Gingival Disease as a Symptom of Stress

Abstract

Stress has become the health epidemic of the twenty-first century; its burden we faced is due to social and professional pressure (spouse death, marital separation and loss of job). If stress is supposed to help an organism to go through daily issue and particular emotional issues, it can be a source of health damage, when sustained. Negative effects of stress can go from change in life style to cardiovascular events and cognitive disorders. Periodontal health can also be affected. During chronic stress, T helper 2 (Th2) lymphocytes are responsible for promoting the destruction of periodontal tissue. Wrong stress management is characterized by changes in life style like poor oral hygiene, smoking, diet modification and parafunctions. This contributes to increase dental biofilm and worsen periodontitis. The most clinically relevant effects are wound healing and response to periodontal treatment. Suppression of immune response components during stress prevents the elimination of damaged tissues as well as any new tissue buildup. Moreover, peripheral vasoconstriction and low oxygen resulting from excessive catecholamine during stress compromise wound healing and response to periodontal treatment. This highlights the importance of knowledge about psychological state of patients with periodontitis and the need for coping strategies’ improvement in an emotionally stressed patient to expect good response to treatment.

1. Introduction

Stress is a common word used in daily life to describe an emotional state during an adverse condition. It is a scope of changes the body adopts to maintain homeostasis when some events require more resources than those available. In the last few decades, we observed a burden of stress linked to professional and social pressure, so that stress has been named by the World Health Organization (WHO) as the “Health epidemic of the twenty-first century.” If stress is designed to prepare the organism to overcome the threat appropriately, it can be dangerous to the body when sustained.

Since antiquity, authors like Aristotle and Hippocrates were aware of stress and its adverse effects. They hypothesized that psychological factors have a part to play in the development of diseases. Nowadays, there are many evidences showing the implication of emotional stress on impaired cognition, mental diseases, systemic disease involving cardiovascular system, central nervous system (CNS) and endocrine system changes. Some life changes are highly associated with health degradation, on the first line, spouse death and marital separation. These are followed by death of a family member or a close friend and loss of employment or frustration from job.

Periodontal diseases are inflammatory disease triggers caused by bacterial formation called biofilm surrounding the teeth. They are divided into two forms: gingivitis that is superficial and reversible and periodontitis that involves supporting tissue destruction and endup with tooth loss. Modification of periodontal health results from desequilibrium between normal oral microorganism colonizing tooth surfaces near gingival margins and the host response. Even if bacteria are known to be the triggers, exacerbated host defense mechanisms seem to be responsible for progressive periodontal tissue damage. Systemic diseases, tobacco use, age and psychological stress are risk factors for periodontal diseases.

Many studies have found that emotional or psychological load (stress) can alter periodontal health directly through a biological mechanism or indirectly by promoting changes in life style. Immune activities during stress can be modulated directly through neurotransmitters or neuropeptides and/or indirectly through hormones. This leads to the conclusion that stress can influence the progression and course of gingivitis and periodontitis. New research provides evidences that there is a network connecting the immune system and the neuroendocrine system, so that products released after the perception of a “stressor” can influence immune response and progression/outcome of diseases like infectious diseases.

This chapter aims to present how stress can disrupt periodontal health, leading to an inflammation state of these tissues and compromising periodontal treatment outcomes. This susceptibility to periodontal events in the presence of psychological stress could have a predictive value for other systemic accidents.

2. Stress

2.1 What is stress?

Studies on stress have started early in antiquity with Aristotle and Hippocrates. Later, Claude Bernard and Walter Bradford Cannon, respectively, from France and the USA explored the normal conditions to provide a steady state and homeostasis. Cannon goes further to describe the response to threat, introducing the concept of “fight or flight.” This concept is an acute stress response observed in animals when they are facing a threat. Acute stress response is under sympathetic nervous system (SNS) influence, which provokes an animal to fight or flight. According to Hans Selye, acute response is the first step of what he called General Adaptation Syndrome (GAS), a universal stress response of vertebrates [1].

