‐adrenal axis, thereby increasing stress hormones and/or neurotransmitters. (6) This then affects gut physiology, habitat, microbiome composition, and bacterial gene expression. (7) Changes in the gut microbiome can result in further systemic inflammation reinforcing the effect on the central nervous system. (8) Further, it may affect periodontal disease by increasing the inflammatory burden. (9) Transmission of the oral bacteria to the gut by saliva may also affect the gut microbiome composition and function. ACTH, adrenocorticotropic hormone; AVP, arginine vasopressin; CRF, corticotropin‐releasing factor