Background: Salivary secretory disorders can be the result of a wide range of factors. Their prevalence and negative effects on the patient's quality of life oblige the clinician to confront the issue.

Background: Gingival enlargement is a known side effect of nifedipine use. This study was conducted to determine the prevalence and risk factors for gingival enlargement in nifedipinetreated patients.Methods: A cross‐sectional study was conducted in a primary care center. Data from 65 patients taking nifedipine were compared with 147 controls who had never received the drug. All patients were examined for the presence of gingival enlargement using 2 different indices: vertical gingival overgrowth index (GO) in 6 points around each tooth, and horizontal MB index in the interdental area. Gingival index, plaque index, and probing depth were also evaluated.Results: The prevalence of gingival enlargement was significantly higher in nifedipine‐treated cases than in controls (GO index, 33.8% versus 4.1%; MB index, 50.8% versus 7.5%, respectively). Higher gingival and plaque indices were observed in patients taking nifedipine. Among the possible risk factors, only the gingival index showed a significant association with gingival enlargement. The risk (odds ratio [OR]) of gingival enlargement associated with nifedipine therapy was 10.6 (3.8‐29.1) for the GO index and 14.4 (6‐34.6) for the MB index. Gingival index‐adjusted ORs were 9.6 (3.3‐28.1) and 9.7 (3.9‐23.3), respectively. In the subset of high nifedipine exposure patients, the odds ratio for gingival enlargement increased to 17.4 (5.3‐56.3) for the GO index and 23.6 (7.7‐72.3) for the MB index. The concordance between GO and MB indices showed a kappa value of 0.689 in controls and 0.642 in patients treated with nifedipine.Conclusions: Patients taking nifedipine are at high risk for gingival enlargement, and gingivitis acts as a predisposing factor. J Periodontol 2001;72:605‐611.

The association between periodontal disease and adverse pregnancy outcomes in Northern Tanzania: a cross-sectional study

Background: Herpes zoster (HZ) presents as a cutaneous vesicular eruption in the area innervated by the affected sensory nerve, usually associated with severe pain. Oral manifestations of HZ appear when the mandibular or maxillary divisions of the trigeminal nerve are affected.Methods: This is a case report of a 63‐year‐old woman with HZ infection with trigeminal nerve involvement that led to a rapid loss of alveolar bone and exfoliation of two teeth.Results: The initial intraoral examination showed redness of the alveolar mucosa and gingiva of the lower right quadrant with multiple well‐delimited and painful erosive lesions affecting the attached gingiva around the teeth. Two weeks later, teeth number 27 (lower right canine) and 28 (lower right first premolar) had class III mobility, flow of purulent exudate from the gingival sulcus, and deep pockets ( >11 mm). The radiological examination showed advanced alveolar bone loss around both teeth. The prognosis for teeth number 27 and 28 was considered hopeless, and they were extracted. Due to extensive necrosis there was no interdental alveolar bone. The case is presented with a review of clinical data from patients with trigeminal HZ infection associated with osteonecrosis or exfoliation of teeth previously reported in the literature. The mechanisms by which the HZ infection leads to the alveolar bone necrosis are discussed.Conclusions: Extensive osteonecrosis and exfoliation of teeth in the area innervated by the nerve affected by HZ has been reported after HZ infection. Clinicians should be aware of this possible outcome after a trigeminal HZ infection. J Periodontol 2005;76:148‐153.

Introduction: Gingival overgrowth has been linked to multiple factors such as adverse drug effects, inflammation, neoplastic processes, and hereditary gingival fibromatosis. Drug-induced gingival overgrowth is a well-established adverse event. In early stages, this gingival enlargement is usually located in the area of the interdental papilla. Histologically, there is an increase in the different components of the extracellular matrix.Objective: The aim of this manuscript is to describe and analyze the different cellular and molecular agents involved in the pathogenesis of Drug-induced gingival overgrowth.Method: A literature search of the MEDLINE/PubMed database was conducted to identify the mechanisms involved in the process of drug-induced gingival overgrowth, with the assistance of a research librarian. We present several causal hypotheses and discuss the advances in the understanding of the mechanisms that trigger this gingival alteration.Results: In vitrostudies have revealed phenotypic cellular changes in keratinocytes and fibroblasts and an increase of the extracellular matrix with collagen and glycosaminoglycans. Drug-induced gingival overgrowth confirms the key role of collagenase and integrins, membrane receptors present in the fibroblasts, due to their involvement in the catabolism of collagen. The three drug categories implicated: calcineuron inhibitors (immunosuppressant drugs), calcium channel blocking agents and anticonvulsant drugs appear to present a multifactorial pathogenesis with a common molecular action: the blockage of the cell membrane in the Ca2+/Na+ ion flow. The alteration of the uptake of cellular folic acid, which depends on the regulated channels of active cationic transport and on passive diffusion, results in a dysfunctional degradation of the connective tissue. Certain intermediate molecules such as cytokines and prostaglandins play a role in this pathological mechanism. The concomitant inflammatory factor encourages the appearance of fibroblasts, which leads to gingival fibrosis. Susceptibility to gingival overgrowth in some fibroblast subpopulations is due to phenotypic variability and genetic polymorphism, as shown by the increase in the synthesis of molecules related to the response of the gingival tissue to inducing drugs. The authors present a diagram depicting various mechanisms involved in the pathogenesis of drug-induced gingival overgrowth.Conclusion: Individual predisposition, tissue inflammation, and molecular changes in response to the inducing drug favor the clinical manifestation of gingival overgrowth.