Hans Hugo Bruno Selye, known as the father of stress research, was the first to introduce the word stress and to provide a simple and general definition of stress: “stress is the non specific response of the body to any demand” [1].

According to Richard S. Lazarus: stress is a condition or feeling experienced when a person perceives that “demands exceed the personal and social resources the individual is able to mobilize.” Therefore, psychological stress is not physical, it is not a pain but the biological response to a “stressor” [1].

Not all types of stress are harmful, stress can be

• Pleasant = good stress or eustress: it comes from funny, motivating or exciting stressor lying in joyful events like birth, wedding or anniversary. This stress is of benefit to the body as it restores energy and improves strength, cognitive and cardiac functions.

• Unpleasant = bad stress or distress: is related to spouse or child death, loss of job or financial issues. This kind of stress has a negative impact on body, mood and performance and results in mental and physical issues. It constitutes the purpose of this chapter.

For both situations, the body always needs to adapt and bring the human back to a peaceful state. Therefore, stressant situation is inevitable because “it is not what happens to you but how you react to what happens”.

2.2 What is the physiology of stress?

Response to stressors in humans is not a stereotype, it takes into account factors associated with the stressor (type, intensity, duration) and factors associated with the host (gender, age, mental health, medical history). The General Adaptation Syndrome (GAS) developed by Hans Selye is a response to stress model made of three steps:

• Alarm is the step corresponding to the fight or flight response. Stress-induced hormones, such as cortisol, adrenaline and noradrenaline, are released to prepare the body either to fight the threat or to escape from it. At this stage, some parameters like heart rate, blood pressure, sudation or blood sugar can be raised.

• Adaptation: when the stressor effect is sustained, the body keeps secreting hormones to adapt to the situation. This is characterized by physical dysfunctions (indigestion, sleep problems, infections, tiredness …), emotional and cognitive impairment (loss of memory, irritability…) as well as life style changes (starting or increased smoking and drinking, reduced oral hygiene).

• Exhaustion or recovery: recovery comes when the body succeeds to overcome the stressor, whereas exhaustion stage results from the failure of the body to maintain normal functions. A long duration of exhaustion stage is responsible for long-term effects of stress, such as hypertension, cardiac diseases and mental illness.

2.3 Physiopathology of stress

Perception of the threat or stressor triggers a stress response that can lead to homeostasis recovery or an exhaustion stage with body damages. Three systems are involved in this response: nervous system, endocrine system and immune system [2, 3]. We will briefly describe the nervous system, endocrine system and the immune system that is the one closely related to disease onset.

In the brain, the perception of a real or imaginary stressor leads through hypothalamus or “seat of emotion” to the activation of autonomic nervous system, secretion of corticotrophin-releasing hormone (CRH) and vasopressin or antidiuretic hormone. The autonomic nervous system consists of sympathetic nervous system and parasympathetic nervous system. SNS is responsible for the release of catecholamines in the fight or flight response with all acute stress symptoms (increased ventilation, heart rate, pupil dilatation, slow digestion), whereas parasympathetic nervous system is involved in relaxation.

Pituitary, adrenal and thyroid glands are the main glands involved in stress, while hypothalamus releases CRH that directly acts on the pituitary gland, also called “master gland”, to induce adrenocorticotropin hormone (ACTH) release. These hormones trigger the release of corticoids (mineralocorticoids and glucocorticoids) at the level of adrenal cortex (Figure 1). Glucocorticoids promote energy release by glycogenolysis and lipolysis as well as depression feeling, appetite and immune system suppression. Mineralocorticoids increase blood volume through sodium ion (Na+) retention. The adrenal medulla reinforces the effect of the sympathetic nervous system by releasing catecholamines (epinephrine and norepinephrine). It therefore appears that effects of catecholamines from SNc constitute immediate effects of stressor when effects of adrenal medulla’s catecholamines are intermediate effects.

