pathway. CRH stimulates thepituitary gland to release adrenocorticotropic hormone (ACTH), which enters thecirculation and ultimately stimulates the cortex of the adrenal glands toproduce glucocorticoids, of which cortisol is the primary stress hormone inhumans. Dehydroepiandrosterone (DHEA) is also released, which is an endogenoushormone that regulates the activity of cortisol. A parallel pathway, the Sympathoadrenalmedullary (SAM) axis activation, results from the sympathetic innervation ofthe adrenal gland’s medulla, which in turn results in the release of adrenal Catecholamines(adrenaline and noradrenaline). All biochemical mediators, glucocorticoids, DHEAand Catecholamines can each independently alter immune function.
Generally,cortisol is an immunosuppressant, known to have strong effects on helper Tcells type 1 (Th1) and type 2 (Th2) (7)responses, through inhibiting the production of IL-12, a major inducer of Th1responses, by antigen-presenting cells, resulting in decreased Th1 cell-derivedinterferon (IFN)-? and increased production of the TH2 cytokinesIL-4, IL-10 and IL-13. As a result, cortisol enhances Th2 functions, such asthe production of immunoglobulins. Whenever the body is exposed tostress, the physiological system responds by stimulating the hypothalamus whichresults in the secretion of Corticotrophin releasing hormone (CRH).
This isreleased into the Hypophyseal portal system, activating the pituitary gland torelease adrenocorticotropic hormone (ACTH), which in turn induces the releaseof corticosteroids from the adrenal cortex. Glucocorticoids, including cortisol(the primary glucocorticoid), exert major suppressive effects through highlyspecific mechanisms at different levels. At the molecular level, they inhibitvital functions of inflammatory cells including macrophages, neutrophils,eosinophils, and mast cells in functions such as Chemotaxis, secretion, anddegranulation. The immune response cascade is also affected as cortisolinhibits the macrophage-antigen presentation, lymphocyte proliferation, andlymphocyte differentiation to effector cell types such as helper lymphocytes,cytotoxic lymphocytes, natural killer cells, and antibody-forming B cells. Corticosteroidsalso inhibit the production of cytokines including IL-1, IL-2, IL-3, and IL-6,tumour necrosis factor, interferon gamma, and granulocyte and monocyte colonystimulating factors. Glucocorticoids inhibit arachidonic acid-derivedpro-inflammatory mediators, anti-inflammatory proteins and lipocortins, andfinally inhibit the generation of eicosanoids.
Therefore, the stress-related stimulation of the HPA suppress immune andinflammatory responses. Otherperipherally generated inflammatory mediators that can activate the HPA axisinclude lymphocyte-derived gamma Interferon, IL-2, IL-6, macrophage-derived IL-1, and tumour necrosis factors (32, 34, 33, 48). (b) Behavioural changesAllostatic load reflects the influence of socialcircumstances and stressful life experiences, as well as behaviours, such assmoking, diet, exercise and alcohol consumption, which have been shown tolargely contribute to the allostatic load construct.
Indeed, health behavioursare well-known risk factors for periodontal disease and several other healthconditions. However, while stress has been shownto correlate with poor health behaviours, some would argue that the role of behaviour in disease has been overemphasized,and that they are rather mediators of the psychosocial environment in whichpeople live, rather than causals themselves. Indeed, social and livingconditions generating psychosocial stressors and material constraints determinewhether individuals’ uptake harmful behaviour and whether they possess thenecessary resources and motivation to care for their oral and overall health. Relatedto this is the link between the social environment and self-perceived healthand health locus of control, which in turn affects one’ s ability to changeharmful behaviours
