Detection of stable and active periodontitis sites by clinical assessment and gingival crevicular acute-phase protein levels

The aim of the present study was to investigate whether incipient periodontal disease breakdown could be associated with changes in gingival crevicular fluid (GCF) acute-phase protein levels. In addition, the potential of clinical indices to act as predictors of significant attachment level (AL) change was investigated. AL measurements were taken at baseline and 3 months using the Florida Probe stent handpiece from a total of 384 sites in 38 patients. The average standard deviation of duplicate AL measurements was 0.423. When the tolerance method was used to detect significant AL change, 3.9% of the sites lost attachment. When a less stringent criterion of AL change of ≥1 mm was used 9.9% of the sites lost attachment during the 3-month period. With the exception of probing depth, baseline clinical parameters failed to predict AL change. Fourteen active periodontitis sites that demonstrated significant attachment loss were paired to stable periodontitis sites within the same patient. The levels of four acute-phase proteins, namely α2-macroglobulin (α2-M), α1-antitrypsin (α1-AT), transferrin (TF) and lactoferrin (LF), and also albumin (Alb) were assessed in the same gingival crevicular fluid sample using sandwich ELISAs. Results were expressed either as ng/30 s and ng/μg Alb. Acute-phase protein levels in GCF failed to differentiate between active and stable periodontitis sites at baseline. In conclusion, the degree of gingival inflammation of the tissues adjacent to the crevice/pocket seems to influence the levels of protease inhibitors and iron-binding proteins in GCF to a greater extent than probing attachment loss.     

The host cytokine response to Porphyromonas gingivalis is modified by gingipains

Background/aims:  Clinical studies indicate that primary proinflammatory cytokines, such as interleukin-1β (IL-1β) are elevated in the gingival crevice around teeth with periodontitis but the secondary cytokines and chemokines, IL-6 and IL-8, are not. The human gingival epithelial cells (HGECs) lining the gingival sulcus respond to perturbation by microbes of dental plaque by releasing a wide range of cytokines. Porphyromonas gingivalis , a putative periodontal pathogen, possesses numerous virulence factors some of which directly impact on the host response. In the present study, we sought to determine how P. gingivalis influences the inflammatory cytokine responses.
Methods:  HGECs were challenged with P. gingivalis and other putative periodontal pathogens, and the resultant production of IL-1β, IL-6, and IL-8 was assayed by enzyme-linked immunosorbent assay (ELISA). Culture supernatants and recombinant human cytokines were challenged with live P. gingivalis wild-type and gingipain-deficient strains and the resultant cytokine profile was assessed by ELISA and Western blot.
Results:  We show here that primary HGECs challenged with live P. gingivalis result in high levels of IL-1β but not the related secondary cytokines IL-6 and IL-8. We further demonstrate that cytokine response differences are the result of the action of P. gingivalis proteases, with lysine gingipain being the most effective.
Conclusion:  We conclude that P. gingivalis , through lysine gingipain, can subvert the protective host proinflammatory response by direct cytokine degradation. Changes in the crevicular cytokine profile have consequences in periodontal disease pathogenesis that should be considered in the development of diagnostic and therapeutic modalities.     

Gingival crevicular fluid IL-6, tPA,PAI-2, albumin levels following initial periodontal treatment in chronic periodontitis patients with or without type 2 diabetes

Objectives  

To evaluate initial periodontal treatment effects on gingival crevicular fluid (GCF) interleukin-6 (IL-6), tissue-type plasminogen activator (tPA), plasminogen activator inhibitor-2 (PAI-2), albumin levels in type 2 diabetic patients.     

儿童间质性肺疾病的分类、诊断和治疗的新观点

刘秀云主任医师很荣幸受《中国循证儿科杂志》编辑部的委托,与申昆玲教授邀请的来自美国哈佛大学医学部麻省总医院儿童呼吸中心主任,T.Bernard Kinane教授就儿间质性疾病,     

Cross-sectional assessment of caries and periodontitis risk within the same subject

Dental caries and chronic periodontitis may be synergistically associated, negatively associated, or completely independent. The present report examines this relationship by comparing the susceptibility to chronic periodontitis and caries within the same individual. From an 800-patient sample, a periodontitis risk score was derived by radiographic assessment of bone loss in quarters of optimum bone height and obtaining for each subject a mean score based on all measurable surfaces. Similarly the caries risk was determined radiographically from the total decayed and filled teeth (DFT), as a percentage of the total teeth measured. The Mantel-Haenszel technique was used for analysis of the relationship between periodontitis and caries and data was stratified on four categories of age, sex, and numbers of teeth present. This analysis revealed no systematic patterns, indicating that the risks of caries and periodontal diseases are unrelated (chi 2 = 0.00; 1 df; P greater than 0.50). In addition, a regression analysis, which was controlled for sex and age, indicated a marked lack of association between caries and periodontitis (P = 0.94). Thus, although these common diseases share putative etiologic factors such as oral hygiene practices and dental attendance pattern, the major risk factors are probably quite different.     