Figure 1.

Physiological response to stress [2].

Adrenocorticotropin hormone (ACTH), vasopressin and thyroxine because of their long half-lives and the reactions they trigger are responsible for the prolonged effects of stress. These hormones raise three biochemical pathways corresponding to physiological axis:

• Adrenocorticotropin hormone (ACTH) axis: also called the hypothalamo-pituitary-adrenal (HPA) axis starts, as we have seen before, with CRF releasing from hypothalamus and ends with cortisol and aldosterone releasing by adrenal glands. In a normal situation, these hormones increase body metabolism and regulate blood pressure. However, when excreted in high levels as in chronic stress period, their effects can be life threatening.

• Vasopressin axis: vasopressin is responsible for fluid loss regulation through the urinary tract. Under normal conditions, vasopressin has a great effect on blood pressure regulation, as it can increase or decrease blood volume to restore physiological homeostasis. However, in case of chronic stress, vasopressin kept increasing blood pressure, even in resting state, causing hypertension.

• Thyroxine axis: thyrotropic hormone (TTH)-releasing factor is released by hypothalamus and stimulates thyrotropic hormone to be secreted by the pituitary gland. At the level of thyroid gland, TTH stimulates the synthesis of hormones aimed to increase basal metabolic rate or overall body metabolism. These pathways have very prolonged effects, leading to gastritis, heart attack, cerebral excitivity or cerebration associated with insomnia/anxiety.

Perception of the stressor can also induce a stress-related inflammatory state. In fact, emotional and psychological stress is a type of “alarmin” that produces a “sterile” inflammation. Alarmin or danger-associated molecular patterns (DAMPs), along with pathogen-associated molecular patterns (PAMPs) when binding to Toll-like receptors (TLRs) of immune cells, can induce synthesis of pro-inflammatory cytokines. These cytokines are signaling molecules that transmit information between immune cells and between immune system, the brain and endocrine system [4]. Cytokines like interleukin 1 beta (IL-1β), interleukin 6 (IL-6) and tumor necrosis factor are involved in stress-associated state of chronic inflammation.

Immune system and central nervous system are highly connected and involved in the impact of stress on disease onset and evolution. Immune system is made of many organs that work together to produce various potent immune cells. Bone marrow is the stem cells producer and the B-lymphocytes manufacturer. The thymus is the place where stem cells mature to become T-lymphocytes. The secondary lymphoid organs: lymph nodes, spleen, tonsils and the gut-associated lymphoid tissue or Peyer’s patches where T-cells and B-cells are stocked for further migration toward target organs. It has been shown that during response to stressors, central nervous system and endocrine system modulate the immune system through three ways:

• The way of autonomic nervous system

• The release of hypothalamic and pituitary hormones

• The release of neuropeptides

All the tissues of immune system are innervated by sympathetic nerve fibers that release adrenaline. Adrenergic receptors are found on cells of the immune system so that adrenaline released from sympathetic nerve fibers and adrenal medulla can promote T-cells differentiation and maturation, cytotoxic T-cells growth and antibodies production from plasma cells.

The hypothalamus-pituitary-adrenal (HPA) axis ends up with the production of glucocorticoids (cortisol). These glucocorticoids have a biphasic effect on the immune response. Initially, after stressor perception, excreted glucocorticoids will inhibit T-cells and macrophages development. But a sustained secretion of glucocorticoids leads to immune response stimulation. Glucocorticoids’ function is to suppress acute stress response and immune response.

The CRF acts on immune cells to induce production of cytokines like interleukin-1 (IL-1) from monocytes. It also enhances the multiplication of T-cells, promotes the release of interleukin 2 (IL-2), and helps in the upregulation of IL-2 receptors of helper T-cells.

The ACTH promotes B-cell proliferation while inhibiting antibody production. It also blocks the activation of macrophages by interferon-gamma (IFN-γ) through the inhibition of IFN-γ production by T-cells and inhibition of the expression of IFN-γ receptors on macrophages.

