No evidence of hepatitis C virus infection in Serbian patients with oral leukoplakia.

BACKGROUND: A review of the literature reveals controversy regarding the relationship between hepatitis C virus (HCV) infection and oral leukoplakia (OL). The aim of this study was to determine the frequency of HCV antibodies in patients with OL and control subjects resident in Serbia. METHODS: In this cross-sectional study 73 consecutive patients with histologically proven OL and 90 control subjects, whose age and gender were matched, were examined for the presence of serological evidence of chronic hepatic disease, hepatitis B surface antigen (HBsAg) and anti-HCV seropositivity. RESULTS: None of the patients with OL or control subjects had antibodies to HCV or HBsAg. All patients with OL and control subjects had normal liver function. CONCLUSION: The present data indicate that patients with OL resident in Serbia do not have evidence of HCV or HBV infection.

Lack of evidence of hepatic disease in patients with oral lichen planus in Serbia.

OBJECTIVE: The reported frequency of chronic liver disease, and particularly, Hepatitis C virus (HCV) infection in patients with oral lichen planus (OLP) shows geographical variation. The aim of this study was to determine the prevalence of chronic hepatic disease, Hepatitis B virus and HCV infection in patients with OLP and control subjects resident in Serbia. PATIENTS AND METHODS: In this prospective study 48 patients with OLP (33 women and 15 men, with a mean age of 49.7 years) and 60 control subjects (38 women and 22 men, with a mean age of 46.7 years) were examined for the presence of serological evidence of chronic hepatic disease, Hepatitis B surface antigen (HBsAg) and anti-HCV seropositivity. RESULTS: All patients with OLP had normal liver function. HBsAg was not found in any of the patients with OLP or control group. None of the patients with OLP or control subjects were HCV seropositive. CONCLUSION: Patients with OLP resident in Serbia do not have evidence of chronic liver disease or infection with HBV or HCV. The exact aetiological role between hepatic disease and OLP remains unclear.

[Clinical use of tetracyclines in the treatment of periodontal diseases]. / Klinicka upotreba tetraciklina u lecenju parodontopatije.

INTRODUCTION: There are a number of chemically different tetracycline homologues. The older group of tetracyclines, which was introduced in the 1950-60s, includes tetracycline, oxytetracycline, chlortetracycline and demeclocycline. The newer group of tetracyclines includes doxycycline, methacycline and minocycline. PHARMACOKINETICS: Elevated concentration of tetracycline in gingival fluid with respect to blood levels was an unexpected phenomenon. Patients given 250 mg every 6 hours had average crevicular fluid concentrations between 4 to 8 g/ml and blood concentrations between 2 to 2.5 g/ml after 48 hours. The levels in crevicular fluid and blood of volunteers who received 250 mg every 12 hours were 2 to 4 g/ml and 0.3 to 1.4 g/ml respectively after 48 hours. The concentration of doxycycline in gingival fluid after administration of 200 mg/1st day and then 100 mg/day achieved average level of 6 g/ml. Minocycline, a semisynthetic derivate of tetracycline, has shown to yield gingival fluid levels 5 times as high as serum levels after administration of 100 mg every 12 hours. MECHANISMS OF ACTION: Tetracycline and its derivates demonstrate high in vitro activity against most periodontal bacteria, including Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Eikenella corrodens, Wolinella recta and Fusobacterium nucleatum. The study of in vitro susceptibility of these 6 bacterial strains showed that, in regard to blood level, minimal inhibitory concentration is higher and it is the concentration of the drug that can be expected in gingival fluid following oral administration of 100 mg per day (doxycycline) (Table 1). The anti-inflammatory effect of tetracyclines was demonstrated histologically not only by reducing the size of the infiltrated connective tissue, but qualitative changes were also observed. Golub and associates have presented evidence that tetracyclines inhibit collagenase activity in gingival fluid and in tissue cultures. Therapeutic concentrations of tetracycline inhibit chemotaxis, phagocytosis and random migration of neutrophils in vitro. ADVERSE EFFECTS: Great amounts of tetracyclines cause gastrointestinal disorders, nausea, vomiting and diarrhea. Tetracyclines suppress activity of the enzymes in the bowel and pancreas. During longlasting administration they can damage the liver and kidneys. Tetracyclines can cause photo-sensibilization. They make deposits with calcium in bones, specially during prenatal period and during growth, so they can cause permanent teeth discoloration and hypoplasia. INTERACTIONS: The most important interaction is with penicillin. These two kinds of antibiotics antagonize and decrease the therapeutic effect of each other, so their administration at the same time should be avoided. A significant interaction occurs between tetracyclines and metal ions. This interaction often has been observed in conjunction with use of various antacids. Tetracyclines can also influence the production and absorption of vitamin K. Nephrotoxicity has been reported when tetracyclines have been administrated in conjunction with methoxyflurane. INDICATIONS: Doxycycline, due to its advantages over tetracycline (Table 2), is indicated in treating destructive periodontal diseases including: juvenile periodontitis and refractory marginal periodontitis. Doxycycline therapy may be used for acute periodontal abscess and if the conditions are accompanied by general symptoms. Prophylactic application is recommended for implant placement procedures including membranes in guided tissue regeneration. RESULTS OF CLINICAL STUDY: ORAL APPLICATION: In spite of great number of published investigations this paper presents only the results of placebo-controlled, double-blind studies. There is evidence that therapy in localized juvenile periodontitis should eliminate Actinobacillus actinomycetemcomitans, since 95% of patients harbored this bacteria. (ABSTRACT TRUNCATED)

