Psychological stress has been postulated as a risk factor for a number of chronic health conditions, such as cardiovascular diseases, diabetes and obesity, among others. Stress induced by poverty, unemployment, job insecurity, high-demand routine jobs and lack. of control in the workplace and at home have been linked to cardiovascular disease, obesity, diabetes, physical limitations and cancer. The vicious cycle between socioeconomic factors, stress and health has perhaps been best described by Evans & Kim as “poverty gets under the skin” .
Stress affects health through different pathways, resulting in a biological impact on the autoimmune and endocrine systems and metabolism.
Stress can also affect health by inducing changes in behaviors. People may adopt some unhealthy behaviors, such as smoking, excessive alcohol consumption, and illicit drug use, to cope with stressful situations. There is also evidence that stress affects oral health .
The use of unhealthy behaviors (such as smoking, drinking alcohol and eating to feel comfortable - comfort foods -) as stress coping mechanisms increase the risk of periodontal diseases, dental cavities and oral cancer. Additionally, biological changes associated with stress are described as risk factors for oral diseases. There is also evidence that stress is related to salivary changes resulting in increased susceptibility to dental caries.
Chronic and repeated exposure to stressors affects periodontal tissues
On the other hand, the biological pathways between stress and periodontal diseases seem to be more evident and have been addressed in several studies. Chronic and repeated exposure to stressors affects periodontal tissues in the same way they affect other body systems. Recent studies on the global burden of oral health suggest that the prevalence of periodontal diseases is increasing, in contrast to a previous review.
Additionally, periodontal diseases appear to result in an increase in disability-adjusted life years (i.e., the number of years lost due to illness, disability, or premature death). Several reviews have addressed proximal risk factors for periodontal diseases, highlighting opportunities to address the burden of disease. Fewer reviews have addressed the role of stress and psychological well-being on periodontal disease. Studies have also examined the mediating role of stress between socioeconomic position and periodontal disease.
While elucidating the relationship between stress and periodontal disease could help identify individuals at high risk, its primary importance lies in highlighting the role of environmental and social factors that could only be addressed at a higher level.
Given the increasing global burden of periodontal diseases and the importance of stress as a modifiable risk factor for periodontal diseases along with other chronic conditions, we conducted this narrative review on the role of stress in periodontal diseases and the different mechanisms through which which stress impacts periodontal diseases.
The role of stress in the complex determinants of periodontal disease
Periodontal disease is a socially patterned condition with a strong behavioral component. Smoking and poor oral hygiene, associated with inadequate personal and professional dental cleaning, are among the main behavioral risk factors for periodontal disease. There is also a strong genetic component that increases susceptibility to periodontal disease. Certain systemic conditions are implicated in predisposing people to periodontitis; These include diabetes, leukemia and acquired neutropenia, among others.
Psychological stressors have repeatedly been shown to play an important role in periodontitis because they can influence behavioral risk factors for periodontitis and/or directly affect periodontal tissues. Studies have shown that people under stress are more likely to smoke, less likely to brush their teeth, and less likely to visit the dentist, behavioral determinants of utmost importance for periodontal disease. On the other hand, stress factors have been shown to have an impact on the body, increasing susceptibility to inflammation and affecting the host immune response and endocrine systems.
These reactions to chronic stressors affect different tissues in the body, including the periodontium. As expected, the common effect of stressors on different organs of the body is implicated in the relationship between systemic conditions and periodontal diseases.
Finally, examination of the contextual determinants of health and related behaviors will allow for the identification of socioeconomic and environmental factors that impact both stress and behaviors, both directly and by limiting the individual’s ability to engage in healthy behaviors. and avoid unhealthy behaviors, and indirectly, through psychological pathways, including stress.
Types of psychosocial stress
Psychosocial stress can be defined as the physiological and psychological changes that occur in the body when an external demand or stressor tests an individual’s adaptive capacity.
Depending on the duration of exposure, stress can be broadly classified into chronic or acute forms ; However, there is no universally accepted definition or established cut-off period for acute and chronic stress.