Neuropeptides, such as substance P (SP), somatostatin, nerve growth factor (NGF), vasoactive intestinal peptides (VIPs), enkephalines and beta-endorphin released from peptidergic nerve fibers, have a modulatory effect on immune response and cytokines releasing.

2.4 Impact of stress on the body

The way we perceive life events modifies the inner composition and functions of the body. The way we respond to this perturbation can affect our physical and mental health. The effects depend on genetic and anthropometric characters as well as past experience of the host and are mainly due to corticoids and adrenaline.

Some of these effects are listed below:

• On cardiovascular system: adrenaline is the first mediator of cardiovascular events during stress. Cortisol and aldosterone play a role in fat accumulation and high blood pressure, respectively. This causes coronary heart disease, obesity and hypertension.

• On digestive system: stressed people usually exhibit acid reflux, diarrhea or constipation and disturbed eating and/or drinking habits.

• On immune system: acute stress induces short-term inflammatory effects through adrenergic mechanisms and chronic stress is associated with low-grade inflammation.

• On reproductive system: glucocorticoids act negatively on reproductive axis by reducing secretion of reproductive hormones (gonadotropin-releasing hormone (GnRH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), estradiol, progesterone and testosterone). This causes decreased libido, erectile dysfunction and poor sperm production in man, dysmenorrhea and other menstrual cycle irregularities in woman as well as sexual dysmorphism and autoimmune disorders in both male and female.

• On others: people living in stressful environment can experience smoking, alcohol consumption and other addictions. Cognitive function and mood can also be affected leading to memory loss, depression, irritability, anxiety and insomnia.

3. Impact of stress on periodontal tissue

Periodontal diseases are made of gingivitis and periodontitis, disease initiation and progression are triggered by an imbalance between oral bacteria and host response. The evolution of the disease is controlled by many risk factors, and stress is one of them. Bhagat et al. agree to say that: “the issue facing us is no longer whether the psyche influences immune cell activities, but rather how influence the development of chronic infections such as gingivitis and periodontitis” [5]. Psychological stress increases the susceptiblity to periodontal diseases by modifying the response of periodontal tissue to bacterial invasion, the healing potential of periodontal lesions and the composition of oral microbiome. Stress is also a risk factor of diabetes and induces smoking, poor oral hygiene habits, which are related to increase periodontal diseases’ incidence (Figure 2).

Figure 2.

Biological mechanism and behaviors linking stress and periodontal disease [6].

3.1 Effect on immunity

Before knowing how stress can modify immune response in periodontal tissue, it is necessary to go back to fundamentals about immune mechanism and inflammatory response in periodontal disease. Inflammation in periodontal tissue is a physiological defense mechanism against microbial assault. So in the presence of supra- or subgingival plaque, we observe gingival inflammation. When plaque is removed, we return to homeostasis but if the lesion persists it turns into periodontitis. Periodontal tissue protection consists of mechanical barrier, here epithelial cell, saliva that contains antimicrobial agents like lactoferrin, lysozyme, peroxidases, and agglutinins. There are others agents called secretory immunoglobulin A which specifically fight bacteria in gingival or periodontal pockets. They constitute the main antibacterial substance in a healthy mouth. Their actions include: bacterial enzyme activity modulation, bacterial agglutination and inhibition of adherence to epithelial cells and teeth.

Immuno-inflammatory events in case of epithelial barrier breakdown are not a continuous process, there are overlapping but two responses that are classically described: innate immune response and adaptive immune response. During innate immune response, pattern models are recognized by pattern recognition receptors (PRRs) including TLRs at the surface of antigen-presenting cells. This stimulates cytokines, chemokines and antimicrobial peptides releasing, activation of complement system and recruitment of neutrophils, lymphocytes and monocytes. The innate immune response signs are inflammation signs. Activation of T- and B-cells mediated by cytokines’ interaction with their receptors triggers acquired immunity. T-cells express on their surfaces CD4+ and CD8+ molecules. CD4+ molecules are also called T-helper cells and are divided into T-helpers 1, T-helpers 2, T-helpers 17 and regulatory T-cells (Tregs). T-helpers 1 secrete interleukin-2 and interferon-γ which act to enhance cell-mediated response, whereas T-helpers 2 secrete interleukin 4, 5, 6 and 10 (IL-4, -5, -6 and -10), which promote B-cell development and increase humoral immune response [7].

