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The clinical manifestations of contact allergic dermatitis to dental materials are not uniform. This study was performed to detect the frequent allergens in the dental series associated with contact dermatitis and to define the causal relationship between the different allergens and the relevant clinical presentations. Between the years 2000 and 2004, 134 patients, aged 20-80 years, were patch tested. 121 patients were included in the study. The most frequent oral manifestations were cheilitis and perioral dermatitis (25.6%), burning mouth (15.7%), lichenoid reaction (14.0%), and orofacial granulomatosis (10.7%). 18 (14.9%) patients were dental personnel, all of whom suffered from hand dermatitis. The common allergens detected included goldsodiumthiosulphate (14.0%), nickel sulfate (13.2%), mercury (9.9%), palladium chloride (7.4%), cobalt chloride (5.0%), and 2-hydroxyethyl methacrylate (5.8%). Positive reactions to metals were frequent in all the different clinical variants, and no specific association between a specific clinical presentation and a particular allergen was found. Allergy to mercury was not a significant factor contributing to the pathogenesis of oral lichenoid reactions. However, a strong association with contact allergy to mercury in dental fillings was found in 2 patients with orofacial granulomatosis.

Apical periodontitis is a chronic inflammatory disorder of periradicular tissues caused by aetiological agents of endodontic origin. Persistent apical periodontitis occurs when root canal treatment of apical periodontitis has not adequately eliminated intraradicular infection. Problems that lead to persistent apical periodontitis include: inadequate aseptic control, poor access cavity design, missed canals, inadequate instrumentation, debridement and leaking temporary or permanent restorations. Even when the most stringent procedures are followed, apical periodontitis may still persist as asymptomatic radiolucencies, because of the complexity of the root canal system formed by the main and accessory canals, their ramifications and anastomoses where residual infection can persist. Further, there are extraradicular factors — located within the inflamed periapical tissue — that can interfere with post-treatment healing of apical periodontitis. The causes of apical periodontitis persisting after root canal treatment have not been well characterized. During the 1990s, a series of investigations have shown that there are six biological factors that lead to asymptomatic radiolucencies persisting after root canal treatment. These are: (i) intraradicular infection persisting in the complex apical root canal system; (ii) extraradicular infection, generally in the form of periapical actinomycosis; (iii) extruded root canal filling or other exogenous materials that cause a foreign body reaction; (iv) accumulation of endogenous cholesterol crystals that irritate periapical tissues; (v) true cystic lesions, and (vi) scar tissue healing of the lesion. This article provides a comprehensive overview of the causative factors of non-resolving periapical lesions that are seen as asymptomatic radiolucencies post-treatment.

In dentistry, a variety of potentially allergenic metals are used, such as mercury, palladium, nickel, gold, chromium, cobalt and other metals. This paper describes a diagnostic approach from a dentist’s point of view, which enables analysis of metals in a patient’s oral cavity. If metal allergy is suspected, a micro analysis can be used to determine which metals are present in the restorations. When the exact composition of the dental materials is known, the patient can be tested in vivo (patch test) and/or in vitro (lymphocyte proliferation test) to reveal sensitization. Two patients with nickel allergy are described where removal of nickel-containing materials (bridge and orthodontic wire) resulted in the marked alleviation of symptoms and improvement of health. Finally, if allergy to specific metals has been established, the restorations containing the implicated metals should be removed to discontinue the exposure and thus facilitate the patient’s health.

OBJECTIVES:
This study was carried out to investigate the potential of titanium to induce hypersensitivity in patients chronically exposed to titanium-based dental or endoprosthetic implants.

METHODS:
Fifty-six patients who had developed clinical symptoms after receiving titanium-based implants were tested in the optimized lymphocyte transformation test MELISA against 10 metals including titanium. Out of 56 patients, 54 were patch-tested with titanium as well as with other metals. The implants were removed in 54 patients (2 declined explantation), and 15 patients were retested in MELISA.

RESULTS:
Of the 56 patients tested in MELISA, 21 (37.5%) were positive, 16 (28.6%) ambiguous, and 19 (33.9%) negative to titanium. In the latter group, 11 (57.9%) showed lymphocyte reactivity to other metals, including nickel. All 54 patch-tested patients were negative to titanium. Following removal of the implants, all 54 patients showed remarkable clinical improvement. In the 15 retested patients, this clinical improvement correlated with normalization in MELISA reactivity.

CONCLUSION:
These data clearly demonstrate that titanium can induce clinically-relevant hypersensitivity in a subgroup of patients chronically exposed via dental or endoprosthetic implants.