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Biomedical subjects

D F Kinane

Publications and source records attributed to D F Kinane.

At least 19 recordsLinked to original sources
PubMed2006

Gingival epithelial cells heterozygous for Toll-like receptor 4 polymorphisms Asp299Gly and Thr399ile are hypo-responsive to Porphyromonas gingivalis.

The Toll-like receptor (TLR)4 is the major sensor for bacterial lipopolysaccharide and its two common co-segregating polymorphisms, Asp299Gly and Thr399Ile, which occur at a frequency of between 6 and 10%, have been associated with infectious diseases, LPS hypo-responsiveness and cardiovascular disease. Porphyromonas gingivalis is a Gram-negative bacterium implicated in chronic periodontitis and is a known TLR4 and TLR2 agonist. We obtained two gingival epithelial cell primary cultures from subjects heterozygous for the TLR4 polymorphism Asp299Gly and compared response characteristics with similar cells from patients (four) with the wild-type TLR4 genes. Cytokine responses and transcriptome profiles of gingival epithelial cell primary culture cells to TNFalpha challenge were similar for all primary epithelial cell cultures. P. gingivalis challenge, however, gave markedly different responses for Asp299Gly heterozygous and wild-type epithelial cell cultures. The epithelial cells heterozygous for the TLR4 polymorphism Asp299Gly were functionally hypo-responsive, evidenced by differences in BD-2 mRNA expression, mRNA response profile by microarray analysis and by pro-inflammatory and chemokine cytokines at the protein and mRNA level. These findings emphasize variance in human epithelial cell TLRs, linked with Asp299Gly carriage, which results in a hypo-responsive epithelial cell phenotype less susceptible to Gram-negative diseases and associated systemic conditions.

Amino Acid Substitution↗
PubMed2005

Clinical and microbiological effect of scaling and root planing in smoker and non-smoker chronic and aggressive periodontitis patients.

OBJECTIVES: To compare the effects of scaling and root planing (SRP) on clinical and microbiological parameters at selected sites in smoker and non-smoker chronic and generalized aggressive periodontitis patients. MATERIALS AND METHODS: Clinical parameters including probing depth (PD), relative attachment level (RAL), and bleeding upon probing (BOP), and subgingival plaque samples were taken from four sites in 28 chronic periodontitis (CP) and 17 generalized aggressive periodontitis (GAgP) patients before and after SRP. Polymerase chain reaction assays were used to determine the presence of A. actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythensis, Prevotella intermedia and Treponema denticola. RESULTS: Both CP and GAgP non-smokers had significantly greater reduction in pocket depth (1.0+/-1.3 mm in CP smokers versus 1.7+/-1.4 mm in non-smokers, p=0.007 and 1.3+/-1.0 in GAgP smokers versus 2.4+/-1.2 mm in GAgP non-smokers, p<0.001) than respective non-smokers, with a significant decrease in Tannerella forsythensis in CP sites (smokers 25% increase and non-smokers 36.3% decrease, p<0.001) and Prevotella intermedia at GAgP sites (smokers 25% reduction versus 46.9% in non-smokers, p=0.028). CONCLUSION: SRP was effective in reducing clinical parameters in both groups. The inferior improvement in PD following therapy for smokers may reflect the systemic effects of smoking on the host response and the healing process. The lesser reduction in microflora and greater post-therapy prevalence of organisms may reflect the deeper pockets seen in smokers and poorer clearance of the organisms. These detrimental consequences for smokers appear consistent in both aggressive and CP.

Adult↗
PubMed2005

The potential role of interleukin-17 in the immunopathology of periodontal disease.