[Clinical significance of analysis of immunoglobulin A levels in saliva]. / Klinicki znacaj analize koncentracije imunoglobulina A u pljuvacki.

SALIVA COLLECTION: Whole saliva is a product of secretion of 3 major glands (parotid, submandibular, sublingual) and many minor glands (labial, buccal, palatal). Unstimulated saliva is usually obtained as the patient spits out every 60 sec. or by forward bended head the patient allows saliva to drip off the lower lip into a cylinder. By collection of saliva in the tube the flow rate per unit time can be measured. When volume measurement is not required the saliva can be collected on cotton rolls, gauze or filter paper. For evaluating salivary gland function or when large volumes of saliva are required for analytic purposes, stimulated whole saliva is used. Method of collection is the same as for unstimulated saliva. The usual masticatory stimuli are paraffin wax or a washed rubber band. A standard gustatory stimulus is obtained by 2% citric acid applied directly to the tongue every 15 to 60 sec. Parotid saliva can be collected by aspiration from the duct opening with a micropipette. Parotid saliva is best collected with Lashley's vacuum chamber. Submandibular and sublingual saliva can be collected by cannulation of the duct with micropipette, but in practice this is both uncomfortable for the patients and technically difficult since the duct orifice is mobile and has a strong sphincter. Because of that, alginate and silicone impression material is used for retention of the collecting tube. As alternative and simple technique is to block off secretion from the parotid glands with absorbent swabs and collect mixed submandibular and sublingual saliva by pipette from the floor of the mouth. Saliva from labial and palatal glands can be collected by filter paper disc or disc of other synthetic materials. SALIVARY IMMUNOGLOBULIN A: The most significant characteristics of the salivary immunoglobulin system are quantitative domination of immunoglobulin A, local synthesis and specific structure. Immunofluorescence studies have shown that immunoglobulin A is produced by plasma cells locally in the salivary glands. There is still little convincing evidence for the origin of predominantly immunoglobulin A secreting plasma cells in salivary glands. DETECTION OF IMMUNOGLOBULIN A IN SALIVA: Radial immunodiffusion (RID) was the most applicable method for detecting salivary immunoglobulin A. However, there are more sensitive and automatic methods such as nephelometry and ELISA. A standard level of immunoglobulin in saliva is still in question since the concentration varies in relation to origin of saliva, method of collection and stimulation of secretion (Table 1). PERIODONTAL DISEASE: Studies of the salivary immunoglobulin A in patients with periodontal disease and healthy persons showed that there are differences which can be used in detection of high-risk groups and individuals. If the bacterial adherence to the mucosa is a prerequisite for bacterial evolution in subgingival or any other region of the oral cavity respectively introduction in periodontitis development, than it is to be presumed that the basic function of salivary immunoglobulin A is inhibition of bacterial adherence rather than antigens destruction. Several bacterial species frequently isolated from the oral cavity of patients with periodontitis have been identified as producers of IgA protease. These enzymes cleave serum IgA and secretory IgA equally well. Additionally, most of the IgA proteases studied have cleaved the A1 and A2 subclass. Several studies have demonstrated that cleavage of human IgA occurs in vivo, resulting in generation of intact Fab alpha and (Fc alpha)2 fragment. Moreover, when bacteria are exposed to Fab alpha fragments released from IgA after cleavage by IgA protease, their surface antigens are likely to be occupied by Fab alpha fragments. These Fab alpha fragments left on the bacterial surface may mediate adhesion. Together, these results indicate that IgA proteases, by promoting adherence, contribute the pathogenic potential of bacteria in the oral c

[Gingival hyperplasia during treatment with nifedipine]. / Hiperplazija gingive u toku lecenja nifedipinom.