In normal state, there is equilibrium between T-helpers 1 and T-helpers 2, but if T-helpers 1 are activated, the IFN-γ they secrete will shut down the expression of cytokines by T-helpers 2, on the same hand, when T-helpers 2 are activated, interleukin 10 (IL-10) downregulates T-helpers 1 response. Dysregulation of this balance can predispose to severe periodontal issues.

It has been stated that psychological stress is an immunosuppressant but when analyzing their effect it seems that there are two phases depending on the duration of the stressor-induced stimulation. In case of acute stress or alarm state, immunoglobulin M (IgM), immunoglobulin G (IgG), complement component 3 (C3), CD4+ T-cells, CD8+ T-cells and natural killer (NK) cells’ plasmatic levels are increased, but after 1 h they come back to their normal ranges. Lymphoid tissues are innervated by sympathetic noradrenaline transmitting nerve fibers and peptidergic sensory nerves. By increasing the secretion of adrenaline and neuropeptides, the stress situation contributes to influencing immune cells’ recruitment, inducing an inflammatory state in gingiva and promoting periodontitis [5, 8].

3.2 Effect on wound healing

Failure to overcome stressant situation is related to increased incidence of advanced periodontal diseases and poor response to non-surgical periodontal treatment in the host. This can be the result of an increased susceptibility to the disease and an impaired wound healing. This will be discussed in the last section on stress and response to periodontal treatment.

3.3 Effect on microbiome

Since many decades, the genesis of periodontal disease has been linked to the modification of biofilm composition for the benefit of species like Porphyromonas gingivalis, Prevotella intermedia and Aggregatibacter actinomycetemcomitans. The concept of microbial endocrinology explores the ability of some bacteria to recognize stress-induced hormones and use them to enhance pathogens’ growth. This leads to a breakdown in biofilm composition. The case of adrenaline and noradrenaline has been well illustrated in in vivo and in vitro studies. From Paudel et al.’s review on the effect of psychological stress on oral–gut microbiota, it appears that noradrenaline decreases the growth of P. gingivalis and A. actinomycetemcomitans and promotes the growth of Actinomyces naeslundii, Actinomyces gerenscseriae, Eikenella corrodens and Campylobacter gracilis (2022). Moreover, noradrenaline reduces the production of an auto-inducer while increasing the expression of genes of a major virulence factor of P. gingivalis called protease arg-gingipainB [9].

3.4 Effect on behaviors

3.4.1 Poor oral hygiene

Stress and psychological disorders have been reported to be associated with neglected oral hygiene and high plaque index.

3.4.2 Smoking

Nicotine has a damaging effect on periodontium, and it induces a noradrenaline and adrenaline-mediated vascular constriction, reducing blood and nutriments’ support to periodontal tissue. It also exhibits the inhibition of neutrophils oral function. This explains why smokers have the greater frequency of severe periodontal disease and the less favorable response to periodontal treatment.

3.4.3 Diet modification

Dietary habits are highly modified by emotional conditions. This includes a high consumption of refined carbohydrates and softer diet that predispose to biofilm accumulation at proximal sites.

3.4.4 Parafunction

Parafunction is a repetitive behavior that targets the oral structures that include digit sucking, tongue thrusting, bruxism, mouth breathing and nail biting. Their apparition can be subsequent to exposition to a stressor. They usually result in tooth mobility or migration and occlusal trauma that aggravate periodontitis.

