Group 8 - Stress
E-facilitator: Sophie

Learning outcomes:
Describe the effects that stress has on the body.
Present a poster on an analysis of why stress is considered as a risk factor for the development of periodontal disease.




Table of Contents:

What is Stress?
Definitions - stress, stressor

Acute Stress
The brain’s response to acute stress
Response by the heart, lungs and circulation to acute stress
The immune system’s response to acute stress
The acute response in the mouth and throat
The skin’s response to acute stress
Metabolic response to acute stress
The relaxation response: the resolution of acute stress

Chronic Stress
Definition
General adaptation syndrome

What is Periodontal Disease?
Definition
Necrotising Ulcerative Periodontitis Vs. Chronic Periodontitis
Epidemiology of Periodontal Disease: the role of bacteria
The role of stress in the initiation and exacerbation of Periodontal Disease



Reference List




What is Stress?

Stress: The pattern of specific and non-specific responses an organism makes to stimulus events that disturb its equilibrium and tax or exceed its ability to cope

Stressor: An internal or external event or stimulus that forces an individual to adapt and induces stress (http://www.helpguide.org/mental/stress_signs.htm)



Acute Stress:

The best way to envision the effect of acute stress is to imagine yourself in a primitive situation, such as being chased by a bear.


The Brain's Response to Acute Stress
In response to seeing the bear, a part of the brain called the hypothalamic-pituitary-adrenal (HPA) system is activated.
Release of Steroid Hormones and the Stress Hormone Cortisol. The HPA systems trigger the production and release of steroid hormones ( glucocorticoids ), including the primary stress hormone cortisol . Cortisol is very important in organizing systems throughout the body (including the heart, lungs, circulation, metabolism, immune systems, and skin) to deal quickly with the bear.
Release of Catecholamines. The HPA system also releases certain neurotransmitters (chemical messengers) called catecholamines , particularly those known as dopamine , norepinephrine , and epinephrine (also called adrenaline).
Catecholamines activate an area inside the brain called the amygdala , which appears to trigger an emotional response to a stressful event. In the case of the bear, this emotion is most likely fear.
Effects on Long- and Short Term Memory. During the stressful event, catecholamines also suppress activity in areas at the front of the brain concerned with short-term memory, concentration, inhibition, and rational thought. This sequence of mental events allows a person to react quickly, either to fight the bear or to flee from it. It also interferes with the ability to handle difficult social or intellectual tasks and behaviors during that time.
On the other hand, neurotransmitters at the same time signal the hippocampus (a nearby area in the brain) to store the emotionally loaded experience in long-term memory. In primitive times, this brain action would have been essential for survival, since long-lasting memories of dangerous stimuli (such as the large bear) would be critical for avoiding such threats in the future.



Response by the Heart, Lungs, and Circulation to Acute Stress
The stress response also affects the heart, lungs, and circulation:
· As the bear comes closer, the heart rate and blood pressure increase instantaneously.
· Breathing becomes rapid, and the lungs take in more oxygen.
· The spleen discharges red and white blood cells, allowing the blood to transport more oxygen throughout the body. Blood flow may actually increase 300 - 400%, priming the muscles, lungs, and brain for added demands.



The Immune System's Response to Acute Stress
The effect on the immune system from confrontation with the bear is similar to organizing a defensive line of soldiers to potentially critical areas. The steroid hormones reduce the activity in parts of the immune system, so that specific infection fighters (including important white blood cells) or other immune molecules can be repositioned. These immune-boosting troops are sent to the body's front lines where injury or infection is most likely to occur, such as the skin and the lymph nodes.



The Acute Response in the Mouth and Throat
As the bear gets closer, fluids are diverted from nonessential locations, including the mouth. This causes dryness and difficulty in talking. In addition, stress can cause spasms of the throat muscles, making it difficult to swallow.



The Skin's Response to Acute Stress
The stress effect moves blood flow away from the skin to support the heart and muscle tissues. This also reduces blood loss in the event that the bear causes a wound. The physical effect is a cool, clammy, sweaty skin. The scalp also tightens so that the hair seems to stand up.



Metabolic Response to Acute Stress
Stress shuts down digestive activity, a nonessential body function during short-term periods of hard physical work or crisis.



The Relaxation Response: the Resolution of Acute Stress
Once the threat has passed and the effect has not been harmful (for example, the bear has not wounded the human), the stress hormones return to normal. This is known as the relaxation response. In turn, the body's systems also return to normal.

Chronic Stress:

A continuous state of arousal in which an individual percieves demands as greater than the inner and outer resources available for dealing with them.

General Adaptation Syndrome:
Hans Selye, a Canadian endocrinologist, investigated the effects of severe stress and the adaptive response of organisms. He developed the General Adapation Syndrome, which describes stages of resistance to stress.