INTRODUCTION: Nifedipine is a relatively new and increasingly used medication for treatment of all kinds of angina pectoris and arterial hypertension. The principal action of nifedipine is to inhibit the influx of extracellular calcium ions across the membranes of cardiac and vascular smooth muscle cells, without changing serum calcium concentration (1). One of the side effects of this drug is gingival hyperplasia which was first described in 1984 by Lederman (2). He noted that gingival hyperplasia is mostly marked on the labial gingiva of the upper and lower anterior teeth and appeared 1 to 2 months after nifedipine therapy began at a dose of 90 mg per day, and never occurs in edentulous areas. This paper reports gingival hyperplasia in a patient treated with nifedipine. CASE REPORT: A 73-year-old man referred to the dental clinic for evaluation of gingival enlargement in the maxillar left quadrant which he had noticed about 3 months after starting the nifedipine therapy. Clinical examination showed gingival enlargement around the teeth 22, 23, 24 and 27, but with normal edentulous area (Fig. 1). The enlarged gingiva was red, smooth and shiny, with no pain on touch, and bled easily on probing. There were metal crowns with overhanging margins and pseudopockets--6 mm with dental plaque and calculus. Radiographs showed moderate alveolar bone resorption of horizontal type. The patient's maxillar left first premolar exhibited severe bone loss, resulting in a hopeless prognosis. This tooth was extracted under local anesthesia. The dental treatment included replacement of the ill-fitting metal crowns, scaling and root planning, and instructions on appropriate method for brushing teeth. 6 weeks later, the hyperplastic tissues were removed surgically. In a 1-year follow-up period, the patient was recalled at regular intervals for control, and no signs of recurrence of gingival hyperplasia have been observed in spite of continued nifedipine treatment. Biopsies taken from the gingivectomy specimens were handled with standard histological method. Histological examination showed a thick epithelium with parakeratosis and acanthosis, and irregular elongation of the rete peg. The underlying connective tissues contained dense fibers with inflammatory cell infiltrate mainly composed of plasma cells. DISCUSSION: The exact mechanism of action of nifedipine in causing gingival enlargement is unknown at present. There is also no answer to the question why gingival enlargement appears in some patients treated with nifedipine, but in others not. The clinical findings (3, 4, 5, 6, 7) and results of in vitro study (8) and this case report showed that hyperplastic change of gingiva started only in areas displaying signs of inflammation, but not in healthy and edentulous areas. These observations suggest that local factors and associated inflammation is essential for onset of the nifedipine-induced gingival hyperplasa. Moreover, it was suggested that duration of nifedipine therapy (more than 2 months) and drug dosage (90 mg per day) could be important (1,2,3). This case report also demonstrates that no signs of recurrence of hyperplasia were observed after elimination of the local inflammatory factors: extensive dental pluque control and surgical removal of the hyperplastic gingival tissue even though administration of nifedipine was continued. CONCLUSION: It was concluded that gingival enlargement occurs in patients with nifedipine therapy only in the areas where local inflammatory factors are present.

The concentration of immunoglobulins A, G, and M in serum of patients with periodontal disease.

The aim of this study was to assess if there are any significant differences of immunoglobulin A, G and M concentration in serum of persons with different stages of periodontal destruction. The study comprised 30 persons (21 female and 9 male) with a mean age of 37.5 years, in whom periodontitis was diagnosed after clinical examination and x-ray analysis. After that the selection of patients was made according to the following criteria: 1. no systemic disease; 2. no basic periodontal therapy undertaken in the last three months; 3. presence of at least 20 teeth; 4. no antibiotics taken in the last three months. The control group consisted of 30 healthy persons with a mean age of 23.0 years in whom healthy periodontium was diagnosed after clinical examination and x-ray analysis, and only 1, 3 and 4 of above-mentioned criteria had to be fulfilled. The seversity of clinical gingival inflammation was determined by gingival index after Loben (5). The severity of periodontal destruction was assessed by measuring the pocket depth. The immunoglobulin A, G and M concentration in serum was determined by method of nephelometry on the day obtaining the sample. The mean values of immunoglobulin A, G and M in serum of patients with periodontitis were in normal ranges and not significantly different compared to the control group (p > 0.05). There is no relationship between the serum immunoglobulins A, G and M and severity of gingival inflammation and periodontal destruction.