Stressors are external stimuli that cause stress in an individual and are classified into 3 groups:
• Disasters or crises . An unpredictable event that is completely outside the individual’s control. For example, devastating natural disasters, such as major floods or earthquakes, or wars.
• Important life events . These are rare events that can be positive or negative and include marital separation, incarceration, death of a close family member, dismissal from work, and personal injury.
• Microstressors . The accumulation of microstressors or daily discomforts can have the same negative impact on our health as experiencing a major stressful event. They occur in the life of each individual; however, they are different for each individual, as not everyone perceives a given event as stressful.
Acute stressors are most commonly short-term, time-limited events, while chronic stressors denote conditions that are longer lasting and may not be attributed to a specific event. The organizational model of the stress process that explains how chronic stress leads to detrimental health outcomes can be classified into 3 broad stages:
- Exposure to environmental demands or negative or stressful life events.
- Self-assessment and assessment of stressors, which could provoke negative responses in the absence of coping skills.
- Activation of the biological system in response to environmental and psychological demand.
This conceptualization of stress serves as a resource for developing stress assessment tools that help researchers select an appropriate measure to use in different studies.
What is allostasis? Allostasis ("stability through change", Peter Sterling) suggests that the goal of regulation is not constancy, but rather maintaining fitness in natural selection (adaptation). The word allostasis means a changing state, while homeostasis means staying in the same state. The idea of allostasis is that the organism will change its internal environment to face the challenge or disturbance that comes to it from the outside. Blood pressure is not constant, but it will be higher if the body has to be very active and lower if that is not necessary. Consistency is not the ideal. The ideal is to have the internal state most relevant to the particular external state (adaptation). Physical condition requires the regulation of aspects of physiology to be efficient in the environment to which the individual is exposed, which implies avoiding errors and minimizing costs. Both needs are best achieved by using prior information to predict demand and then adjusting all parameters to meet it. Therefore, allostasis considers the unusual value of a parameter not as a failure with respect to a supposed mechanism that should defend a fixed reference point, but rather as an adaptive response to some prediction. This model attributes diseases such as essential hypertension and type 2 diabetes to sustained neural signals arising from unsatisfactory environmental interactions with high demand. |
Clinical-biochemical measures
Neuroendocrine biomarkers
Whenever a stressor induces chronic physiological stress, some alterations occur at the systemic level, as well as an increase in energy production to maintain homeostasis. The neuroendocrine system is the first to activate and this will initiate the release of endocrine markers that can be effectively detected. The various neuroendocrine biomarkers of chronic stress currently in use include cortisol, dehydroepiandrosterone, epinephrine, norepinephrine, and dopamine.
Cortisol and dehydroepiandrosterone
The cortisol level is one of the most used measures to quantify physiological stress. As a mediator of many secondary outcomes, cortisol captures the state of hypothalamic-pituitary-adrenal axis function. The immediate sources of cortisol are blood (plasma or serum) and saliva. Dehydroepiandrosterone is also a marker of chronic stress and functions as an antagonist of the hypothalamic-pituitary-adrenal axis.
Dehydroepiandrosterone measurements directly capture the state of hypothalamic-pituitary-adrenal axis functioning. However, due to the large diurnal variation in cortisol or dehydroepiandrosterone levels, which makes it difficult to determine levels from a single measurement, these are generally not effective as biomarkers for chronic stress.
In recent years, researchers have also become increasingly interested in hair samples as another potentially practical way to assess cumulative stress exposure.
Unlike other less reliable measures, non-invasive hair sampling has several advantages in terms of collection, storage and transportation. Additionally, the level of cortisol in hair can also reflect both acute and chronic stress.
Epinephrine, dopamine, aldosterone and norepinephrine
The levels of these biomarkers consistently show an increase in response to stress, regardless of whether the stress is perceived as a threat or an opportunity for gain. Therefore, these measures may not necessarily be static measures of stress.
However, when used in conjunction with other markers of chronic stress in an allostatic load model , norepinephrine and dopamine may be useful indicators of the sympathetic nervous system and cardiovascular functioning, respectively.
