2005 Self Learning Assessment (February 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.

QUESTION 5

Which of the following characteristics of cut dentin will affect local adhesion of dentin bonding restorative materials?

1. Density of dentinal tubules.

2. Dentinal tubular length and size.

3. Degree of dentin sclerosis.

4. Smear layer.

A. 1, 2, 3D. 4 only

B. 1 and 3E. All of the above

C. 2 and 4

Rationale

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 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.”

Self-etching systems are less technique-sensitive because of the reduced number of clinical steps in the process. Although resin tags into the dentin are shorter, a good seal is provided. Furthermore, susceptibility to moisture contamination from dentinal fluid is lessened, although some transmission of fluid can occur. However, the strength of the bond to dentin is dependent on the aggressiveness of the self-etching primer’s ability to penetrate the smear layer.

Another factor affecting dentin adhesion is the number of tubules available for mechanical retention. The length and orifice size of the tubules also affect the end result. Since sclerosis of dentin increases with age and the number of dentinal tubules decreases, this should be taken into account when dentin bonded restorations are being considered in the older patient, especially in a Class V restoration.

REFERENCE

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.

QUESTION 6

An eleven-year-old boy sustained a blow to his mouth about one hour ago, resulting in a 2mm intrusion of the right maxillary central incisor. There is no fracture of the tooth. You would

A. allow the tooth to reposition itself.

B. reposition the tooth orthodontically over time.

C. reposition the tooth immediately.

D. reposition the tooth immediately and perform root canal therapy.

Rationale

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. It was once thought that the stage of root development was the determining factor for the outcome of an intruded tooth, but it would appear that the degree of intrusion is the determining factor.

Intrusions of up to 3mm have an excellent prognosis, whereas prognosis of incisors with severe (>6mm) intrusions is poor because of accompanied inflammatory root resorption and pulp necrosis. Incisors intruded less than 3mm are best left to reposition themselves, although natural obturation of the pulp canal is frequently associated with these intrusions. Incisors intruded between 3 and 6mm 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. Incisors 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.

REFERENCE

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

QUESTION 7

Alveolar bone loss in chronic periodontitis is

1. influenced by genetics.

2. affected by the host’s reaction.

3. caused by specific organisms.

4. constant over time.

A. 1, 2, 3D. 4 only

B. 1 and 3E. All of the above

C. 2 and 4

Rationale

Patient response to periodontal infections is complex. Genetic factors are seen to be responsible for increased susceptibility to periodontal diseases. One such example is localised juvenile periodontitis where neutrophil function is altered.

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.

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.

REFERENCES

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.

QUESTION 8

Examination of a patient reveals erosion of the lingual and occlusal surfaces of the posterior teeth. This may be due to

1. excessive ingestion of carbonated beverages.

2. gastroesophageal reflux disease.

3. occupational exposure to corrosive agents.

4. bulimia.

A. 1, 2, 3D. 4 only

B. 1 and 3E. All of the above

C. 2 and 4

Rationale

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 reg
urgitation 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.

REFERENCES

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.

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