Bruxism corresponds to repetitive, involuntary and unconscious masticatory movements and grinding (and/or tightening) of teeth, with no functional purpose, and is associated with an abnormal tooth position and jaw muscle discomfort. According to Vlăduțu et al. [10], it can be considered like a marker of chronic stress.

4. Evidences

4.1 Association between periodontal parameters and blood/salivary levels of stress-related markers

Many stress-related markers with biological properties that may influence periodontal disease development have been found in saliva [4, 11]:

• Cortisol, which reflects hypothalamic-pituitary-adrenal (HPA) axis activity, can be detected in blood, saliva and gingival crevicular fluid (GCF). This hormone is an anti-inflammatory substance and an immunosuppressant, which inhibits T-lymphocytes formation and suppresses natural killer cells or macrophages function.

• α-Amylase is one of the major salivary enzymes and it is an indirect indicator of the function of the autonomic nervous system (ANS).

• Secretory immunoglobulin A [12].

• Catecholamines (dopamine, norepinephrine and epinephrine) are synthesized and released by noradrenergic neurons. They are the most important substances displaying information from the central nervous system to the immune system. They are involved in the suppression of lymphocytes proliferation, suppression of antibody production and cytolytic activity as well as pro-inflammatory cytokines inhibition (interleukin-2, interleukin-6 (IL-6), interleukin-12 (IL-12), tumor necrosis factor-α and interferon-γ).

• Neuropeptides involved in neurogenic inflammation are mainly represented by substance P and vasopressin. Substance P plays a role in the initiation and maintenance of inflammation and limitation of transforming growth factor-β (TGF-β) and interferon-γ-activated macrophages.

4.2 Association between periodontal disease and stress

Gingival inflammation and periodontitis have been associated with psychological stress in different populations. This association was evocated in 1983 and exploration of the relationship between periodontal destruction and stress has permitted to find that poor coping strategies are related to periodontal inflammation [13, 14]. Islam et al. [15] have evaluated the influence of occupational stress and coping style on periodontal disease in Japanese workers. They found that workers with periodontitis were different from those without periodontitis in terms of body mass index (BMI), smoking status, daily alcohol consumption and stress-coping style. Workers with periodontitis presented high stress-low coping condition compared to non-periodontitis workers. A logistic regression analysis allows them to found that high stress-low coping condition is associated with periodontitis in Japanese workers. In the same year, Goleli et al. evaluated the effects of academic stress on periodontal tissues. They compared the periodontal parameters of a group of students before, during and after exam period and their results showed that gingival index, sulcus bleeding index and gingival crevicular fluid flow rate changes between exams period and after exams were significant [16]. A cross-sectional multicenter study was performed in four cities in France in 2017 to identify the main factors related to self-reported gingival bleeding [17]. It revealed that population of patients with higher severe anxiety have a higher self-reported gingival bleeding frequency compared to those with no or moderate anxiety. Gingival bleeding is known to be the clinical sign of periodontal inflammation. It can occur during gingivitis, necrotizing ulcerative gingivitis/periodontitis, acute periodontitis and chronic periodontitis.

Those studies show that stress promotes gum inflammation and severe periodontal tissue destruction. Chronic stress results in the chronic production, but a low-grade state of inflammatory factors is called low-grade inflammation. This is the great connector between non-communicable diseases like cardiovascular disease, obesity, diabetes and depression which, in turn, are related to periodontitis.

4.3 Stress and response to periodontal treatment

The aim of periodontal treatment is a periodontal healing based on probing pocket depth (PPD) reduction, probing clinical attachment level (CAL) maintenance and suppression of gingival inflammation. Stress seems to have an impact on periodontal healing with a high rate of non-surgical periodontal treatment failure. This can be the result of impaired wound healing triggered by stress and behavioral changes it induced. Wound healing involves the elimination of damaged tissue by immune cells and new tissue building up by epithelial cells and fibroblasts. By suppressing some components of immune response as natural killer cells activity, antibody and cytokine synthesis, stress could modify the wound healing process and affect the management of periodontal disease [5, 18].

