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Notes: Objective: To compare the progression of periodontal destruction in people with and without HIV.Method: Relative attachment loss on 6 index teeth was compared between 19 people with HIV and 17 people without HIV infection over 12 and 18 month follow ups.Results: The proportions of sites with 1, 2 or 3 mm of relative attachment loss were similar in the study and control groups. Mean maximum relative attachment loss was similar in both groups after 12 months but greater in the study group after 18 months.Conclusions: The data are not compelling evidence of greater periodontal destruction associated with HIV infection. Large scale cohort studies or meta-analyses would be more conclusive.

Notes: Background: Inactivation of the elastase inhibitor, α1 proteinase inhibitor (α1PI), may be of pathogenic significance in inflammatory diseases like periodontal disease. Two key mechanisms of inactivation appear to be (a) the formation of an α1PI–elastase complex and (b) proteolytic cleavage by elastase or other enzymes such as metalloproteinases of host origin or enzymes of bacterial origin. Based on the different heat stabilities of the intact, complexed and proteolytically cleaved forms of α1PI, an enzyme-linked immunosorbent assay (ELISA) that allowed the simultaneous measurement of native and inactive forms of α1PI was developed.Methods: The ELISA method described employs a commercially available antibody and represents a rapid, reproducible and sensitive method for studying α1PI inactivation in human inflammatory diseases. The assay was applied to normal human plasma and to human extracellular fluids obtained from patients with inflammatory diseases such as adult periodontitis and rheumatoid arthritis. Samples from patients with osteoarthritis, a “non-inflammatory” joint disease, were also studied.Results: The findings expressed as the mean percentage (±SD) of the total α1PI that was inactivated were as follows: gingival crevicular fluid from adult periodontitis patients: 73.5±16.6% (n=12); normal human plasma: 8.4±4.9% (n=13); knee-joint synovial fluid (SF) from rheumatoid arthritis patients: 12.5±4.5% (n=15); plasma from rheumatoid arthritis patients: 8.0±1.8% (n=15); knee-joint SF from osteoarthritis patients: 8.6±8.2% (n=14); plasma from osteoarthritis patients: 5.7±4.8% (n=14). The results obtained by ELISA were in good agreement with those obtained by the semi-quantitative method of SDS–PAGE and Western blotting.Conclusions: We have shown that the differential heat stability of α1PI may be utilised as the basis for a rapid, sensitive and reproducible ELISA assay of α1PI inactivation. In gingival crevicular fluid from periodontal disease patients, α1PI is mainly inactivated and the extent of this inactivation is much higher than in inflammatory fluids from other chronic diseases such as rheumatoid arthritis. This assay could be useful in monitoring the progression of periodontal disease.

Notes: Abstract Periodontal microbiology is reviewed with regard to the potential of certain characteristics to serve as markers of high risk groups or individuals for periodontal diseases. The generally accepted associations between particular organisms and the various periodontal diseases are discussed. The usefulness of various clinical study designs is reviewed. The ecology of the subgingival plaque microflora is discussed and a number of suggestions for future research are made. We have concluded that there is no monospecific aetiology to any of the various periodontal conditions. Nevertheless, we give particular attention to the role of the black-pigmented bacteroides based upon our belief that they, and Bacteroides gingivalis in particular, are fundamental to our understanding of the biology of periodontal diseases in humans and other animals. Consequently, the contribution of its various virulence factors and their potential as markers of disease susceptibility and activity is addressed.

Notes: Abstract. The total protein concentration of gingival crevicular fluid (GCF), sampled repeatedly over a 10-min period with the minimum of physical irritation to the sulcus. was evaluated in a group of 32 healthy adolescent. The mean concentration of the 1 st sample was comparable to that of normal tissue fluids and lymph, irrespective of the state of inflammation of the sample site. However, during repeated sampling, the values rose to resemble serum protein levels, except at those sites with no clinically detectable inflammation. Gel eletrophoretic analysis confirmed the increasing proportion of serum-derived molecules in the more proteinaceous GCF samples. The results demonstrate the extreme sensitivity of the gingival vasculature to GCF sampling and consequently the need for accurate standardisation of GCF collection protocols. This will apply particularly when compositional data is to be normalised with respect to the total protein content or when the levels of a serum constituent are being examined.

Notes: Abstract The evidence for systemic predisposition to periodontal diseases is reviewed in relation to cellular and humoral immunity, drug therapy, diet and nutrition and stress. It is concluded that, apart from defects of polymorphonuclear leukocytes (PMN) and Ehlers-Danlos Syndrome, little firm evidence exists for other diseases, though insulin-dependent diabetes and acquired immune deficiency syndrome (AIDS) may accelerate and/or potentiate the damage of existing disease. The precise role of drugs, diet and nutrition and stress remain to be elucidated, but recent advances in these areas offer the prospect of assessing risk using carefully controlled studies.