BACKGROUND: Interleukin-17 (IL-17) is exclusively produced by activated T cells, and this cytokine can induce inflammatory responses, support immune responses (Th1), and stimulate osteoclastic bone resorption in combination with receptor activator of NF-kappaB (RANK) and RANK ligand (RANKL). These biological functions are relevant to the aetiopathogenesis of periodontitis, and thus we sought to investigate whether IL-17 is produced in periodontal lesions and to assess the relationship of gene expression between IL-17 and other cytokines, and to determine the effect of IL-17 on IL-6 production in human gingival fibroblasts (HGF). MATERIALS AND METHODS: IL-17 was detected and measured in periodontal tissues obtained as biopsy samples during periodontal surgery and in the cell-free culture supernatants cultured ex vivo, by using Western immunoblotting and enzyme-linked immunosorbent assay, respectively. IL-17 and other cytokine gene expression were investigated by the reverse transcription-polymerase chain reaction (RT-PCR) method. The contribution of IL-17 to IL-6 production by HGF was studied. RESULTS: IL-17 protein was moderately detected in periodontal tissues. In contrast, IL-17 mRNA was expressed only in nine of 23 periodontitis tissue samples by RT-PCR. The IL-17 mRNA-positive samples simultaneously expressed mRNAs encoding interferon (IFN)-gamma, IL-2, RANK, and RANKL, but not IL-4. IL-10 (Th2 cytokine) was detected more frequently in the samples than IFN-gamma and IL-2 (Th1 cytokine). Recombinant human IL-17 induced IL-6 production from HGF in a dose- and time-dependent fashion. CONCLUSIONS: These results indicate that IL-17 is produced in periodontal lesions, which may be involved in Th1 modulation and enhance inflammatory reactions via gingival fibroblast-derived mediators in periodontal disease. Thus, IL-17, together with other cytokines, has a potential role in the aetiopathogenesis of periodontal disease.

Adult↗
PubMed2005

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.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed2005

Impact of smoking on the clinical, microbiological and immunological parameters of adult patients with periodontitis.

OBJECTIVES: The aim of the current study was to assess the impact of smoking on the clinical indices, the humoral immune response and the detection frequency of putative periodontal pathogens in patients with periodontitis cross-sectionally and following therapy. MATERIAL AND METHODS: Clinical measurements, subgingival plaque samples, gingival crevicular fluid (GCF) and sera were collected from 40 untreated patients with moderate-to-advanced chronic periodontitis before and after treatment over a period of 6 months. The treatment consisted of the initial therapy of scaling and root planing. Smoking status was self-reported and was confirmed by cotinine enzyme inhibition assay (CEIA). Whole-mouth clinical measurements were recorded with a manual periodontal probe at baseline (BAS) and at 6 months (RAS). Selected-site analyses were performed on the deepest site in each quadrant before and after therapy and clinical indices were recorded with an electronic pressure-sensitive probe. GCF sample volume was quantified using the Periotron 6000. Polymerase chain reaction (PCR) was utilized to determine the presence of Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Prevotella intermedia, Treponema denticola and Tanerella forsythensis in subgingival plaque. Enzyme-linked immunosorbent assay examined the systemic antibody titres to these bacteria, and thiocyanate disassociation determined the antibody avidity to these organisms. RESULTS: At baseline, smokers showed significantly less gingival inflammation and lower GCF volume compared with non-smokers. After treatment, a compromised clinical outcome was noted for smokers in terms of pocket depth reduction and gain in attachment levels. No significant differences in the detection of putative periodontal pathogens in subgingival plaque existed between smokers and non-smokers. A consistent trend was noted in that smokers had lower sera immunoglobulin G antibody titres to these organisms before and after treatment (statistically significant for A. actinomycetemcomitans). This pattern was less clear when antibody avidities were considered, revealing only small differences, if any, between the two groups of patients. CONCLUSION: Current data indicate that smokers with periodontal disease have a suppressed inflammatory response, a significantly less favourable clinical outcome and seem to have an altered host antibody response to antigenic challenge than non-smokers. In contrast, the subgingival microflora of smokers appears similar to that of non-smokers.

Adult↗
PubMed2005

Generation of inflammatory stimuli: how bacteria set up inflammatory responses in the gingiva.

OBJECTIVES: The primary aetiologic factor of periodontal disease is the bacterial biofilm. Gram-positive and gram-negative bacteria possess a plethora of structural or secreted components that may cause direct destruction to periodontal tissues or stimulate host cells to activate a wide range of inflammatory responses. These responses are intended to eliminate the microbial challenge, but may often cause further tissue damage. METHODS: This review has been divided into three parts: (a) bacterial virulence factors, which includes basic information on bacterial virulence factors, and the principle inflammatory responses that host cells elicit against these factors, (b) main receptors and signalling pathways, which includes basic information about the main receptors that interact with the bacterial virulence factors, the nature of these interactions, and the activated signalling pathways that lead to inflammatory responses, and (c) initiation of inflammation, which includes a model by which the virulence factors may interact with host cells and lead to inflammatory responses in the gingiva. FINDINGS AND CONCLUSIONS: Bacterial components/virulence factors may be involved in modulating inflammatory responses and include: lipopolysaccharides (LPS), peptidoglycans, lipotechoic acids, fimbriae, proteases, heat-shock proteins, formyl-methionyl peptides, and toxins. Potential host cell receptors involved in recognizing bacterial components and initiating signalling pathways that lead to inflammatory responses include: Toll-like receptors (TLRs), CD14, nucleotide-binding oligomerization domain proteins (Nod) and G-protein-coupled receptors, including formyl-methionyl peptide receptors and protease-activated receptors. Of the above bacterial and host molecules, evidence from experimental animal studies implicate LPS, fimbriae, proteases, TLRs, and CD14 in periodontal tissue or alveolar bone destruction. However, evidence verifying the involvement of any of the above molecules in periodontal tissue destruction in humans does not exist.

