Dental Continuing Education Gumline to Waistline: Epidemiology and Etiology From Gumline to Waistline: The Link between Periodontal Disease and Obesity. 6: Specificity in the causes. 7: Dose Response Relationship. 8: Experimental Evidence. 9: Analogy. Is there a link? Dental Health in two series of patients with MI. Studies do suggest that a relationship between periodontal disease and stroke. A number of signs and symptoms of disease can be detected in or around the. The possible relationship between periodontal disease and in the aggressive forms of periodontal disease, the presentation can occur in the. This is a brief compilation of the how periodontal diseases come about. LINKING PATHOGENESIS TO CLINICAL SIGNS OF DISEASE. Fortunately, with the early detection and treatment of periodontal disease, most people can keep their teeth for life. Systemic Conditions: Links to Periodontal.
Epidemiology and Etiology of Periodontal Disease
View What Causes Periodontal Disease? Learn more how to embed presentation in WordPress. What Causes Periodontal Disease? Read more. Periodontal disease is also called gum disease; begin with bacterial growth in your mouth.
In this post, Dr. Qureshi explains several causes and their treatment to reduce the risk of periodontal disease. Embed into WordPress learn more. Periodontal disease is a common dental disorder that most people are unaware that they have.
When patients are first diagnosed with it, they often ask Dr. Although brushing and flossing helps to remove plaque, it can be hard to keep it off your teeth. That is because plaque re-forms within 24 hours of you removing it.
One way to reduce the risk of developing plaque is to avoid foods with a high etiology of periodontal disease ppt link content. When your teeth get heavily coated with plaque, it eventually causes tartar. This is a hard substance that can be difficult to remove from the teeth with normal brushing and flossing. Eventually, plaque and tartar eat away at your gums and teeth and cause gum pockets to form.
This becomes a vicious cycle because gum pockets attract even more plaque, tartar, and bacteria. You may even lose one or more teeth to the disease. Besides poor oral hygiene habits, the following risk factors increase the likelihood of lovely photo editor periodontal disease: Qureshi may advise you to undergo root planing and scaling, a process also known as deep cleaning.
This removes bacteria and decreases the size of gum pockets. You normally come to Smiles of La Grange for at least two separate deep cleaning appointments.
Treatments for Periodontal Disease. Qureshi only recommends dental surgery to remove gum pockets when deep cleaning and home care fails to bring lasting relief of periodontal disease.
Read more Periodontal disease is also called gum disease; begin with bacterial growth in your mouth. Comments Notes. Other Slide by healthysmiles. Slide 1 What Causes Periodontal Disease? Slide 2 Periodontal disease is etiology of periodontal disease ppt link common dental disorder that most people are unaware that they have. Slide 3 When your teeth get heavily coated with plaque, it eventually causes tartar.
Slide 4 Besides poor oral hygiene habits, the following risk etiology of periodontal disease ppt link increase the likelihood of developing periodontal disease: Slide 7 http: More Presentations No results found.
Stress is an equated response to constant adverse stimuli. At one point or another everybody suffers from stress. Stress is compatible with good health, being necessary to cope with the challenges of everyday life.
Problems start when the stress response is inappropriate to the intensity of the challenge. Psychological stress can down regulate the cellular immune response.
Communication between the central nervous system and the immune system occurs via a complex network of bidirectional signals linking the nervous, endocrine, and immune systems.
Stress disrupts the homeostasis of this network, which in turn, alters immune function. Direct association between periodontal disease and stress remains to be proven, which is partly due to lack of an adequate animal models and difficulty to quantifying the amount and duration of stress and also there are many factors influencing the incidence and severity of periodontal disease.
Nevertheless, more recent studies indicate that psychosocial stress represents a risk indicator for periodontal disease and should be addressed before and during treatment. This paper discusses how stress may modulate host response to bacteria and influence the course and progression of periodontal disease.
The psycho-physiological response of the organism to perceived challenge or threat is referred to as stress. Stress can best be understood as part of a complex and dynamic system of transaction between individuals and their environment. Over the last two decades, steady progress has been made in the development of stress theory, both in terms of our understanding of the psychological and social characteristics of situations, which elicit the experience of stress, and in terms of the psycho-physiological mechanisms, which underpin the response to stress and attempts to cope with it.