Relative avidity of serum antibodies to putative periodontopathogens in periodontal disease

ELISA was used to determine both the avidity and titre of IgG, IgA and IgM antibodies to the gram-negative anaerobe. Porphyromonas gingivalis, in twenty periodontitis patients enrolled in a longitudinal study of attachment loss and eleven non-periodontitis affected subjects. The avidity and titre of IgG antibodies to Actinobacillus Actinomycetemcomitans were also examined. A cross-sectional analysis of the longitudinal patients at baseline and non-periodontally affected controls confirmed earlier findings that IgG and IgA antibody titres to P. gingivalis were higher in periodontitis patients than in individuals who were not periodontally affected. In this cross-sectional analysis, IgG antibody avidities to P. gingivalis were not found to be significantly higher in periodontitis than in control subjects (p = 0.065). However, indications of the potential prognostic value of antibody avidity was demonstrated by the higher IgM avidities to P. gingivalis in patients who did not experience attachment loss during the three-month monitoring period than in those who did (p=0.0005).     

A six-month comparison of three periodontal local antimicrobial therapies in persistent periodontal pockets

BACKGROUND: Currently, several local antimicrobial delivery systems are available to periodontists. The aim of this 6-month follow-up parallel study was to evaluate the efficacy of three commercially available local delivery systems as adjuncts to scaling and root planing in the treatment of sites with persistent periodontal lesions. METHODS: Seventy-nine patients with 4 pockets > or = 5 mm and bleeding on probing and/or suppuration were randomized into 4 treatment groups which included: scaling and root planing alone (S) (20 patients), or in conjunction with the application of 25% tetracycline fibers (S+Tet) (19 patients), or 2% minocycline gel (S+Min) (21 patients), or 25% metronidazole gel (S+Met) (19 patients). Clinical measurements were taken at baseline, 6 weeks, 3 months, and 6 months after antimicrobial application. Treatments were applied using the distributors' recommended protocols. RESULTS: All 4 therapies resulted in significant improvements from baseline in probing depth, attachment level, bleeding on probing, and the Modified Gingival Index (MGI) scores. The improvements in clinical parameters were greater in all 3 adjunctive treatment groups than scaling and root planing alone. The mean probing depth reductions at 6 months were: scaling + tetracycline = 1.38 mm; scaling + metronidazole = 0.93 mm; scaling + minocycline = 1.10 mm; and scaling alone = 0.71 mm. The probing depth reduction at all time points was significantly greater in the scaling plus tetracycline fiber group than the scaling and root planing alone group (P<0.01). There was also a significant improvement for scaling plus tetracycline fiber application over scaling and metronidazole at both 6 weeks and 3 months, although this did not remain significant at the 6-month visit. While the frequency of sites with suppuration was markedly reduced following all antimicrobial treatments, the most effective reductions were seen in the scaling plus tetracycline fiber group, followed by the minocycline group. CONCLUSIONS: Although all 3 locally applied antimicrobial systems seem to offer some benefit over scaling and root planing alone, a treatment regimen of scaling and root planing plus tetracycline fiber placement gave the greatest reduction in probing depth over the 6 months after treatment.     

Immune processes in periodontal disease: a review

The inflammatory and immune processes in periodontitis are complex and, although a great deal of information is available, many questions remain. Variation in human susceptibility to periodontitis has long been accepted, but the pathological basis of this is poorly understood. Similarly, we know little of the differences, if any, between the pathology of chronic and aggressive periodontitis. Genetics and environmental influences play a role in the susceptibility process, but if and how that translates through the immune and inflammatory processes to produce the plasma cell-dominated lesions seen in periodontitis remain to be elucidated. This review will focus on immunological aspects of the inflammatory changes seen in gingivitis and periodontitis, addressing both humoral and cellular responses to the microbial insult from dental plaque. A tendency for an individual or site to form an extensive plasma cell infiltrate may indicate an inability to defend against periodontopathogens and thus a predisposition to periodontitis. The issues to be considered include: 1) homing of immune and inflammatory cells to target tissues; 2) their local proliferation and synthetic activity; 3) the cytokine profile of the leukocytes; 4) the immunoglobulin subclasses of locally produced antibodies; 5) mucosal and systemic immune characteristics of the response; 6) the humoral immune response in periodontal health and disease states; and 7) the antigenic target of the immune response in periodontal lesions.     

