Periodontology Risk Factors Question And Answers

Risk Factors

Question 1: Define risk. Enumerate the various risk factors influencing periodontium.
Answer:

• Risk is the probability that an individual will develop a specific disease in a given period.
• The determination of risk is an essential part of diagnosis as it can modify the course of periodontal disease and have an impact on treatment planning.
• Risk has different elements such as risk factors, risk determinants, risk indicators, and risk markers.

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Risk Factors

Risk factors, when present in an individual increase the likelihood of developing the disease. The risk factors of periodontal disease are broadly divided into modifiable and non-modifiable risk factors.

• Modifiable risk factors are those that can be altered by the patient to reduce disease occurrence or progression.
• Modifiable risk factors include biological such as diabetes mellitus, environmental such as smoking, and behavioral such as poor oral hygiene. Non-modifiable risk factors include age, and genetic risk factors.

Risk Determinants:

Risk determinants are those factors that cannot be modified. For example, genetic factors, age and gender of the patient, socioeconomic status, and stress.

Risk Indicators:

Risk indicators are factors that can probably cause periodontal disease. They are identified through cross-sectional studies. for example., osteoporosis, HIV, and noncompliant patients.

Risk Markers:

Risk markers do not cause the disease, but are associated with greater risk for disease. for example., bleeding on probing and previous history of periodontal disease.

Question 2: Discuss the effect of smoking on periodontium. Classification of Smokers
Answer:

• The center for Disease Control and Prevention (CDC) classified smokers as
• Current smokers: Those who smoked 100 or more cigarettes over their lifetime and smoked at the time of the interview.
• Former smokers: Those who had smoked 100 or more cigarettes in their lifetime but were not currently smoking.
• Non-smokers: Those who had not smoked more than 100 cigarettes in their lifetime.

Smoking and Oral Disease:

The habit of smoking and the use of smokeless tobacco is associated with premalignant lesions such as oral leukoplakia and malignancies such as squamous cell carcinoma.

Smoking and Periodontal Disease:

• Smokers exhibit greater prevalence and severity of gingivitis and periodontitis. Current smokers exhibit greater destruction of periodontal tissues when compared to former and non-smokers.
• Several studies have shown alterations in the host-bacterial interaction resulting in more aggressive forms of the disease.

Effect on Microbiology:

• Smoking favors the habitat of P.gingivalis, P.intermedia, and A.actinomycetemcomitans in even shallow pockets.
• There is a reported greater presence of gram-negative anaerobic bacilli in pockets in smokers when compared to non-smokers.

Effect on Microvasculature:

• Smokers have a higher proportion of smaller blood vessels and lower proportions of larger blood vessels.
• This difference in blood vessels is due to the suppression of the inflammatory response.
• In the periodontal environment, this means that there is an increased progression of disease without external signs of inflammation.
• Hemorrhagic responsiveness is suppressed in smokers.

Effect on Tissues of Periodontium;

• Nicotine adversely affects the proliferation, attachment, and chemotaxis of periodontal ligament cells.
• Nicotine affects the attachment of fibroblasts and affects the collagen and noncollagenous proteins by gingival fibroblasts.
• Cotinine enhances the effects of toxins from periodontopathogens increasing the severity of periodontal disease. Certain components of tobacco smoke affects cell adhesion and their structure.

Effect on Clinical Features of Periodontal Disease:

Greater plaque index but fewer bleeding sites decreased redness, and decrease in GCF.

• More attachment loss, more probing depths, more bone loss, more tooth mobility, more missing teeth, greater recession, and furcation involvement, with fewer bleeding sites and fewer plaque accumulation.
• More loss in the maxillary lingual area, possibly because of the local effect. Bone loss is higher in smokers in spite of good oral hygiene.

Immunoinflmmatory Response

The condition of former smokers was intermediate between current smokers and non-smokers.

• No difference in plaque accumulation between smokers and non-smokers.
• Smoking suppresses inflammatory response.
• Reduced volume of GCF among smokers.
• Increased MMP-8 activity. The lower level of IgG2, which may impair neutrophil function and
• aggravate disease process.
• Increases expression of ROS and its effects on periodontium
• Reduced levels of antibodies to Aa, Pi, and Td indicate a disruption of the immune response.

Effect on Periodontal Treatment

Reduction in regeneration after using enamel matrix derivative and guided tissue regenerations.

Smoking, Genetic Polymorphism, and Periodontal Disease

Patients with the interleukin-1 genotype who were smokers exhibited greater attachment loss and bone loss when compared to patients who were IL-1 genotype and non-smokers.

Question 3: Describe the relationship between diabetes and periodontium.
Answer:

Patients with diabetes show an increased prevalence of gingivitis and periodontitis.
A greater incidence of gingival inflammation is seen in children with type I diabetes mellitus.

• Poorly controlled DM patients have greater gingival inflammation than well-controlled patients, irrespective of the amount of plaque.
• Improvement in glycemic control decreases gingival inflammation.
• The level of clinical attachment loss is directly proportional to the duration of DM.
  Increased number of bleeding sites, greater gingival inflammation, more severe periodontal destruction, increased risk of periodontitis, increased extent and severity of periodontitis, greater mean attachment loss.
• Increased prevalence of deeper pockets, increased risk of progressive bone loss, and tooth loss are seen in poor metabolic control patients.