Additionally, the excess levels of catecholamines result in a peripheral vasoconstriction and low oxygen, which compromise wound healing. Figure 3 and Table 1 illustrate the effect of stress on wound healing, with a mention that the stress-induced modifications in life style or behavior can also alter healing potential of periodontal tissue. For example, poor oral hygiene due to stress promotes oral biofilm growth, even after a well-performed non-surgical periodontal treatment. Stress-induced smoking habits impair collagen synthesis and increase matrix metalloproteinase (MMP) level in a wound. Disturbed sleep is also a risk factor of wound healing impairment because of the reduction in growth hormone level it can cause.

Figure 3.

The effects of chronic stress axes on the periodontium and wound healing. The three axes involved in chronic stress include the hypothalamic-pituitary-adrenal axis (HPA). Behavioral axis, and adrenergic axis (neurovascular). Concomitant aberrance to homeostasis via these three mechanisms result in diminished wound healing capacity and susceptibility to progressive periodontal/peri-implant disease [17].

Health-impairing behaviors

Pathophysiological effects

Poor oral hygiene; Increased consumption of cigarettes; Increased alcohol consumption; Forgetfulness and difficulty concentrating; Disturbed sleeping patterns; Poor nutritional intake

Higher glucocorticoid levels (cortisol) and higher catecholamine levels (epinephrine and norepinephrine), which may lead to any or all of the following: Hyperglycemia, which may impair neutrophil function and impair the initial phase of wound healing; Reduced levels of growth hormone, which may downregulate the tissue repair response; Altered cytokine profiles, which may affect the recruitment of cells important to wound remodeling, such as macrophages and fibroblasts; Reduced tissue matrix metalloproteinase (MMP) levels, leading to impaired tissue turnover and reduced wound remodeling; Decreased natural killer cell levels, reducing the host ability to mount an appropriate immune response to periodontal pathogens; Altered Th1/Th2 ratio, leading to an increased susceptibility to periodontal disease

Table 1.

Mechanisms by which stress may affect periodontal wound healing [7].

Th1, T helper 1 cell; Th2, T helper 2 cell.

When evaluating the influence of psychological stress on non-surgical periodontal treatment outcomes in patients with severe chronic periodontitis, it has been found that worsened periodontal outcomes are observed in patients with increased stress, anxiety and depression scores as well as those exhibiting negative coping strategies [19]. Coping behaviors refer to measures or strategies adopted to respond to stress in order to reduce or overcome it. Recently, in a short-term (3-month) evaluation of the impact of psychological stress and coping behaviors (ignoring or denying the problems, canceling plans, procrastinating, alcohol consumption smoking…) on clinical response to non-surgical periodontal therapy (NSPT), Romano et al. [20] found that psychosocial stress and avoidance coping strategy seem to negatively influence full-mouth bleeding score (FMBS), mean probing pocket depth (PPD), the number of residual pathological pockets and full-mouth plaque scores (FMPS). Poor coping strategies are therefore a rick factor of poor response to periodontal treatment.

5. Conclusion

Relation between stress and periodontal disease is the domain of psychoneuroimmunology. The three systems involved are responsible for gingival inflammation, advanced periodontal tissues’ destruction and poor response to periodontal treatment. Stress indirectly influences the onset and the course of periodontitis by promoting changes in behavior and inflammation-modulated diseases like diabetes, which are periodontal disease risk factors. In a clinical context, it is now possible to understand sudden gingival bleeding, swelling and pain on previously healthy periodontal sites, steady periodontal pockets or persistent bleeding and pockets after well-performed NSPT. Acute periodontal destruction in response to psychological stress becomes a complex entity, whose management depends on psychological dispositions of the host. In that case, if periodontal healing is expected, it could be interesting in collaboration with other professionals to detect the stressor and explore the ways to improve coping strategies of the patient.