Bacteria, Anaerobic↗
PubMed2004

Quadrant root planing versus same-day full-mouth root planing. I. Clinical findings.

OBJECTIVES: The aim of this study was to test the hypothesis that same-day full-mouth scaling and root planing (FM-SRP) resulted in greater clinical improvement compared to quadrant scaling and root planing (Q-SRP) in chronic periodontitis patients over a period of 6 months. MATERIAL AND METHODS: Forty patients were recruited into this study. Subjects were randomised into two groups. The FM-SRP group received full-mouth scaling and root planing completed within the same day, while the Q-SRP group received quadrant root planing at 2-weekly intervals over four consecutive sessions. Whole-mouth clinical measurements were recorded with a manual periodontal probe at baseline (BAS) and at reassessment 1 (R1) (approximately 6 weeks after the completion of therapy), and at reassessment 2 (R2) (6 months after the initiation of therapy). Selected site analyses were performed on the deepest site in each quadrant before and after therapy (R1 and R2) and clinical indices were recorded with an electronic pressure sensitive probe. In addition, during the active phase of treatment clinical data were collected at 2-weekly intervals from the remaining untreated quadrants in the Q-SRP group only. RESULTS: Both therapies resulted in significant improvements in all clinical indices both at R1 and R2. A continuous clinical improvement was seen for both treatment groups during the experimental period, which reached peak levels at 6 months (DeltaPD=1.8 mm, DeltaCAL=1.1 mm, p<0.001; PD: pocket depth; CAL: clinical attachment level). The selected-site analysis revealed no significant differences in any clinical index between the two treatment groups at R2 (DeltaPD=2.8 mm, DeltaRAL=1.1 mm; RAL: relative attachment level). At the selected sites, the analysis of the deep pockets (>7 mm) showed a significantly greater gain in RAL for the FM-SRP group compared to the Q-SRP group at R2 (p<0.05). The results of this analysis however, should be interpreted with care due to the small number of deep pockets. Data from the Q-SRP group provided an insight into how treated and untreated quadrants responded during the initiation of plaque control measures. There were significant reductions in PD, suppuration (SUP), modified gingival index (MGI) and plaque index (PI) in the remaining untreated quadrants in the Q-SRP group during the initial phase of treatment (p<0.05), while minimum changes in RALs and bleeding on probing (BOP) occurred. Nevertheless, the improvement in PD was clearly inferior to that seen after scaling and root planing. CONCLUSION: Following both therapeutic modalities, there were marked clinical improvements at both R1 and R2 (6 months) from baseline. The current study, in contrast to previous findings, failed to show that FM-SRP is a more efficacious periodontal treatment modality compared to Q-SRP. However, both modalities are efficacious and the clinician should select the treatment modality based on practical considerations related to patient preference and clinical workload.

Adult↗
PubMed2004

Quadrant root planing versus same-day full-mouth root planing. II. Microbiological findings.