Aldosterone may be a useful measure of adrenal gland function when used in conjunction with other biomarkers of allostatic load . Importantly, it is the frequency of acute stressors that is detrimental to health.
Immune biomarkers
Other commonly used chronic stress biomarkers are circulating levels of interleukin-6, tumor necrosis factor alpha, C-reactive protein, and insulin-like growth factor. The secretion of immunological biomarkers can be altered by chronic exposure to stress.
Interleukin -6 , a proinflammatory cytokine that functions synergistically with tumor necrosis factor alpha and interleukin-1, may indirectly capture hypothalamic-pituitary-adrenal axis dysfunction mediated by glucocorticoid signaling.
The level of C-reactive protein has been used in many studies as one of the inflammatory responses to chronic stress.
However, these biomarkers are markers of inflammation and are not used as primary markers of stress. They are rather indicators of how stress can affect the immune system. Although these biomarkers are used with other primary markers (such as epinephrine and cortisol) to test the relationship between stress and cardiovascular and periodontal diseases, they can also be found in the body system as markers of inflammation in the absence of stress.
Metabolic biomarkers
Changes in metabolism have been used as secondary and tertiary markers of stress. Studies have used biomarkers such as cholesterol, albumin, waist-to-hip ratio, and glycated hemoglobin levels in combination with other biomarkers discussed above. However, these biomarkers are mainly confounded by many variables, making them less reliable and less valid in epidemiological studies.
allostatic load
No metric can accurately measure chronic stress, and this deficiency is managed by using a compendium of biomarkers , released from different body systems, known as allostatic load , which is generally defined as the ’price the body pays for being forced to adapt’ to adverse psychological or physical situations, and represents the presence of too much stress or the ineffective functioning of the stress hormone response system.
Allostasis is an active physiological or biochemical adaptation that helps the body restore homeostasis after exposure to a stressor.
While the acute stress response is critical for survival, repeated or chronic exposure to stressors can have detrimental effects on the nervous and endocrine systems and immune functions. When people are repeatedly exposed to chronic stressors, biological responses are induced to cope with these stressors, leading to wear and tear of the immune, cardiovascular, metabolic and nervous systems, and this is mainly characterized by elevated levels of epinephrine and cortisol in the body. a phenomenon known as allostatic load .
Since chronic exposure to stress hinders the normal functioning of the physiological regulatory system, the state of the biological system must be considered for the measurement of allostatic load. The first study to validate these interconnections. Cascading relationships were initially validated by McArthur’s studies on successful aging. The study contains information on the 10 parameters that determine the physiological state of the hypothalamic-pituitary-adrenal axis, sympathetic nervous system, metabolic processes and cardiovascular system.
The first four primary mediators (dehydroepiandrosterone, cortisol, epinephrine and norepinephrine) related to the stress response were identified .
Other mediators were outcome indices:
- Metabolic (eg, insulin, glucose, total cholesterol, high-density lipoproteins, cholesterol, triglycerides, visceral fat deposits).
- Cardiovascular (eg, systolic and diastolic blood pressure).
- Immune (eg, fibrinogen, C-reactive protein).
Most of the biomarkers measured to derive the allostatic load score are biologically interconnected .
Although allostatic load reflects cumulative exposure to stress over many years, most studies of allostatic load are cross-sectional in nature. Longitudinal measurement of allostatic load can provide information about an individual’s allostatic profile at various stages of the development of stress-related health outcomes. This may shed some light on the pathophysiology pathways that lead to the development of the disease.
Stress pathways for periodontal diseases
biological changes
In response to chronic stressors, a cascade of reactions occurs.
First, the hypothalamus releases corticotropin-releasing hormone from the periventricular nucleus, initiating the hypothalamic-pituitary-adrenal pathway, which in turn stimulates the pituitary gland to release adrenocorticotropic hormone. Due to the stimulating effect of circulating adrenocorticotropic hormone, glucocorticoids, such as cortisol (primary stress hormone), are produced by the cortex of the adrenal glands. Dehydroepiandrosterone , an endogenous cortisol-regulating hormone, is also released .