Changes in Microbiota

• Greater presence of gram-negative rods and filaments.
• Increased proportions of Capnocytophaga
• Increased proportions of Pi and Pg in diseased sites.

Changes in GCF

Increased glucose levels in GCF in patients with elevated blood glucose levels, can affect the local host response to microbial challenge and wound healing response.

Changes in Tissue Homeostasis

• Changes in collagen synthesis, maturation, and turnover.
• Changes in collagen metabolism contribute to alteration in wound healing and increase
• predisposition to periodontal disease initiation and progression.
• Decreased rate of collagen and glycosaminoglycan production.
• Increased destruction of the newly formed collagen by the enzyme collagenase and MMP.
• Accumulation of advanced glycation end products (AGE) in the periodontium affects the microvasculature causing the thickening of blood vessels.
• Decreased tissue turnover leads to decreased wound healing response.

Changes in Host Immunoinflmmatory Response

• Reduction in PMN functions such as chemotaxis, adherence, and phagocytosis. This results in the impairment of effective microbial evasion.
• Neutrophil chemotaxis improved in patients with better glycemic control.
• Hyper-responsive neutrophils and monocyte/macrophages result in greater tissue destruction.
• Increased production of proinflammatory cytokines IL-1β and TNF-α by monocytes.
• Increased production of PGE2
• Increased oxidant stress within tissues results in greater tissue destruction.

Treatment Response of Diabetic Patients

• Poorly controlled diabetes patients have less favorable responses to periodontal treatment than well-controlled patients.
• Well or moderately-controlled diabetic patients similarly respond to periodontal therapy to non-diabetic patients and are ideal candidates for implant treatment.

Question 4: Discuss the role of stress on periodontium.
Answer:

• Stress is defined by Selye as a response state of the organism to forces acting simultaneously on the body which, if excessive, led to disease adaptation and eventually to diseases of exhaustion and death.
• The forces that had the potential to challenge the adaptive capacity of the organism are defined as ‘stressors’. Stressors can be physical or mental.
• The stressors can bring about positive or negative changes in the body.
• The state of positive change (for example., excitement) is called ‘eustress’ and the state of negative change (pain, discomfort) is called ‘distress’.

Mechanism Of Stress

The basic pathways of stress are via the

• Hypothalamic- pituitary- adrenal axis
• Adreno-medullary sympathetic nervous system.

The corticotrophin-releasing hormone and the locus-ceruleus-norepinephrine system are the two principal brain components that act through these pathways to modulate the widely dispersed effects of stress between the brain and the peripheral organs. The regulation of glucocorticoids and catecholamines from the brain, adrenal cortex, and adrenal medulla maintain stress-related homeostasis

Stress and Immunoinflmmatory Mechanisms

The stress system responds to immune and inflammatory signals to combat any stressor and bring about homeostasis.

• The activation of the immune system, associated with an increase in the circulating levels of interleukin-1 and interleukin-6, increases activity to the hypothalamus-pituitary axis, and increases cortisol levels which modulate the stress system.

Stress and Periodontal Disease

Stress is a major risk determinant of periodontal disease. Stress can have an effect on diabetes and smoking which in turn may influence periodontal disease.

• Psychosocial stressors are the major stressors that influence susceptibility to periodontal disease.
• The symptoms such as pain, bleeding and fetid odor associated with periodontal disease can cause distress to the patient resulting in activation of the stress pathways, resulting in immunosuppression and further periodontal breakdown.
• Loosening and loss of teeth can have a negative impact on the patient’s emotional well-being and can act as a potential negative stressor leading to further worsening of the periodontal condition.
• Periodontal treatment reduces the signs and symptoms of the disease and boosts the emotional status of the patient which prevents further hard and soft tissue breakdown.

Question 5: Write a note on the non-modifiable risk factors.
Answer:

It has been estimated that about 50% of the difference in host response to periodontopathogenic bacteria is a result of genetic factors. These genetic factors may influence the host response in the following ways;

1. Alteration in immune cell activity in disease sites relates to either too little or excessive inflammatory cell infiltrate in the affected site.
2. Excessive cytokine production by the inflammatory cells present in the inflammatory milieu.

• These are by large the most studied genetic factors in periodontal disease. Several genetic alterations grouped under the term cytokine polymorphisms have been reported in periodontitis.
• The effect of this polymorphism is excessive production of various pro-inflammatory cytokines such as Il-1, IL-6, and TNF-α, which result in prolonged inflammatory responses that may lead to tissue damage. Kornman proposed the periodontal susceptibility test (PST) based on the presence of the IL-1 composite genotype which was thought to make genotype-positive individuals more susceptible to periodontal disease as a result of excessive IL-1 production.

Conclusion

The presence of risk factors must be recognized because they contribute to the etiology although they cannot cause disease by themselves. It is therefore important to control, and modify the risk factors during therapy in order to achieve success in periodontal therapy.