OBJECTIVES: The aim of this study was to test the hypothesis that over a period of 6 months, same-day full-mouth scaling and root planing (FM-SRP) resulted in greater reductions in the detection frequency of five putative periodontal pathogens compared with quadrant scaling and root planing (Q-SRP) in chronic periodontitis patients. MATERIALS AND METHODS: Forty patients were recruited into this study. Subjects were randomised into two groups. The FM-SRP group received full-mouth scaling and root planing completed within the same day, while the Q-SRP group received quadrant root planing at 2-weekly intervals over four consecutive sessions. Selected-site analyses were performed on the deepest site in each quadrant before and after therapy, at approximately 3 and 6 months from baseline (R1 and R2) and clinical indices were recorded with an electronic pressure-sensitive probe. In addition, subgingival plaque samples were collected from these sites at baseline (BAS), at reassessment 1 (R1), approximately 6 weeks after the completion of therapy and at reassessment 2 (R2), 6 months from baseline. Polymerase chain reaction (PCR) was used to determine the presence of Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Prevotella intermedia, Treponema denticola and Bacteroides forsythus in plaque. RESULTS: Both therapies resulted in significant improvements in all clinical indices both at R1 and R2. A marked reduction in the presence of all candidate periodontal pathogens was noted after both treatment modalities, reaching statistical significance for the majority of the test organisms. These improvements were maintained over a period of 6 months. When the two treatment groups were compared, a significantly higher percentage of Q-SRP patients was positive for P. intermedia at R1 compared with FM-SRP patients (p<0.05). In addition, a greater reduction in the patient prevalence for T. denticola was found for the FM-SRP group than the Q-SRP group at R1 and R2 from baseline (p<0.005), but the significance of this is questionable given the skewed detection frequency of this organism at baseline between the two treatments (p<0.01). CONCLUSION: This study failed to confirm that same-day FM-SRP resulted in greater microbiological improvements compared with Q-SRP at 2-weekly intervals over a 6-month period, as determined by PCR.

Adult↗
PubMed2004

Quadrant root planing versus same-day full-mouth root planing.

OBJECTIVES: The aim of this study was to determine whether same-day full-mouth scaling and root planing (FM-SRP) and quadrant scaling and root planing (Q-SRP) resulted in variations in the systemic humoral immune response dynamics (antibody titres and avidity) during active treatment and 3 and 6 months post-therapy. MATERIALS AND METHODS: Forty patients with chronic periodontitis were recruited into this study. Subjects were randomised into two groups and received either scaling and root planing quadrant by quadrant at 2-weekly intervals (Q-SRP group) or same-day full-mouth scaling and root planing (FM-SRP group). Clinical measurements and serum samples were obtained at baseline and approximately 6 weeks after the last clinical intervention (R1) and 6 months after the initiation of therapy (R2). Furthermore, serum samples were obtained from each patient undergoing therapy (Q-SRP and FM-SRP) at 3 bi-weekly instances so as to determine the short-term effects of each session of scaling and root planing on the dynamics of the humoral immune response. Serum antibody titre was assayed by enzyme-linked immunosorbent assay (ELISA) and antibody avidity was measured by thiocyanate dissociation against five putative periodontal pathogens: Porphyromonas gingivalis; Actinobacillus actinomycetemcomitans; Prevotella intermedia; Treponema denticola and Bacteroides forsythus. RESULTS: Both therapies resulted in similar antibody titre reductions against the majority of the organisms tested and although there was a distinct trend for antibody avidity to increase following therapy, this was not found to be statistically significant, reflecting marked inter-individual variation. In addition, no evidence emerged from this study to support increased antibody titres following the active phases of both treatment approaches due to an inoculation effect. Nevertheless, significant short-term increases in antibody avidity to most test bacteria were noted for both treatment strategies. CONCLUSION: Both therapies were associated with a reduction in antibody titres and an increase in the binding ability or avidity of antibodies, but there was a marked inter-subject variability and statistical significance was reached for only some of the test bacteria. No significant differences in the humoral antibody dynamics were found between the two treatment approaches.

Adult↗
PubMed2004

Smoking, periodontal disease and the role of the dental profession.

Epidemiological investigations support a firm relationship between smoking and periodontal disease. The likely benefits of smoking cessation programmes are considerable for periodontal disease, cancers and nearly all chronic systemic diseases. The mechanisms by which smoking may influence the development and progression of periodontal disease are as yet unclear, but may include changes in the vasculature, the immune and inflammatory systems, tissue oxygenation and the healing processes. Unfortunately, although dental professionals have more opportunities to encourage smokers to quit (most people visit their dentist more frequently than their doctor), dentists claim that they are not well informed on this subject. The purpose of this review is to describe the evidence for a link between smoking and periodontal disease, the possible pathology induced by smoking on the periodontal tissues and its impact on therapy, and to outline the smoking cessation techniques that are currently available.

Dentists↗
PubMed2003

Teaching periodontal pocket charting to dental students: a comparison of computer assisted learning and traditional tutorials.

