Acute-phase proteins in gingival crevicular fluid during experimentally induced gingivitis

The dynamics of four acute-phase proteins were investigated in gingival crevicular fluid (GCF) during the course of a 21 day experimental gingivitis study. These acute-phase proteins were the protease inhibitors α2-macroglobulin (α2-M) and α1-antitrypsin (α1-AT) and the iron-binding proteins transferrin (TF) and lactoferrin (LF). 6 healthy volunteers ceased all oral hygiene procedures for 3 weeks. GCF was sampled at seven day intervals from two sites per subject by paper strips for 30 s during the experimental gingivitis period and for two additional weeks after the reinstitution of oral hygiene. The mainly serum derived α2-M, αl-AT and TF exhibited very similar dynamics which reflects their common origin in GCF. Their levels increased significantly from baseline and remained high for at least one week after the reinstitution of oral hygiene measures (repeated measures MANOVA; α2-M: p=0.015; α1-AT: p=0.012; TF: p=0.02). This probably reflects increased vascular permeability in the gingivae and, to a lesser degree, local production by gingival inflammatory cells. In contrast to the serum derived acute-phase proteins, the neutrophil derived LF rose significantly from baseline (repeated measures MANOVA; p=0.001) but dropped rapidly after the reinstitution of oral hygiene measures. This could be because dental plaque was removed and thus neutrophil chemotactic agents in the crevice were decreased.     

Quantitative and qualitative detection of cytomegalovirus-specific antibodies using two types of enzyme-linked immunosorbent assay

An indirect ELISA and an inhibition ELISA were developed for the detection of cytomegalovirus (CMV)-specific immunoglobulin G (IgG) and CMV-specific total immunoglobulin, respectively. Both assays were more specific than the complement fixation (CF) test, and titres of positive sera were 660 times higher by IgG ELISA and 6 times higher by inhibition ELISA than titres by the CF test. Titres by IgG ELISA were reliably determined using the absorbance obtained at a single serum dilution of 1/1,000 in conjunction with a standard graph. Both ELISAs compared favourably with each other in sensitivity and specificity in determining CMV immune status. The inhibition ELISA, in particular, provides a simple and reliable method of screening sera, which requires no control antigen or predilution of sera. It should prove useful for large-scale screening procedures, such as blood donor testing.     

The serology of delta hepatitis and the detection of IgM anti-HD by EIA using serum derived delta antigen

A sensitive and specific capture assay for IgM antibody to hepatitis D virus (HDV) was developed employing serum-derived delta antigen (HDAg). In a retrospective and prospective study of an outbreak of hepatitis B (HB), 135 hepatitis B surface antigen (HBsAg) positive drug-abusers with acute hepatitis and 18 HBsAg carriers, attending various hospitals and clinics in Dublin, were found to be infected with HDV. Serological follow-up was available from 24 of those with acute hepatitis allowing a comparison of the duration and level of IgM anti-HD with the more commonly used markers, HDAg and anti-delta (anti-HD), and an assessment of the usefulness of each. HDV and HB serology was grossly altered by human immunodeficiency virus (HIV) in two patients, with severe clinical manifestation in one. All 135 patients with HDV co-infection had delta antigenaemia. In co-infections with optimum sampling times, the mean duration of delta antigenaemia was 21 days. IgM anti-HD was always found between HDAg and sero-conversion to anti-delta and was the only 'window' marker present in five cases. The mean duration of IgM anti-HD was four weeks (optimum at 2.8 weeks) and was of moderate or low titre and occurred simultaneously with HDAg in 78%. In HDV-infected HBsAg carriers, high-titre IgM anti-HD (greater than 1/10,000) persisted for the duration of the study and is a useful indicator of chronic HDV infection. IgM anti-HD was not found in 202 random blood donors nor in 205 patients with non-B hepatitis or other disorders.(ABSTRACT TRUNCATED AT 250 WORDS)     

Periodontitis modified by systemic factors

Microbial dental plaque is the initiator of periodontal disease but whether it affects a particular subject, what form the disease takes, and how it progresses, are all dependent on the host defenses to this challenge. Systemic factors modify all forms periodontitis principally through their effects on the normal immune and inflammatory defenses. Some good examples of this effect exist such as when there is a reduction in number or function of polymorphonuclear leukocytes (PMNs) that may result in an increased rate and severity of periodontal destruction. Many other systemic factors are much less clear cut and are difficult to causally link to periodontitis. In many cases the literature is insufficient to make definite statements on links between systemic factors and periodontitis. It is also at times difficult to be precise regarding the causative agent in systemic exposures such as smoking and even prescribed drug therapy. The possible role of systemic diseases and systemic exposures in initiating or modifying the progress of periodontal disease is clearly a complex issue. It is however generally agreed that several conditions may give rise to an increased prevalence, incidence, or severity of gingivitis and periodontitis. The categorization of the systemic modifying factors causing periodontitis and the evidence to support the role of these factors are the focus of this review. An attempt has been made to consider the conditions under broad headings, but it will be clear that many conditions fall within more than one category and that for several conditions only case reports exist whereas in other areas an extensive literature is present.