Oral Health Group

2005 Self Learning Assessment (January 01, 2005)

January 1, 2005
by Oral Health

The SLSA program is based on current, referenced literature and consists of 40 questions, answers, rationales and references. Answers appear at the end of each quiz.

Dentists who complete the 15 question quiz in the November, 2005 issue of Oral Health may be eligible to receive continuing education points. The names and license numbers of all who complete the quiz will be forwarded to their respective provincial licensing authorities.



Which of the following is/are the cause(s) of dentin hypersensitivity?

1. Bruxism.

2. Gingival recession.

3. Malocclusion.

4. Erosion.

A. 1, 2, 3D. 4 only

B. 1 and 3E. All of the above

C. 2 and 4


Two processes are essential for the development of dentin hypersensitivity. Dentin must become exposed and the dentin tubules must be open to both the oral cavity and the pulp. Dentin hypersensitivity is characterized by short, sharp pain arising from exposed dentin in response to stimuli typically thermal, evaporative, tactile, osmotic or chemical, which cannot be ascribed to any other form of dental defect or disease. The diagnosis of dentin hypersensitivity is one of exclusion. Erosion, abrasion, attrition and possibly abfraction lead to exposure of tubules. Gingival recession (a predisposing factor) is not a cause by itself. Neither bruxism nor malocclusion has been identified as a causative factor. A study of a representative sample of the Canadian population found that the incidence of hypersensitivity is about 30 percent in adults aged 18 to 64. The most widely accepted mechanism of dentin hypersensitivity is the hydrodynamic theory proposed by Brnnstrm, whereby fluid flow within the tubules is altered by various stimuli near the exposed surface of the tubules, which leads to stimulation of certain fibres surrounding the odontoblasts. It should be noted that reversible procedures should be used before non-reversible. In the initial management of dentin hypersensitivity predisposing factors and causes should be removed or modified and desensitizing toothpastes should be used daily.


1.Holland, G.R., Narhi, M.N., Addy, M. et al. Guidelines for the design and conduct of clinical trials on dentine hypersensitivity, J Clin Periodontol, 24:808-813, 1997.

2.Canadian Advisory Board on Dentin Hypersensitivity. Consensus-based recommendations for the diagnosis and management of dentin hypersensitivity. J Can Dent Assoc. 69:221-226, 2003.


A patient on long-term corticosteroid therapy

1. does not require steroid cover before a gingivectomy.

2. is prone to oral candidiasis.

3. is prone to aspiration pneumonia.

4. requires prior steroid cover before a gingivectomy.

A. 1, 2, 3D. 4 only

B. 1 and 3E. All of the above

C. 2 and 4


Although physiological adrenocortical suppression occurs when exogenous steroids are taken, recent studies suggest such suppression is not clinically significant. Twenty patients on long-term steroids requiring bilateral gingivectomy and acting as their own controls formed the study group. The surgery on one side was done with a prior intravenous injection of 100 mg hydrocortisone hemisuccinate. At a later date, when the contralateral side was treated, the patient received a placebo injection. Blood pressure measurements throughout the operations showed no changes in either systolic or diastolic pressures. Thus, administration of steroids before minor dento-alveolar surgery using local anaesthesia is not required. Dentists may encounter patients who are on long-term steroid use for management of conditions such as rheumatoid arthritis and other collagen diseases, certain dermatological disorders, blood dyscrasias, certain malignant diseases, adrenal insufficiency and organ transplants.

Chronic use of systemic and inhaled corticosteroids predisposes patients to microbial infections of which oral candidiasis is high on the list. In the older patient, frequently with poorer oral hygiene there is an increase in the anaerobic organisms of the gingival crevice and the saliva. From this source and frequent swallowing dysfunction as a result of debilitation or medication, there is an increased risk of aspiration pneumonia. Patients at risk require routine dental examinations and treatment.


1.Seymour, R.A. Dentistry and the medically compromised patient. Surg J R Coll Surg Edinb. 1.207-214, 2003.

2.Ship, J.A., and Chavez, E.M. Management of systemic diseases and chronic impairments in older adults: Oral health considerations. General Dentistry. Sept/Oct. 555-565, 2000.


