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Anxiety, gingival inflammation and periodontal disease in non-smokers and smokers - an epidemiological study.

OBJECTIVES: The aim of the present study was to investigate the influence of anxiety, measured by one single question, on gingival inflammation and periodontal disease in non-smokers and smokers. MATERIAL AND METHODS: The participants were 144 subjects with untreated periodontal disease 30-40 years of age, and 26 healthy controls, 30-40 years of age. All subjects were clinically examined and answered an uncomplicated question regarding anxiety in every day life, as well as smoking habits. The periodontitis subjects were divided into; an aggressive periodontitis (AP)-group and a chronic periodontitis (CP)-group. Fisher's exact probability t-test, analysis of variance (anova), Mann-Whitney U-test and analysis of covariance (ancova) were used as statistical methods. RESULTS: Anxious subjects had a significantly higher gingival index than non-anxious subjects, when controlling for smoking (p<0.01). The healthy anxious non-smokers had an average score of GI 1.6 (+/-0.4 SD) compared with 1.2 (+/-0.4 SD), p<0.05 for the non-anxious non-smokers. Anxious smokers with periodontits (AP-/CP-group) had significantly more sites with pockets >/=5 mm, compared with non-anxious smokers, (p<0.05). CONCLUSIONS: The results of the present study, suggest that self-reported anxiety was associated with an adverse affect on the gingiva. Anxiety seemed to be associated with increased severity of periodontal disease in smokers.

Acute Disease↗

[Immunoglobulin bearing cells and complement 3 in periodontal diseases].

Frozen gingival tissue sections from marginal gingivitis (MG), juvenile periodontitis (JP), adult periodontitis (AP) patients and clinical healthy subjects (H) were immunohistochemically stained with specific antibodies to aid in identification and quantification of different Ig bearing cells in inflammatory infiltrates. IgG, IgA, IgM, K and lambda were present in all specimens studied. The numbers of Ig cells in disease groups were much greater than in H group, especially the IgG cells. The numbers of IgG cells in AP and JP were most abundant, followed by MG and H. The correlation between the number of IgG cells and the percentage of infiltrated connective tissue was obtained by linear correlation analyses (r = 0.534, P < 0.001). This means that the inflammatory infiltration became heavier as the number of IgG cells increased. It is the new finding that the number of IgA cells was smaller than the IgM cells in JP, the IgA/total heavy chains ratio was much lower than other groups. The C3 deposition was found in all of the gingival specimens. In healthy gingival tissue, C3 mainly deposited in both of the surface of inflammatory cells and vessels. In diseased status C3 located not only in these two, but also in sulcular (pocket) epithelium and oral epithelium, Igs were also observed in these areas. It is suggested that immunocomplex may deposit in gingival tissue.

Adolescent↗

Adult linear immunoglobulin A disease manifesting as desquamative gingivitis.

Desquamative gingivitis is a manifestation of various dermatoses, particularly lichen planus and mucous membrane pemphigoid. A rare example of adult linear immunoglobulin A disease manifesting as desquamative gingivitis is presented. Although the initial clinical features were typical of desquamative gingivitis, the persistence of ulceration after dental extractions was unusual, and the management of the oral lesions proved difficult. The clinical, immunopathologic, and therapeutic aspects of linear immunoglobulin A dermatoses are reviewed.

Aged↗

Characterization of collagens of diseased human gingiva.

In the gingiva and other connective tissues, alteration in the collagens is primarily responsible for their functional impairment during disease. To study the collagen alterations, we extracted diseased human gingival tissue with neutral and acidic solvents and then with pepsin. The pepsin extract was separated into proteins soluble in 2.5 and 1.5 M NaCl and proteins insoluble in 1.5 M NaCl. By the criteria of solubility behavior in NaCl solutions, elution from (carboxymethyl)cellulose (CM-cellulose) columns, sodium dodecyl sulfate (NaDodSO4)-polyacrylamide gel electrophoresis, CNBr peptide pattern, and amino acid composition, the collagens of acidic and neutral solvent extracts and 1.5 M soluble fraction of pepsin extract were characterized as type I collagen and the 1.5 M NaCl insoluble collagen as type III. The 2.5 M NaCl fraction contained alpha 2, A, and B chains. The alpha 1 chains resembled alpha 1[I] in amino acid composition, and, since alpha 2 chains were lacking, it appeared that these chains derived from type I trimer collagen. The A and B chains were purified from the 2.5 M NaCl fractions by salting out at acidic pH. The final (A plus B) chain fraction was resolved into two major and one minor protein peaks by phosphocellulose chromatography. The major peaks were characterized as A and B chains on the basis of amino acid composition and CNBr peptide patterns. The minor peak had electrophoretic mobility slightly less than B chains, and the amino acid composition was different. Analysis of the proportion of different collagen types extracted indicated that type III collagen, which is the second major fraction in other connective tissues, is only a minor constituent in the gingiva. More interestingly, A and B chains accounted for a greater proportion than type III. Unlike the fibroblast cultures, the type I trimer formed only a small proportion of collagens of diseased gingival tissue.

Acetates↗

Desquamative gingivitis: early presenting symptom of mucocutaneous disease.

Desquamation of the gingiva is a sign that may be encountered in clinical practice. Various diseases can affect the gingival tissues. Mild desquamation that is localized may be associated with mechanical irritation or induced by trauma. Moderate to severe generalized desquamation associated with ulceration and erythema may be indicative of a more serious systemic condition. Although often overlooked, mucocutaneous diseases frequently present with gingival desquamation as an early presenting symptom. The most common mucocutaneous diseases that affect the oral cavity are lichen planus, pemphigus, and mucous membrane pemphigoid. This article reviews the etiology, signs and symptoms, and therapies for these disorders. Increased knowledge of mucocutaneous diseases can help the clinician recognize these disorders and enable the patient to receive appropriate therapy.

Anti-Inflammatory Agents, Non-Steroidal↗

Predictive dentistry: a study in carbohydrate metabolism.

The virtues of prediction in the so-called health sciences are well-known. There is still small but burgeoning interest in predictive medicine; little has been done in predictive dentistry. The evidence presented in this report suggests that carbohydrate metabolism may be utilized as a predictive instrument in dentistry. While the emphasis in this document rests on biochemical techniques, there are other avenues, physiologic ones, such as photomotogrammetry, which can also be used. It is hoped that these paradigms will catalyze interest in this fascinating subject and generate research by others along these lines.

Blood Glucose↗

Detection of localized tooth-related factors that predispose to periodontal infections.

The primary goal of periodontal therapy is to produce an environment that is conducive to oral health. This is achieved by eliminating the subgingival infection and implementing supragingival plaque control measures designed to prevent the re-colonization of the sulcus. Local etiologic factors, as described above, my prevent the removal of subgingival plaque, and may even contribute to destruction of the periodontal tissues. Thus, it is crucial to be able to recognize and, when possible, eliminate any plaque-retentive factor that could contribute to disease progression. Iatrogenic factors such as subgingival margins, restorative overhangs, overcontoured restorations and unpolished surfaces can be altered. Similarly, cervical enamel projections, enamel pearls and, in certain instances, palatal grooves can be removed or recontoured to enable the patient to access the area for good plaque control. There are some things that we cannot alter. Anatomic anomalies, particularly in posterior teeth, cannot be changed. However, awareness of potential anatomic variations and early detection of them may be able to prevent future attachment loss.

Causality↗