Self Learning Assessment 2005 (July 01, 2005)

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.


The smear layer, produced on cutting enamel and dentin

1. is 10 to 15 microns thick.

2. contains denatured collagen.

3. is firmly attached to the underlying dentin.

4. contains hydroxyapatite crystals

A. 1, 2, 3

B. 1 and 3

C. 2 and 4

D. 4 only

E. All of the above


The smear layer produced on cutting enamel and dentin contains hydroxyapatite crystals and denatured collagen. It is 1-5 microns thick. Although in part porous, the smear layer is weakly attached to the underlying dentin.

Current dental adhesives use two methods to achieve micromechanical retention between the resin and dentin. The first method removes the smear layer and demineralizes the subsurface of intact dentin through acid etching. After rinsing, a multiple step application of a primer and adhesive or a simplified self-priming adhesive is applied to the conditioned surface to complete the bonding. The second method uses the smear layer using it as a bonding substrate. Self-etching primers are then applied to this smear layer covered dentin for a specific time. Then, without rinsing, a layer of adhesive resin is placed. In this system, the smear layer is incorporated into the “hybrid layer.”


1.Tay, F.R., Pashley, D.H. Aggressiveness of contemporary self-etching systems. Depth of penetration beyond dentin smear layers. Dental Materials. 17:296-308. 2001.

2.Tay, F.R., Pashley, D.H. Have dentin adhesives become too hydrophilic? J Can Dent Assoc 69:726-731, 2003.


Which of the following is the determining factor for the successful outcome of an intruded tooth?

A. Age of patient

B. Stage of root development

C. Degree of intrusion

D. Type of force causing intrusion


It was once thought that the stage of root development determined the outcome of an intruded tooth, but it would appear that the degree of intrusion is the determining factor. Tooth intrusion can be a complicated and controversial luxation injury. A severe intrusion produces extensive injury to the alveolar bone, destroys cells of the periodontal ligament (PDL) and crushes the apical vascular system.

Intrusions of up to 3 mm have an excellent prognosis, whereas prognosis of teeth with severe (>6 mm) intrusions is poor because of accompanied inflammatory root resorption and pulp necrosis. Teeth intruded less than 3 mm are best left to reposition themselves, although natural obturation of the pulp canal is frequently associated with these intrusions. Those intruded between 3 and 6 mm have an unpredictable prognosis because of potential pulp necrosis. The clinician may opt to allow these teeth to reposition themselves or actively reposition them by orthodontics. However, it must be ensured that in such teeth endodontic access can be achieved within 1 to 2 weeks to remove the dental pulp. Teeth intruded beyond 6 mm are firmly held by compressed bone. Such teeth can be extracted or immediately repositioned followed by root canal treatment. For very severe intrusions, there is no chance of PDL regeneration. In these cases another option may be considered-extraction, removal of the damaged PDL, immediate extraoral root canal treatment and replantation. The outcome for such teeth is analogous to replantation of avulsed teeth.


Kenny, D.J., Barrett, E.J., Casas, M.J. Avulsions and intrusions: The controversial displacement injuries. J Can Dent Assoc. 69:308-313, 2003.


Which of the following can contribute to disease advancement in a patient with chronic periodontitis?

1. Immunosuppressive drugs

2. Radiotherapy

3. HIV infection

4. Osteoporosis

A. 1, 2, 3

B. 1 and 3

C. 2 and 4

D. 4 only

E. All of the above


Irradiation and immunosuppressive drugs which interfere with the normal host defence mechanisms are contributory to disease advancement. So too are osteoporosis and HIV infection. Risk assessment of patients must take into account the existing periodontal status, family history of periodontitis and genetic factors, as well as other diseases if treatment planning and therapy are to be effective in the long term.

Periodontal diseases are chronic, but bone loss is not constant over time. Instead, there are healing periods following periods of active tissue destruction in given sites. Specific periodontal bacteria trigger inflammatory host responses which lead to tissue destruction.

Data accumulating from clinical and in vitro studies suggest that the neutrophil/antibody/complement axis is critical for protection against periodontal diseases. Abnormalities in this axis often lead to increased susceptibility.


1.Rosling, B., Serino, G., Hellstrm, M-K. et al. Longitudinal periodontal tissue alterations during supportive therapy. J Clin Periodontol. 28:241-249. 2001.

2.Rutger Persson, G., Mancl, L.A., Martin, J. et al. Assessing periodontal disease risk. JADA. 134:575-582. 2003.


A patient presents with erosion of the labial and occlusal surfaces of the maxillary anterior teeth, which may be caused by

1. recurrent vomiting of pregnancy.

2. xerostomia.

3. regurgitation secondary to chronic gastritis.

4. extrinsic factors.

A. 1, 2, 3

B. 1 and 3

C. 2 and 4

D. 4 only

E. All of the above


Dental erosion can be caused by extrinsic or intrinsic factors. Both in the primary and permanent dentitions the mandibular molars are the teeth most commonly subject to erosion. Extrinsic factors include carbonated or acidic beverages, acidic foods, citric lozenges, various medications, oral hygiene swab sticks, saliva substitutes, recreational exposure to water in gas-chlorinated swimming pools and occupational exposure to corrosive agents such as battery acid fumes and industrial aerosols. Extrinsic factors cause more damage to the labial or occlusal surfaces of the maxillary anterior teeth with the severity decreasing posteriorly.

Intrinsic causes of dental erosion include bulimia, rumination (voluntary reflux phenomenon), subclinical regurgitation due to chronic gastritis associated with alcoholism, xerostomia, malabsorption syndrome, recurrent vomiting of pregnancy and gastroesophageal reflux disease.

Intrinsic acid causes more damage to the lingual and occlusal surfaces of teeth, particularly in the maxilla, as the tongue tends to force the regurgitated acid over the tongue, along the palate, over the occlusal surfaces and into the buccal vestibule, where salivary buffering action reduces the acidity. Thinning of the enamel imparts a yellowish hue to the teeth. Once dentin is exposed, loss of dentin progresses faster than enamel, such that “cupping” lesions occur. Amalgam restorations appear highly polished and seem to stand above the surface.

Management of this condition is to identify the cause and eliminate it if possible. Attempts must be made to prevent the salivary pH from falling below 5.5, at which point demineralization occurs. Chewing antacid tablets or rinsing with sodium bicarbonate can neutralize the effect of acid on the dentition. Fluoride can facilitate remineralization.


1.Barron, R.P., Carmichael, R.P., Marcon, M.A. et al. Dental erosion in gastroesophageal disease. J Can Dent Assoc. 69:84-89, 2003.

2.Lazarchik, D.A., Filler, S.J. Dental erosion: predominant oral lesion in gastroesophageal reflux disease. Am J Gastroenterol 95 (8 suppl): S 33-38, 2000.

Answers to the June 2005 SLSA Questions

21. C

22. C

23. B

24. E