Periodontal disease has been suggested to be an important risk factor for preterm low birthweight (PLBW). Here we report a case-control study of 236 cases (infants < 37 wks and weighing < 2499 g) and a daily random sample of 507 controls (> or = 38 wks and weighing > or = 2500 g). Clinical periodontal indices were measured on the labor wards. Associated risk factors for periodontal disease and PLBW were ascertained by means of a structured questionnaire and maternity notes. The risk for PLBW decreased with increasing pocket depth (odds ratio [OR] 0.83, 95% confidence interval [CI] 0.68 to 1.00). After adjustment for maternal age, ethnicity, maternal education, smoking, alcohol consumption, infections, and hypertension during pregnancy, this decreased further (OR 0.78, 95% CI 0.64 to 0.99). We found no evidence for an association between PLBW and periodontal disease. Our results do not support a specific drive to improve periodontal health of pregnant women as a means of improving pregnancy outcomes.

The influence of subject-based and environmental factors on the balance between the subgingival microbial challenge and the host response in periodontal diseases illustrates the intimate link between oral and systemic health. From this stems the hypothesis that the persistent Gram-negative challenge and associated inflammatory sequelae in periodontal disease may have consequences extending beyond the periodontal tissues themselves. This paper addresses the design of a case-control study to examine the relationship between preterm low birth weight (PLBW) and maternal periodontal disease. We present preliminary data on the prevalence of these 2 conditions in a group of mothers at the Royal Hospitals Trust, London, U.K. Cases are defined as mothers delivering an infant weighing less than 2,500g before 37 weeks gestation and controls as mothers delivering an infant of more than 2,500g after 38 weeks. We estimated that a study involving 800 mothers (1:3 case:control) should have sufficient power to detect an association with a minimum odds ration of 3 at the 5% significance level. Demographic details of 177 subjects demonstrated that they were representative of the local population, and the prevalence of PLBW was within the expected range. However, the extent and severity of periodontal disease were higher than predicted and may have reflected elevations in gingival inflammation associated with pregnancy. The final outcome of the study should help determine the need for further interventionist studies to demonstrate a causal relationship between periodontal disease and PLBW, as well as provide information on the prevalence of periodontal diseases in this study population.

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.

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Gingival crevicular fluid (GCF) sampling was performed on 2 occasions separated by 1 year, at 2 sites in the mouths of 102 male adolescents, mean age 17.85 years. Samples were collected onto 5 filter paper strips which were sequentially applied to the mouth of the crevice over a 9-min collection period. Volume and flow rates of GCF were determined for each site and were compared with clinical measurements of plaque, gingival colour, bleeding, gingival index (GI) and pocket depth, using a general linear models (GLM) procedure. While the initial volume of GCF showed no association with any clinical measurement, there was an association between flow rate of GCF and gingival colour. The volume of GCF collected in the final, 5th sample was associated with the GI. The sample site strongly influenced all measures of GCF volume. It is proposed that the flow rate of GCF may be a better indicator of gingival inflammation than the more imprecise clinical assessments of inflammation, since GCF flow rates more precisely reflect changes in tissue permeability. The association between the final sample, collected after 9 min, and clinical measurements, was probably a reflection of the association between clinically-detectable inflammation and the susceptibility of the site to mild irritation.

The Arg-and Lys-gingipains of Porphyromonas gingivalis are important virulence determinants in periodontal disease and may correspond to targets for immune-or drug-based treatment strategies. In this investigation we aimed to determine which of these enzymes represents the most promising molecular target for protease inhibitor-based therapy and to examine the effectiveness of the resultant compound in a murine virulence assay. Isogenic mutants with mutations in rgpA and rgpB (encoding Arg-gingipains) and in kgp (encoding Lys-gingipain) and a double mutant with mutations in rgpA and rgpB were prepared by using P. gingivalis W50. The virulence of these mutants indicated that Kgp is a promising drug target. Combinatorial chemistry was used to define the optimal substrate of Kgp, and from this information a specific slowly reversible inhibitor with a nanomolar K i was designed and synthesized. Growth of P. gingivalis W50 in the presence of this compound resembled the phenotype of the kgp isogenic mutant; in both instances bacterial colonies failed to form pigment on blood agar, and only poor growth was obtained in a defined medium containing albumin as the sole protein source. Furthermore, pretreatment of the wild-type organism with the Kgp inhibitor led to a significant reduction in virulence in the murine assay. These data emphasize the conclusion that Kgp is an important factor for both nutrition and virulence of P. gingivalis and that inhibitors of this enzyme may have therapeutic potential for the control of P. gingivalis infections. Protease inhibitors may be a potentially novel class of antimicrobial agents with relevance to the control of other bacterial pathogens.

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 rôle 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.