Another parallel pathway, the medullary sympatho-adrenal axis , also operates at the same time in the medullary cortex of the adrenal gland, resulting in the release of epinephrine and norepinephrine (together called catecholamines).
Glucocorticoids, including cortisol, exert important suppressive effects, through very specific mechanisms, at different levels. At the molecular level, they inhibit vital functions of inflammatory cells, such as macrophages, neutrophils, eosinophils and mast cells, in functions such as chemotaxis, secretion and degranulation. Immune function can be altered independently by the release of all of these biochemical mediators into the system.
Cortisol is an immunosuppressant and its main effects are on helper T cell responses: it suppresses the production of interleukin-12, the main inducer of type 1 helper T cells; and improves the production of T-helper type 2 cytokines (interleukins 4, 10 and 13), which in turn stimulate the functions of T-helper type 2 cells.
Consequently, cortisol inhibits macrophage antigen presentation and lymphocyte proliferation and differentiation. and a general deregulation of the immune system occurs. Prolonged stress-related stimulation of the hypothalamic-pituitary-adrenal axis suppresses both immune and inflammatory responses and biological adjustments occur.
Behavior changes
Allostatic load reflects the influence of stressful social circumstances and life experiences, as well as behaviors such as smoking, diet, exercise, and alcohol consumption, which have been shown to contribute, in large part, to allostatic load. In fact, unhealthy behaviors are well-known risk factors for periodontal disease and several other health conditions.
However, although stress has been shown to correlate with poor health behaviors, some would argue that the role of behavior in illness has been overemphasized and that health behaviors are mediators of the psychosocial environment in which people live. , more than causes in themselves.
The social and living conditions that generate psychosocial stressors and material limitations determine whether people adopt unhealthy behaviors and whether they have the necessary resources and motivation to take care of their oral and general health. Related to this is the link between the social environment and self-rated health and locus of control for health, which in turn affects one’s ability to change unhealthy behaviors.
Furthermore, since the association between stress and periodontal disease needs to be clarified, prospective studies should take health behaviors into account to determine their contribution to the relationship between stress and periodontal disease.
Allostatic load and periodontal diseases
Several studies have examined the association between allostatic load and specific biological markers of stress, on the one hand, and periodontal diseases, on the other. Bakri et al, using longitudinal data, found that patients with stress indicated by a high level of C-reactive protein and a high Perceived Stress Scale at baseline had worse periodontal outcomes than those with lower levels of stress. The study was hampered by having a small sample.
Another study used a longitudinal design to examine the relationship between socioeconomic position, C-reactive protein (as a stress marker), and periodontitis. However, both C-reactive protein and periodontitis were assessed at the same time point. Almost all other studies used case-control or cross-sectional data. In several studies, an association between salivary cortisol, interleukin-1beta, interleukin-6 and periodontitis was demonstrated. It should be noted here that salivary cortisol is a marker of acute stress and is therefore difficult to determine. verify a possible causal relationship with periodontal disease.
Two well-known studies used a combined variable of different biological markers as indicators of allostatic load, using data from different waves of the National Health Survey.
Sabbah et al14 used an aggregate variable of 7 biomarkers of allostatic load, namely C-reactive protein, fibrinogen, high blood pressure, waist circumference, triglycerides, plasma glucose, and high-density lipoprotein-cholesterol to assess whether stress indicated by Allostatic load mediates the relationship between socioeconomic conditions and each of the periodontal and ischemic heart diseases. The authors found an association between allostatic load and each of the conditions and argued that biological markers of stress possibly mediate the association between socioeconomic position and these health outcomes.
Similarly, Borrell and Crawford argued that a combined variable of allostatic load, which included blood pressure, body mass index, glycated hemoglobin, triglyceride level, C-reactive protein, homocysteine level, total cholesterol level, albumin and creatinine, explains ethnic inequalities in periodontal diseases.
Although these 2 studies used objective indicators of stress (allostatic load) and large, nationally representative samples of the US population, their conclusions do not support temporality.
Conclusions
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