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Questions and Answers
What is the primary etiologic agent of periodontal disease?
What is the primary etiologic agent of periodontal disease?
What is the ultimate outcome of untreated periodontitis?
What is the ultimate outcome of untreated periodontitis?
What is the most significant known risk factor for periodontitis?
What is the most significant known risk factor for periodontitis?
What is the Task Force of the 2017 AAP/EFP World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions recognizing?
What is the Task Force of the 2017 AAP/EFP World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions recognizing?
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What is the effect of nicotine on fibroblasts?
What is the effect of nicotine on fibroblasts?
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What are the primary risk factors for periodontal disease?
What are the primary risk factors for periodontal disease?
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What is the cause of periodontitis?
What is the cause of periodontitis?
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What is the effect of smokeless tobacco use on teeth?
What is the effect of smokeless tobacco use on teeth?
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What is the effect of smokeless tobacco use on teeth?
What is the effect of smokeless tobacco use on teeth?
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What are the risk factors for periodontal disease?
What are the risk factors for periodontal disease?
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What is the cyclic nature of periodontitis?
What is the cyclic nature of periodontitis?
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How can periodontitis be prevented?
How can periodontitis be prevented?
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What is the cycle of periodontitis?
What is the cycle of periodontitis?
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Study Notes
- The etiology of periodontal disease is a bacterial infection of the periodontium.
- Bacteria are the primary etiologic agents in the initiation of periodontal disease.
- There are risk factors for periodontal disease, which can be either local or systemic.
- The most significant known risk factor for periodontitis is cigarette smoking.
- Periodontitis is a condition in which the tissues that support the teeth become inflamed and damaged.
- The disease is often cyclic, with periods of remission and recurrence.
- The cause of periodontitis is unknown, but may be related to the accumulation of plaque and bacteria in the mouth.
- Periodontitis can be prevented by good oral hygiene and by treating active periodontal disease.
- Periodontitis is classified by the risk factors of the individual: systemic disease, genetic information, personal habits, and characteristics.
- Periodontitis can be prevented by assessing an individual's risk factors and taking appropriate preventive measures.
- Cigarette smoking increases the risk for periodontal disease by at least two to three times.
- Tooth loss is the ultimate outcome of untreated periodontitis.
- Smokers are at higher risk for tooth loss due to periodontal disease.
- Cigar and pipe smoking are also significant risk factors for attachment loss.
- Smokeless tobacco use is associated with severe recession and loss of attachment to buccal surfaces of teeth where the smokeless tobacco was placed.
- Heavy smokers (more than 10 cigarettes/day) have greater odds for more severe attachment loss compared to nonsmokers.
- The Task Force of the 2017 AAP/EFP World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions recognizes that cigarette smoking is a major risk factor for periodontal diseases and peri-implant diseases:
- smoking increases the rate of progression of periodontitis,
- it alters the patient’s responsiveness to standard therapeutic principles,
- it influences general health or systemic disease, and
- it could cause the disease to progress from one stage to the next.
Therefore, a clinician should make every effort to assess a patient’s smoking status and integrate this pertinent information, along with other risk factors, to formulate the grade of periodontitis.
- Smoking has negative effects on the immune system, cellular and humoral inflammatory response systems, and bone metabolism.
- Smoking is also associated with environmental tobacco smoke, which has significant effects on the oral cavity.
- Chemical products and toxins in cigarette smoke may delay wound healing by impairing the biologic progression of healing and by inhibiting the basic cellular functions necessary for the initiation of wound healing.
- Fibroblasts exposed to nicotine produce less extracellular matrix, less collagen, and more collagenase. These negative effects on fibroblast functions influence wound healing and progression of periodontitis.
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