Antibody responses against Porphyromonas gingivalis infection in patients with early-onset periodontitis

BACKGROUND, AIMS: The aim of this study was to evaluate antibody responses against Porphyromonas gingivalis (P. gingivalis) infection in early-onset periodontitis (EOP) patients to elucidate further the host-parasite interactions in the pathogenesis of EOP. METHOD: 16 P. gingivalis-infected EOP and 20 adult periodontitis (AP) patients, and 18 periodontally healthy subjects (HS) participated in this study. Serum immunoglobulin G (IgG) antibody levels and avidities against extracted P. gingivalis whole cells were measured. The components of P. gingivalis outer membrane antigens (OMA) reacting to patients' sera were analysed from the molecular weights by Western blotting. Serum antibody levels against P. gingivalis lipopolysaccharide (LPS) were also measured. The ability of the patients' sera to block interleukin-1beta (IL-1beta) production by human mononuclear cells in response to P. gingivalis LPS was examined. RESULTS: Antibody levels were positively correlated with antibody avidities in both EOP and AP patients (r=0.91, r=0.72, p<0.0005, respectively), while not significantly so in HS (r=0.09). There was variability in the antigen recognition of P. gingivalis OMA in EOP and AP patients. Smear and 53-kDa protein were more frequently recognized by sera of EOP and AP patients rather than that of HS (p<0.05). The smear was partly diminished by absorption with P. gingivalis LPS, indicating the smear antigen was partly composed of LPS. There was high correlation between antibody levels against P. gingivalis whole-cell extracts and LPS in EOP and AP patients (r=0.81, p=0.0002, r=0.87, p<0.0001, respectively), while not significant in HS (r=0.22). The sera of EOP and AP patients with high IgG titre to P. gingivalis LPS blocked IL-1beta production more effectively than that of the patients with low IgG titre to P. gingivalis LPS. CONCLUSIONS: These results indicate that EOP patients' antibody response against P. gingivalis infection does not differ significantly from that of AP patients. The person-to-person heterogeneous antibody production against P. gingivalis LPS could contribute to our understanding of the relationship between the defensive ability of EOP patients and their chronic infection with this pathogen.     

Lipoprotein-associated phospholipase A2 and plasma lipids in patients with destructive periodontal disease

OBJECTIVES: Periodontitis is believed to be an independent risk factor of cardiovascular disease (CVD) and to be associated with a moderate systemic inflammatory reaction and hyperlipidaemia. Lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) is an enzyme that has been shown to be a risk factor of CVD and that is involved in the degradation of the phospholipid mediator platelet-activating factor (PAF), a potent mediator of inflammation. MATERIAL AND METHODS: In the present study, we measured concentrations of plasma lipids and plasma activity of Lp-PLA(2) in 32 patients (mean age 43+/-11 years) with moderate-to-severe periodontitis before and 3 months after local treatment. RESULTS: Periodontal therapy resulted in a significant reduction of local inflammation and tissue destruction as reflected in reduced pocket depths and reduced bleeding indices. Pre- and post-treatment plasma lipid levels were (median and range, mmol/l): total cholesterol (C) 5.01 (3.94-7.15) and 4.91 (3.32-8.01); low-density lipoprotein-cholesterol (LDL-C) 3.14 (2.40-4.84) and 2.96 (1.39-5.04); HDL-C 1.27 (0.73-2.17) and 1.25 (0.74-2.55); triglycerides 1.37 (0.48-5.11) and 1.14 (0.38-792). Using the Wilcoxon's rank test, neither parameter showed a significant change. In contrast to the lacking response of plasma lipids, we observed a significant reduction in the activity of Lp-PLA(2). Local treatment lowered the enzyme activity by about 10% from 3.61+/-0.99 to 3.29+/-0.94 micromol/ml/h (mean+/-SD; p<0.001). The pre-treatment values of Lp-PLA(2) and LDL-C significantly correlated with clinical parameters of inflammation and periodontal destruction. CONCLUSION: This study indicates that treatment of periodontitis significantly reduces the serum activity of Lp-PLA(2), which is believed to be an independent cardiovascular risk factor.