agents repeatedly was associated with a significant reduction in adjusted DFT increment over the course of 18 months. Dentists should consider these nonoperative approaches more often.
Chaffee BW, Cheng J, Featherstone JDB: Non-operative anti-caries agents and dental caries increment among adults at high caries risk: A retrospective cohort study. BMC Oral Health 15:111, 2015 Reprints available from Center to Address Disparities in Children’s Oral Health, UCSF School of Dentistry, 3333 California St,Suite 495, San Francisco, CA 94143-1361; e-mail: [email protected]
Caries adjacent to restorations Background.—Few studies have indicated what happens to the surfaces adjacent to decayed surfaces after restoration. Cavity preparation has been related to damage of adjacent surfaces, but adjacent surfaces have significantly less caries development when they are in contact with fluoride-releasing materials such as glass ionomer cement, resin-modified glass ionomer cement, and compomer compared to amalgam. The effect of composite on adjacent surfaces is unknown. Among the possible factors that influences caries development are previous caries experience, tooth anatomy, and dentist skill level. A practice-based study was undertaken to identify the risk factors for caries development on tooth surfaces adjacent to recently placed Class II composites. Methods.—Dentists participating in the Public Dental Service (PDS) in Norway placed Class II composite restorations. A total of 750 surfaces, either sound or with caries confined to enamel, and in contact with the restorations were evaluated using standard clinical and radiographic measures. The mean age of the patients was 15.1 years and 52.8% were female. Results.—The patients’ caries experience ranged from decayed-missing-filled-teeth (DMFT) of 1 to 23, with a mean of 6.6. At baseline the number of restorations and contact surfaces placed by the dentists ranged from 1 to 84. Various brands of composite were used. After a mean of 4.9 years (range 4 to 7.3 years), 38.8% of the initial sound surfaces remained sound. Caries developed in 34.0% of the surfaces and caries in dentin developed or had been restored in 27.2%. When the caries were confined to enamel at baseline, 57.3% remained confined to enamel and the rest had progressed into dentin or had been restored. Almost 8% of the contact restorations were replaced. Risk factors related to caries development on sound contact surfaces included patients with poor or medium
oral hygiene; patients with higher DMFT; having contact surfaces in molars, on distal surfaces, in maxillary teeth, or on the right side; and having the restorations placed by certain dentists. After adjustments, poor or medium oral hygiene, higher DMFT, maxillary teeth, and teeth on the right side remained significantly more often associated with a higher risk of developing caries in the dentin of contact surfaces. Surfaces next to restorations placed by one dentist were more likely to become decayed than those placed by any of the other dentists. Higher DMFT, surfaces adjacent to restorations made with Herculite XRV, those placed by certain dentists, and those placed without an approximal protection shield during cavity preparation were shown to be related to a higher risk for progression of caries lesions from enamel to dentin. With adjustments, only higher DMFT remained as a risk factor. Dentist-related factors with a higher risk of caries progression included restorations placed by a single dentist. Those placed by two other dentists had a significantly lower risk of caries development. The former used Herculite XRV; the latter used Tetric Ceram. Discussion.—Sound surfaces that were in contact with composite restorations were more likely to develop dentinal caries when the patients practiced poor or medium oral hygiene, had a higher DMFT, had maxillary teeth involved, or had teeth on the right side of the mouth involved. In addition, the treating dentist significantly influenced the development of caries.
Clinical Significance.—Clinicians should be aware that caries can develop more often on adjacent surfaces when they place a restoration. The risk is especially high in patients at high risk for caries development overall. Preventive strategies should be employed to reduce the
risk. Alternatively, nonoperative treatment may be required. These adjacent surfaces should be regularly evaluated for the presence of caries development or progression.
Kopperud SE, Espelid I, Tveit AB, et al: Risk factors for caries development on tooth surfaces adjacent to newly placed class II composites – a pragmatic, practice based study. J Dent 43:1323-1329, 2015 Reprints available from SE Kopperud, Nordic Inst of Dental Materials (NIOM), Sognsveien 70a, NO-0855 Oslo, Norway; fax: þ47 99 64 35 36; e-mail: [email protected]
Endodontics Failed anesthesia in acutely inflamed pulp Background.—Anesthesia is considerably more difficult in situations where there is acute irreversible pulpitis. The specific combination of having an acutely inflamed mandibular molar (AIMM) with acute irreversible pulpitis (AIP) presents perhaps the most difficult challenge for achieving profound pulpal anesthesia when administering an inferior alveolar nerve block (IANB). Conventional approaches are only successful 20% to 50% of the time. As a result, practitioners prescribe antibiotics, refer for secondary care, or begin treatment without achieving proper anesthesia of the tooth. Detailed analysis of the clinical presentation, the pathophysiological situation, pulpal anesthesia facts, and theories to explain failure of pulpal anesthesia offers practitioners principles for achieving proper anesthesia in any tooth. Clinical Presentation.—The severity of the pain that accompanies AIP is described as a severe dull throbbing ache made worse by thermal or postural changes during sleep. Patients may also report spontaneous sharp bursts of pain and referred pain. With progression, cold stimulation may actually alleviate symptoms, which indicates a partially necrotic state has developed. Without periapical pathosis, pain may be hard to localize and the tooth will exhibit no response when percussed. Visually, the tooth may have a deep carious lesion or extensive restoration with poor margins. If trauma or heavily restored adjacent teeth are part of the picture, it may be hard to pinpoint which tooth is involved. The clinician should note especially any subtle signs such as cracks or discolored areas and use all available tools for analysis. Electric pulp testing (EPT) can give false positives in the presence of large restorations, partial vitality, and suppuration and should only be used when thermal testing is inconclusive and sufficient natural tooth structure remains. A detailed history and examination are essential. It is useful to adopt a practical classification system where diagnostic terms represent clinical findings.
Pathophysiology.—Pulpal inflammation begins when the carious lesion passes the amelodentinal junction and enters dentin (Fig 1). Odontoblasts deposit tertiary and intra-tubular dentin to increase the resistance against the lesion. Acidic bacterial by-products enter the pulp chamber and stimulate dentinal nerve endings and fast-acting Ad nociceptors. The result is an increase in the pulp’s hemodynamic pressure, which the Ad fibers translate into short, sharp pain. If the process continues without treatment, bacteria enter the pulp chamber, leading to pulpal inflammation and creating an acute inflammatory reaction. As deeper slow-acting C nociceptors are activated, neuropeptides and inflammatory cytokines are secreted from leukocytes, which alter the blood flow to the pulp. Hemodynamic pressures are further amplified, but the rigid walls of the root canal system cannot accommodate the edema. The vasculature collapses, sensitizing pain fibers to produce dull, persistent pain typical of AIP. Further progression increases hemodynamic pressures again, stressing nociceptors and producing a hyperalgesic response to thermal stimuli. With further pulp deterioration, the pulp becomes necrotized, so that cold stimuli actually relieve symptoms. With complete necrosis of the pulp, invading bacteria feed on the material, leaving a pulpless, infected root canal system with suppuration extending into the periapical area, forming an abscess. This stage occurs 2 to 10 months after the first bacterial invasion and causes pain when apically placed forces are applied to the tooth. Pulpal Anesthesia Methods.—Subjective methods are commonly used to evaluate the efficacy of local anesthetics in creating an IANB. These include probing the gingiva and checking for lip numbness. Both are unreliable and indicative solely of soft tissue anesthesia. Pulpal anesthesia and soft tissue anesthesia do not necessarily occur at the same point. If the tooth responds to sensitivity tests after the