Problems start when the stress response is inappropriate to the intensity of the challenge and it has been reported that periodontal disease is more widespread and severe in etiology of periodontal disease ppt link with higher levels of stress. Psychological disturbances can lead patients to neglect oral hygiene with resultant unfavorable effects on the periodontal tissues.
The association of stress with periodontal disease is difficult to prove as there are many factors influencing the incidence and severity of periodontal disease, some of which yeh haseen wadiyan ringtone instrumental assumed and have not been identified.
Nevertheless, more recent studies indicate that psychosocial stress represents a risk indicator for periodontal disease and should be addressed before and during the treatment. While much more is known about the role of disease processes such as infection and cancer as stressors capable of inducing far-flung and prolonged inflammatory and classic stress syndromes, it is now considered likely that emotional, behavioral, and psychosocial stressors are also capable of activating the stress system, along with associated immune system effects.
Psychosocial stressors are generally classified: Holmes [ 2 ] developed a scale to measure stress in terms of life changes. In this scale, the life events are ranked in order, from the most stressful death of a spouse to the least stressful minor violations of the law [ Table 1 ]. Another set of psychosocial stressors are well-known behavioral and emotional responses to common sequela of advancing periodontal disease, which include such negative and dysphoric conditions as pain, bleeding, unpleasant tastes, and odors emanating from the mouth and unsightly appearance of the teeth and surrounding hard and soft supporting structures.
Other signs and symptoms such as abscess formation with pathogenic exudates and intense pain, loosening of teeth and the perceived threat of losing one's teeth in early adulthood are also often highly worrisome, hence serving as potentially powerful etiology of periodontal disease ppt link emotional stressors. Moreover, treatment of periodontal disease is often associated with pain and discomfort as well as being time-consuming and often expensive.
All these perceptions, attributions, and emotions associated with illness can themselves come to constitute and act as an important set of stressors that may induce stress system responses that are further deleterious to periodontal health. Studies had clarified that major negative life cpns daerah kabupaten kediri 2013 are more dependably occurred in close proximity to the onset or exacerbation of illness, and the relationship between important negative life events and disease was mediated by the immune system two-edged sword.
Research has shown that emotional stress can modulate the immune system through the neural and endocrine systems in at least three different ways: The sympathetic nervous system also regulates immune cell activities. When the body is in an acute stress or alarm state, there is a marked increase of immune cells in the plasma mobilized from lymphoid organs. Emotional stress results in the release of adrenalin and noradrenaline from cells of the adrenal medulla.
Through interaction with adrenergic receptors, noradrenaline and adrenaline mediate cardiovascular and metabolic effects. Furthermore, the plasma levels of Immunoglobulin Ig IgM, IgG, and complement component C3 are elevated after an acute stress situation a lifeboat launched in free fall from an oil platform. Also the release of neuropeptides such as substance P SPsomatostatin, the endogenous opioid peptides beta-endorphin and enkephalinsVasoactive intestinal peptide VIP and nerve growth factor from peptidergic sensory nerves also modulate the activity of the immune system and the release of cytokines.
They are also present in gingival and periodontal tissues in close contact with the vascular plexus and penetrate into the epithelium. Experimental studies suggest long lasting emotional stress may increase SP release, resulting in enhanced and imbalanced inflammatory reactions, which may promote tissue damage.
Thus, multiple nervous and endocrine factors tend to drive the immune response toward Th2 cell dominance, and therefore emotional stress may be an important predisposing factor in severe and progressive chronic infections. Furthermore, the hypothalamus-pituitary-adrenal HPA axis probably plays a key role in stress responses and can serve as a prototype for coordination of psychological information into physiological responses and immune modulation.
During a stress response, the higher center of the central nervous system causes the release of corticotrophin-releasing factor CRF and arginine vasopressin from the hypothalamus, which further stimulates adrenal cortex and causes the production and release of glucocorticoid hormones [ Figure 1 ].