Notes: Aim: The aims of this study were to monitor the prevalence and progression of lifetime cumulative attachment loss (LCAL) in a group of young British male military recruits over a 3-year period, and to determine the relationship between signs of LCAL and selected periodontal variables.Methods: 100 subjects, aged 16–20 years (mean 17 years) at baseline, were examined at 0 (baseline), 12 and 30 months. LCAL, probing depth, plaque, bleeding on probing, gingival colour and supra- and subgingival calculus were assessed on the mesio-buccal, disto-buccal, mesio-lingual and disto-lingual surfaces of all teeth present, excluding third molars. Data were analysed cross-sectionally at each examination.Results: Over the period of the study, the prevalence of LCAL 〈inlineGraphic alt="geqslant R: gt-or-equal, slanted" extraInfo="nonStandardEntity" href="urn:x-wiley:03036979:JCPE281010:ges" location="ges.gif"/〉1 and 2 mm ranged from 95–100%, whereas LCAL 〈inlineGraphic alt="geqslant R: gt-or-equal, slanted" extraInfo="nonStandardEntity" href="urn:x-wiley:03036979:JCPE281010:ges" location="ges.gif"/〉3 mm ranged from 40–47%. The extent of LCAL 〈inlineGraphic alt="geqslant R: gt-or-equal, slanted" extraInfo="nonStandardEntity" href="urn:x-wiley:03036979:JCPE281010:ges" location="ges.gif"/〉1 mm ranged from 76–86%. However, the extent of LCAL 〈inlineGraphic alt="geqslant R: gt-or-equal, slanted" extraInfo="nonStandardEntity" href="urn:x-wiley:03036979:JCPE281010:ges" location="ges.gif"/〉2 mm was dramatically lower (10.5–12.7%), and LCAL 〈inlineGraphic alt="geqslant R: gt-or-equal, slanted" extraInfo="nonStandardEntity" href="urn:x-wiley:03036979:JCPE281010:ges" location="ges.gif"/〉3 mm was uncommon (0.5–0.9%). Examining the number of subjects according to the number of sites affected above a threshold, showed that a small number of subjects have a large number of sites above threshold. Using Pearson’s rank correlation coefficient a significant correlation (p〈0.05) was found between LCAL and the periodontal variables of gingival bleeding and supra- and subgingival calculus.Conclusions: These data suggest that the onset and progression of chronic periodontitis can be seen in young adults, and in this group gingival bleeding and supra- and subgingival calculus are the variables most strongly associated with early periodontitis.

Notes: Abstract We have estimated the levels of Interleukin-1 beta (IL-1β) by ELISA in gingival crevicular fluid (GCF) at 58 sites from 37 patients with adult periodontitis. GCF was collected for 5 s on filter papers and a 2nd sample was collected for 30 s 1 min later. 68/116 strips yielded detectable levels of IL-1β. IL-1β was present in both the 1 st and 2nd samples at 28 sites, in the 1 st only at 4 sites and in the 2nd only at 8 sites; 18 sites were below the level of detection for the assay. When the concentrations of IL-1β were calculated in the original volume of GCF on each strip, the mean value for positive strips was 34.16±29.45 (SD) pg/μ1 with a range from 1.75 to 97.13 pg/μ. There were no statistically significant correlations with the plaque index, bleeding index or probeable crevice depth (pocket depth). The results indicate that IL-1 is present in the GCF from a proportion of sites with evidence of previous periodontal destruction.

Notes: Abstract We have reviewed the recent literature on the humoral immune responses to a variety of subgingival plaque bacterial species in patients with destructive periodontal diseases. We do not feel that the information presently available on the specific antibody responses to proposed pathogens such as Bacteroides gingivalis and Actinobacillus actinomycetemcomitans allows antibody responses to be diagnostic. All control subjects without periodontal destruction have antibodies to candidate pathogens but the generally higher levels in patients are not sufficiently elevated to be diagnostic. Nor can they be used to predict the initiation of disease or the onset of new episodes of destruction where disease had previously occurred. Successful treatment of patients may lead to lower levels of antibodies to some organisms, including possible pathogens, and thus support a given species in the aetiopathogenesis of disease. It appears that unsuccessful treatment may be accompanied by continuing high antibody levels to some organisms and further studies may enable this observation to be used to monitor therapy. There is some evidence from serological studies that each destructive episode may be induced by a different bacterial species or consortium. The start of studies using single antigens and the techniques of molecular biology will provide not only antibody-based diagnostic methods but also allow us to determine which bacterial antigens are virulence factors and thus the role of the antibody responses, whether protective or damaging, in the periodontal diseases.

Notes: Abstract It is argued that the periodontal diseases can no longer be regarded as universally prevalent conditions to which all members of the world's population are at equal risk if they fail to practise good oral hygiene. Rather, they should be regarded as a range of different diseases for each of which certain individuals, which together comprise certain minority groups, are at relatively high risk. The epidemiological evidence for the existence of high-risk groups is reviewed, from which it is concluded that world-wide the prevalence of severe destructive periodontitis is of the order of only 7–15% of the adult dentate population. A working classification of the different types of gingivitis and periodontitis is offered, as is a summary of the theoretically possible approaches to the detection of high-risk groups and individuals which are explored in detail in subsequent papers. Successful identification of such individuals will permit scientifically valid, rational and targetted prevention and treatment.

Notes: Abstract The use of saliva as a source of components that may identify subjects at risk of developing destructive periodontitis. or provide markers of disease potential or activity, has been reviewed. It was concluded that bacteria, their constituents or products are unlikely to be rewarding and that host-derived salivary factors such as enzymes cannot identify risk, as deficiency states for these do not exist. Secretory IgA, plasma IgA and IgG isotype levels and specific antibodies may be associated with risk, but probably only if levels fall below those which are protective or a specific antibody response is absent. More work is needed to distinguish between monomeric and dimeric IgA antibodies and to identify IgG antibodies in longitudinal clinical studies. In general, although saliva may prove to be useful as a source of indicators of current disease activity or as a means of assessing responses to treatment, it is unlikely to provide evidence for the existence of risk factors.