Acute apical periodontitis in the permanent dentition can be characterized by which of the following?

1. Constant pain.

2. No radiographic bony changes.

3. Pain on biting.

4. Widening of the periodontal ligament space.

A. 1, 2, 3D. 4 only

B. 1 and 3E. All of the above

C. 2 and 4


Acute apical periodontitis (AAP) is a periapical inflammation resulting from an untreated, non-vital pulp. Features of AAP are constant pain which has occurred over a short period of time with marked pain on biting or percussion of the associated tooth. Rarely is there sensitivity of the tooth to thermal changes. There is a delayed or negative response to vitality tests and no radiographic bony changes are seen, although there may be some evidence of widening of the periodontal ligament space. Swelling, periapical radiolucency and systemic changes are not associated with AAP.

A review of the literature has provided the basis for practice guidelines and the recommendations are:

Root canal therapy should be started as soon as possible.

Analgesics (NSAIDs if not contraindicated) should be given preoperatively, or immediately post-operatively and continued as needed.

If root canal therapy cannot be started immediately, appropriate analgesics should be prescribed.

Extraction may be an alternative to endodontic therapy for some patients.

If the tooth is in hyperocclusion, it should be relieved if possible.

Antibiotic therapy and bony trephination are not indicated for this condition.


Sutherland, S., Mathews, D.C. Emergency management of acute apical periodontitis in the permanent dentition: A systematic review of the literature. J Can Dent Assoc. 69:160-161, 2003.


In maintenance therapy of periodontal disease, reduction of supragingival plaque results in

1. alteration of subgingival microflora.

2. reduced gingival inflammation.

3. decreased flow of gingival crevice fluid.

4. reduction in pocket depth.

A. 1, 2, 3D. 4 only

B. 1 and 3E. All of the above

C. 2 and 4


Repeated removal of supragingival plaque affects the subgingival plaque biofilm by altering the subgingival microflora along with which there is a reduction in pocket depth. Removal of supragingival plaque has at least three benefits:

A decrease in the reservoir for colonisation by periodontal pathogens.

A reduction of gingival inflammation with decrease in damage to adjacent connective tissues of the periodontium.

Alteration in the composition and numbers of subgingival microorganisms which in part occurs as a result of decreased flow of gingival crevice fluid needed for growth of subgingival plaque.

Dental plaques are now recognized as organized microbial biofilm communities. In these biofilms, the organisms are protected by an extracellular matrix, which must be penetrated by an antimicrobial agent to be effective in preventive care. Agents with this ability are chlorhexidine, Triclosan, cetylpyridinium chloride and a fixed combination of essential oils. These are found in both toothpastes and mouthwashes.

A recent study simulated conditions of a typical patient on a maintenance oral hygiene therapy regimen. It compared use of dental floss and toothbrushing with toothbrushing and an essential oil mouthrinse. The flossing group was demonstrably less effective in reducing both interproximal plaque levels and gingivitis. Another study showed that toothbrushing with an antimicrobial dentifrice is as good as
dental floss in control of interproximal gingivitis. Flossing is not effective in patients showing exposed roots with root surface concavities and grooves which harbour plaques that floss cannot reach. The mechanics of flossing will not control subgingival pathogenic bacteria. An additional study has demonstrated how an essential oil mouthrinse becomes an effective adjunct to brushing and flossing for patients on maintenance therapy.


1.Banroth, K., Charles, C.H., Mancodi, S.M. et al. The efficacy of an essential oil antiseptic mouthrinse vs. dental floss in controlling interproximal gingivitis. JADA. 134:359-365. 2003.

2.Sharma, L., Charles, C.H., Lynch, M.C., et al. Adjunctive benefit of an essential oil containing mouthrinse in reducing plaque and gingivitis in patients who brush and floss regularly. JADA 135:496-504, 2004.


1. A

2. A

3. E

4. C

5. C

6. E

7. A

8. A

9. E

10. E

11. E

12. C

13. D

14. C

15. D

Funding for the SLSA program has been provided by:

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