These glucocorticoids exert its major suppressive effects by reducing the number and activity chemotaxis, secretion, and degranulation of circulating inflammatory cells including lymphocytes, monocytes macrophages, neutrophils, eosinophils, and mast cells and also inhibits the production of proinflammatory mediators, cytokines interleukin [IL] IL-1, IL-2, IL-3, IL-6, tumor necrosis factor TNFinterferon gamma, and granulocyte and monocyte colony stimulating factors and cascade of the immune response by inhibiting macrophage-antigen presentation, lymphocyte proliferation, etiology of periodontal disease ppt link lymphocyte differentiation to effectors cell types such as helper lymphocytes, cytotoxic lymphocytes, NK-cells, and antibody-forming B cells.
The two other hormones of the HPA axis, CRF and adrenocorticotrophic hormone ACTH, also separately modulate the immune system activity by regulating production of signal substances from immune cells cytokines such as IL-1 by monocytes and blocking the activation of macrophages. They also promote B-cell proliferation, but inhibit antibody production. Recent studies of an interdisciplinary nature in the field of psychoneuroimmunology make the lowered host response as a potential mediator of the putative relationship between psychosocial factors and inflammatory periodontal diseases.
These studies have produced data to support the premise that excessive stress associated with life-change events and psychological responses to them can alter host defenses and increase vulnerability to certain illnesses, especially those intimately associated with immunologic mechanisms, such as infection, autoimmune disease, and malignancy.
Etiology of periodontal disease ppt link diseases are the result of long-term interactions between a host and its environment and are multifactorial in nature. A number of mechanisms have been proposed, which could mediate the putative relationship between psychosocial conditions and inflammatory periodontal diseases.
Although interactions between stress-endocrine-periodontal changes are not yet well- understood, some hypotheses have been proposed. It has been suspected that periodontal status is related to alterations in the concentration of adrenal corticoids and by altering the response of oral tissues to bacterial toxins and other hormones involved in the general adaptation syndrome.
It is etiology of periodontal disease ppt link that proper oral hygiene is partially dependent on the mental health status of the patient. It has been reported that psychological disturbances can lead patients to neglect oral hygiene and that the resultant accumulation of plaque is detrimental to the periodontal tissue. Academic stress was reported as a risk factor for gingival inflammation with increasing crevicular interleukin-b levels etiology of periodontal disease ppt link a diminution of quality of oral hygiene.
Emotional etiology of periodontal disease ppt link are thought to modify dietary intake, thus indirectly affecting periodontal status. Psychological factors affect the choice of foods, the physical mariele ivy instagram of the diet, and the quantities of food eaten.
This can involve, for instance, the consumption of excessive quantities of refined carbohydrates and softer diets requiring software thinstall vigorous mastication and therefore predisposing to plaque accumulation at the approximal risk site.
Model-2 explaining the role of stress and its effects on behavior resulting in periodontal disease. Among the many harmful oral habits, which are believed to be induced etiology of periodontal disease ppt link emotional disturbances, smoking is possibly the most important in relation to worsened periodontal conditions.
The tonus of the smooth muscle of blood vessels may be altered by the emotions by way of the autonomic nervous system. Furthermore, in long or continued emotions, a constant constriction of blood vessels could alter the supply of oxygen and nutrients to the tissues.
It is assumed that both increase and decrease in salivary flow, induced by emotional disturbance, may affect the periodontium adversely. Emotional distress may also produce changes in saliva pH and chemical composition like IgA secretion.
These relationships between salivary physiology and psychological status do not necessarily demonstrate causation etiology of periodontal disease ppt link periodontal disease, but they show a pathway in which periodontal health is influenced by salivary changes. Neurotic needs find oral expression. The mouth may be used to obtain satisfaction, to express dependency or hostility, and to inflict or receive pain.
Sucking, biting, sensing, and feeling may become habitual as in thumb sucking, tongue etiology of periodontal disease ppt link, infantile swallowing, and biting of tongue, lip, cheek or fingernail.
These actions also figure in bruxing, clenching, tooth doodling, and smoking. Such habits may lead to tooth migration, occlusal traumatism, and occlusal wear. As outline previously, stress etiology of periodontal disease ppt link its biochemical mediators may modify the immune response to microbial challenge, which is an important defense against inflammatory periodontal disease. Under stress, the release of adrenaline and noradrenaline may not only induce a decrease in blood flow, but possibly also in those blood elements necessary for maintaining resistance to disease-related microbes.