After being exposed to a stressor, the body's resistance is diminished until the physiological response returns it to the normal level. If the stressor continues, resistance to the particular stressor increases but drops for other stressors. The adaptive resistance returns the body to its normal level of functioning. Following prolonged exposure to the stressor, adaptation breaks down, stressor effects are irreversible and the individual becomes ill.

General Adaptation Syndrome: Physiological Response to Stress
Stage I:
  • Alarm Reaction
  • Enlargement of adrenal cortex & lymphatic system
  • Increase in hormone levels, epinephrine release
  • Greater susceptibility to illness & increased intensity of stressor

Stage II: Resistance
  • Shrinkage of adrenal cortex, lymph nodes return to normal size, hormone levels sustained
  • High physiological arousal
  • Counteraction of parasympathetic branch of ANS
  • Heightened sensitivity to stress

Stage III: Exhaustion
  • Dysfunction of lymphatic structures
  • Increase in hormone levels and depletion of adaptive hormones
  • Affective experience, often depression
  • Illness, including periodontal infection & disease

(This table adapted from Gerrig & Zimbardo 2005, p.410)






What is Periodontal Disease?

Periodontal Disease: Chronic bacterial infection of gingiva and surrounding periodontal tissue; caused predominantly by bacterial plaque and calculus and can be worsened by smoking, smokeless tobacco, genetic predisposition, pregnancy, puberty, stress, poor nutrition, diabetes mellitus, and other systemic diseases. Immunologic reactions are also involved. (Stegman, 2007 pp. 416).



Necrotising Ulcerative Periodontitis Vs. Chronic Periodontitis

There are several forms of periodontal disease for which stress can be a systemic risk factor for. This includes Necrotising Ulcerative Periodontitis which can progress rapidly from ulcerative gingivitis, and Chronic Periodontitis, which develops over a number of years. The bacteria involved in these two types of periodontal disease are different, and they can present differently clinically as well. Ulcerative periodontitis, or NUP (necrotising ulcerative periodontitis) stems from necrotising ulcerative gingivitis (NUG) and both diseases can be present at the same time. The disease begins with ulceration and eventual destruction of the gingiva (often the interdental papilla is the initial site of destruction) with consequent alveolar bone loss. Pocket probing depths are usually shallow as the gingiva and periodontium are destroyed simultaneously (Wolf & Hassell, 2006). Chronic periodontitis usually progresses from pre-existing plaque-induced gingivitis and can also include gingival shrinkage, which can sometimes occur in sub-acute stages of the disease. Symptoms of periodontal disease include gingival shrinkage or swelling, pocket activity (bleeding, exudates, and pus), pocket or furcation abscess, fistula, tooth migration and tipping, tooth mobility and eventual tooth loss.


The above image (www.perio.org) depicts the changes from a healthy periodontium to a diseased periodontium.





Epidemiology of Periodontal Disease: the role of bacteria

Under normal circumstances there are many different species of bacteria found in the oral cavity. Bacteria which are linked to periodontal diseases are called periodontopathic bacteria (Wolf & Hassell, 2006). Numbers of these harmful bacteria can be controlled with a combination of good oral hygiene and a healthy immune system. However, their growth can be facilitated by excessive plaque accumulation in conjunction with several risk factors, including stress and smoking, which are proven to compromise the immune system's response to infection. In high risk individuals, a predominance of periodontopathic bacteria, such as spirochetes, fusiforms, P. intermedia and sometimes Selenomas and Porphyromonas in NUP; and P. gingivalis, P.intermedia, Fusobacterium nucleatum and A. actinomycetemcomitans in chronic periodontal disease (Wolf & Hassell, 2006) can initiate the progression of the disease. These harmful bacteria form secondary colonies and compete with less destructive bacteria to begin the process that leads to gingivitis and eventually periodontitis.

Periodontal disease progresses further as pockets around the root of the tooth form as a result of bone resorption. This process is termed attachment loss (Wolf & Hassell, 2006). Severe attachment loss around molar teeth can result in furcation involvement, where the root trunks of the teeth become exposed. These sites (pockets and furcations) are favourable sites for the proliferation of bacteria and can further destroy the periodontium and increase the severity of the disease.

The micro-organisms present in plaque release chemicals called cytokines and interleukins, which trigger the immune system to respond to infection by mobilizing fibroblasts (connective tissue cells), mast cells and white blood cells (macrophages, monocytes and lymphocytes) to the site of infection. The mast cells, which are found in connective tissue, release chemicals including histamine, which causes dilation and increased permeability of the surrounding capillaries, allowing more neutrophils and macrophages to move from the blood into the damaged tissues (Campbell et al, 2006). Activated macrophages then release chemicals, including prostaglandins, which promote blood flow to the site of infection. The increased local blood supply causes a normal inflammatory response in the surrounding tissue and aids in the elimination of the pathogens. The inflammatory response is what causes swollen gums, erythema (redness) and sometimes pus. The vascular changes deliver microbial proteins and clotting factors to the site. Blood clotting prevents the movement of pathogens to other parts of the body, and also aids in the repair of the damaged tissues (Campbell et al, 2006). The following image, from www.biol.andrews.edu, depicts the inflammatory response to a pin-prick, but the methods of pathogenic invasion are similar to that of gingivitis and periodontitis.


