pathway. function. Generally, cortisol is an immunosuppressant, known to

pathway. CRH stimulates the
pituitary gland to release adrenocorticotropic hormone (ACTH), which enters the
circulation and ultimately stimulates the cortex of the adrenal glands to
produce glucocorticoids, of which cortisol is the primary stress hormone in
humans. Dehydroepiandrosterone (DHEA) is also released, which is an endogenous
hormone that regulates the activity of cortisol.  A parallel pathway, the Sympathoadrenal
medullary (SAM) axis activation, results from the sympathetic innervation of
the adrenal gland’s medulla, which in turn results in the release of adrenal Catecholamines
(adrenaline and noradrenaline). All biochemical mediators, glucocorticoids, DHEA
and Catecholamines can each independently alter immune function. Generally,
cortisol is an immunosuppressant, known to have strong effects on helper T
cells type 1 (Th1) and type 2 (Th2) (7)
responses, through inhibiting the production of IL-12, a major inducer of Th1
responses, by antigen-presenting cells, resulting in decreased Th1 cell-derived
interferon (IFN)-? and increased production of the TH2 cytokines
IL-4, IL-10 and IL-13. As a result, cortisol enhances Th2 functions, such as
the production of immunoglobulins. Whenever the body is exposed to
stress, the physiological system responds by stimulating the hypothalamus which
results in the secretion of Corticotrophin releasing hormone (CRH). This is
released into the Hypophyseal portal system, activating the pituitary gland to
release adrenocorticotropic hormone (ACTH), which in turn induces the release
of corticosteroids from the adrenal cortex. Glucocorticoids, including cortisol
(the primary glucocorticoid), exert major suppressive effects through highly
specific mechanisms at different levels. At the molecular level, they inhibit
vital functions of inflammatory cells including macrophages, neutrophils,
eosinophils, and mast cells in functions such as Chemotaxis, secretion, and
degranulation. The immune response cascade is also affected as cortisol
inhibits the macrophage-antigen presentation, lymphocyte proliferation, and
lymphocyte differentiation to effector cell types such as helper lymphocytes,
cytotoxic lymphocytes, natural killer cells, and antibody-forming B cells. Corticosteroids
also inhibit the production of cytokines including IL-1, IL-2, IL-3, and IL-6,
tumour necrosis factor, interferon gamma, and granulocyte and monocyte colony
stimulating factors. Glucocorticoids inhibit arachidonic acid-derived
pro-inflammatory mediators, anti-inflammatory proteins and lipocortins, and
finally inhibit the generation of eicosanoids. 
Therefore, the stress-related stimulation of the HPA suppress immune and
inflammatory responses.  Other
peripherally generated inflammatory mediators that can activate the HPA axis
include lymphocyte-derived gamma Interferon, IL-2, IL-6, macrophage-derived IL-
1, and tumour necrosis factors (32, 34, 33, 48).

 

(b) Behavioural changes

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Allostatic load reflects the influence of social
circumstances and stressful life experiences, as well as behaviours, such as
smoking, diet, exercise and alcohol consumption, which have been shown to
largely contribute to the allostatic load construct. Indeed, health behaviours
are well-known risk factors for periodontal disease and several other health
conditions. However, while stress has been shown
to 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 which
people live, rather than causals themselves. Indeed, social and living
conditions generating psychosocial stressors and material constraints determine
whether individuals’ uptake harmful behaviour and whether they possess the
necessary resources and motivation to care for their oral and overall health. Related
to this is the link between the social environment and self-perceived health
and health locus of control, which in turn affects one’ s ability to change
harmful behaviours