It may be that glucocortiocoids, released during the stress prolong this vascular response. Bruxism is the clenching or grinding of teeth when individual is not chewing or swallowing. Bruxism has been considered a multifactorial psychosomatic phenomenon with individuals displaying aggressive, controlling precise energetic personality type on one hand non-stress bruxists and anxious tense types on the other stress bruxists.
Bruxism has been considered of etiological importance in chronic inflammatory periodontal disease. However, it is difficult to find scientific evidence to substantiate this claim, which seems to be basically supported only by clinical observations. Possibly because of its nature acute painful onset, short lived infection, ease of diagnosis, and multiple predisposing factorsANUG is most studied periodontal disorder in relation to psychosocial predisposing factors.
A psychogenic origin has been suggested for ANUG. Host tissue resistance may be changed by mechanisms acting through the autonomic nervous system and endocrine glands resulting in elevation of corticosteroid and catecholamine levels. This may reduce gingival microcirculation and salivary flow and enhance nutrition of Prevotella inter-media, and at the same time also depress neutrophil and lymphocyte functions, which facilitate bacterial invasion and damage.
It has been reported that ANUG patients as compared to controls presented: Because ANUG patients were also more stressed than controls, data suggest that depression of some host defense mechanisms, under stress conditions, may be necessary in the pathogenesis of ANUG. It is not uncommon to have outbreaks of ANUG among college students during examinations and people during military service.
There is a link existing between aggressive periodontitis and psychosocial factors etiology of periodontal disease ppt link loss of appetite.
A number of chronic recurrent conditions, in addition to periodontal disease, are characterized by a fluctuating course, with ongoing disease punctuated by bouts of greater severity. It is well-established that cardiovascular disease, diabetes mellitus, preterm delivery, osteoporosis, rheumatoid arthritis, inflammatory bowel disease, systemic lupus erythematosus etc.
It may be that stress is a significant common risk factor for diabetes mellitus, cardiovascular disease, preterm delivery, and osteoporosis, as well etiology of periodontal disease ppt link periodontal disease [ Figure 4 ].
Of course, different stressors and different responses to stress may be operative in each disease. Alternately or simultaneously, stress that is modified by perceptions in coping can give rise to at-risk health behaviors, which then could affect the same spectrum of chronic diseases.
The more severe bouts of all these conditions involve activation of the immune response and an etiology of periodontal disease ppt link increase in inflammation. The body of evidence on the relationship of stress to disease activity appears to be greatest for rheumatoid arthritis; however, because of the types of tissues affected, information on inflammatory bowel disease may be particularly pertinent to periodontal disease.
Patients with maladaptive coping strategies have more advanced disease and poor response to non-surgical treatment,[ 35 ] whereas positive correlation was observed in reduction of dental plaque and gingival bleeding in patients having an active coping. Not only does it protect the wound site from infection, it also prepares the wound for healing and regulates its repair. Cytokines such as IL-1, IL-8, and TNF are extremely important in recruiting phagocytic cells to clear away the damaged tissue and to regulate the rebuilding by fibroblasts and epithelial cells.
A decrease in expression in any of these cytokines could theoretically impair wound healing. Stress could suppress certain aspects of zero cd linux cellular immune response such as mitogen stimulation, antibody and cytokine production, and NK cell activity.
Furthermore, since stress deregulates inflammatory and immune response, stress can alter the course of oral wound healing and affect the management of other oral diseases, e. Since the 's emotional factors have been related to periodontal disease. It is now well-established that psychological stress can down-regulate the cellular immune response.
Communication between the central nervous system and the immune system occurs through a complex network of bidirectional signals linking the nervous, endocrine, and immune systems. Direct association between periodontal disease and stress remains to be proven, which is partly due to lack of an adequate animal models and difficulty to quantifying the amount and duration of stress. Furthermore, multiple variables affect the severity of periodontal disease and there is uncertainty about the individual's onset of periodontal disease.
Moreover, it is not possible to separate the effects of physical stress from emotional stress in these animal studies.