One cytokine signals the production of enzymes called matrix metalloproteinases. These enzymes break down collagen in the tissues surrounding teeth. Collagen is a fibrous material that is a constituent of bone, cartilage and connective tissue. Its destruction produces deep pockets in between teeth and gums and eventually destroys the structures that hold teeth in place.

Chemicals produced by the micro-organisms and affected tissues can have an effect on the osteoblast and osteoclast activity in the periodontium. These chemicals include cytokines and interleukins, specifically IL-1 and IL-6, which are produced by host cells as part of the inflammatory response. These chemicals induce the osteoblasts (bone forming cells) to produce the lipid mediator Prostaglandin E2 (PGE2). This chemical then stimulates the production of adenylate cyclase which ultimately supports osteoclast formation (bone resorbing cells) (Inada et al, 2006). This process is key to the progression of bone resorption associated with inflammation.





The role of stress in the initiation and exacerbation of periodontal disease:

As previously discussed, stress can adversely affect the immune system, placing individuals with high stress levels at risk of local and systemic infections as a result of suppressed immune function. Stressed individuals may possess less than ideal personal oral hygiene habits, and this can allow plaque to accumulate within the oral cavity and cause gingivitis, the common pre-cursor to periodontal disease. Specifically, stressed individuals may not rate oral hygiene high on their list of priorities, brushing technique and regularity may suffer as a result of stress and these lapses in effective oral hygiene can result in flourishing oral micro-flora and the development of plaque-induced gingivitis. Stressed individuals may also experience problems with clenching and bruxism, which can place further pressure on the periodontal ligament and aggravate any existing mobility from periodontal disease (Heasman & Millett, 1996). An important consideration to make is the fact that many psychosocial and stress disorders are frequently treated with psycho-pharmaceutical drugs, with side effects such as reduced salivary secretion (Axelsson, 2002). The decreased saliva flow may allow bacterial colonies to flourish more readily.



References

American Academy of Periodontology 2003, Oral Health Information for the Public, AAP, viewed 2 October 2007,
<http://www.perio.org/consumer/proto2/healthygums.htm>.

Andrews University, Department of Biology 2007, Chapter 43: The Immune System, Berrien Springs, Michigan, viewed 7 October 2007, <http://www.biol.andrews.edu/fb/spring/Chap.43-Immunology/4305.jpg>.

Axelsson, P 2002, Diagnosis and Risk Prediction of Periodontal Diseases, Quintessence Publishing, Carol Stream IL.

Campbell, NA, Reece, JB & Meyers, N, 2006, Biology, 7th Edition, Australian Version, Pearson Education Australia, Frenchs Forest, NSW.

Gerrig, RJ & Zimbardo, PG 2005, Psychology and Life, 17th Edition, Pearson Education, United States of America.

Heasman, PA, Millett, DT & Chapple, IL 1996, The Periodontium and Orthodontics in Health and Disease, Oxford University Press Inc, New York.

Inada, M, Matsumoto, C, Uematsu, S, Akira, S & Miyaura, C, 2006, 'Membrane-Bound Prostaglandin E Synthase-1-Mediated Prostaglandin E2 Production by Osteoblast Plays a Critical Role in Lipopolysaccharide-Induced Bone Loss Associated with Inflammation', The Journal of Immunology, vol 177: 1879-1885, viewed 6 October, 2007, <http://www.jimmunol.org/cgi/content/full/177/3/1879>.

Jaffe–Gill, E, Smith, M, Flores Dumke, L, Larson, H & Segal, J 2007, Stress: signs, symptoms, causes and effects, helpguide.org, viewed 30 September 2007, <http://www.helpguide.org/mental/stress_signs.htm>.

Marieb, EN & Hoehn, K 2007, Human Anatomy and Physiology, 7th Edition, Pearson Education, San Francisco

Mostofsky, DI, Forgione, AG & Giddon, DB (eds), 2006, Behavioral Dentistry, Blackwell Publishing, Ames, Iowa.

Stegman, JK (Senior Publisher), 2007, Stedman's Medical Dictionary for the Dental Professions, Wolters Kluwer Health/Lippincott Williams and Wilkins, Philadelphia.

Wolf, HF & Hassell, TM 2006, Colour Atlas of Dental Hygiene: Periodontology, Georg Thieme Verlag, Stuttgart.