AIM: The aim of this study was to compare the effectiveness of a computer assisted learning (CAL) programme with that of traditional small group tutorials in teaching theoretical and practical aspects of periodontal pocket charting. METHOD: Sixty-one third year undergraduate dental students were randomized to either receive a tutorial or to work through the CAL programme. Students using the CAL programme completed questionnaires relating to previous computer experience and the ease of use of the programme. All students were assessed immediately after the intervention by means of a confidence log, a practical exercise and a further confidence log. They were assessed again three weeks later by means of a confidence log and a multiple-choice written test. RESULTS: There were very few significant differences between groups for any of the assessments used. However, subjective comments indicated that students occasionally felt disadvantaged if they had not received a tutorial. CONCLUSION: CAL and traditional teaching methods are equally effective in teaching periodontal pocket charting to undergraduate dental students.

Clinical Competence↗
PubMed2003

The systemic immune response is more prominent than the mucosal immune response in the pathogenesis of periodontal disease.

BACKGROUND/AIM: The diseased periodontium appears to express features of a systemic and a mucosal immune response. Our aims were to determine differences in immunoglobulin expression between gingivitis and periodontitis lesions and to ascertain whether immune and inflammatory cells were recruited into the diseased periodontium by the mucosal addressin adhesion molecule (MAdCAM-1). METHODS: In situ hybridization and immunohistochemistry were used to detect the expression of chemokines, adhesion molecules and immunoglobulins in tissue sections of gingival and granulation tissues excised from periodontitis-affected sites and of healthy tissue and gingivitis-affected tissue excised during crown-lengthening procedures. RESULTS: Greater numbers of plasma cells were observed in periodontitis gingival/granulation tissue lesions compared with gingivitis lesions. While IgA1 were predominant in all lesions, IgA2 and J-chain expressing plasma cells were present in increased proportions in gingival tissues compared with granulation tissue. Intracellular adhesion molecule-1 (ICAM-1) was higher in periodontitis than in gingivitis and interleukin-8 mRNA was higher in lesions with a pronounced neutrophil infiltrate. Vascular cell adhesion molecule-1 (VCAM-1) localized to the deep connective tissue and indicated the presence of a systemic type of immune response in this region. Periodontal tissues (n=71 biopsies) did not appear to express MAdCAM-1, in positive control sections of small intestine where it was detected. CONCLUSION: Overall, the systemic-type immune response is predominant, and although the mucosal immune response is minor and limited to the superficial tissues it may have an important role in the host defense to periodontal pathogens.

Adult↗
PubMed2003

Changes in gingival crevicular fluid matrix metalloproteinase-8 levels during periodontal treatment and maintenance.

OBJECTIVES: The aim of this study was to investigate the effect of scaling and root planing (SRP) and the maintenance phase of treatment on the gingival crevicular fluid (GCF) matrix metalloproteinase-8 (MMP-8) levels. MATERIALS AND METHODS: Clinical measurements and GCF samples were taken from four sites in 20 adult periodontitis patients before and after SRP and during a 3-month maintenance phase of treatment. MMP-8 levels were measured from GCF samples by time-resolved immunofluorometric assay (IFMA) with monoclonal antibodies. RESULTS: SRP improved the clinical indices as would be predicted, 6.1 mm (SD = 1.4) at baseline compared with 4.3 mm (SD = 1.6) post-treatment (P < 0.001). Attachment level (AL) reduced but not significantly between these two visits 13.4 mm (SD = 2.4) compared with 12.8 mm (SD = 2.4) (P < 0.08) post therapy. GCF MMP-8 levels reduced after initial treatment from 33.8 micro g/30 s sample to 23.5 micro g/30 s, which just failed to reach statistical significance (P = 0.07). However, when MMP-8 levels were expressed as a concentration, the differences following initial therapy were significant (54.1 ng/ micro L at baseline compared with 34.2 ng/micro L post treatment; P < 0.005). The difference, however, between the baseline MMP-8 levels (33.8 ng/30 s) and the final visit (16 ng/30 s) following maintenance was markedly significant (P < 0.001) for both absolute amounts and on a concentration basis. CONCLUSION: In conclusion, clinical improvement following SRP was associated with significant reductions in MMP-8 levels. The GCF concentration of MMP-8 decreased after initial therapy but reduced even more dramatically (approximately 50%) following a 3-month period of maintenance (P < 0.001).

Adult↗
PubMed2003

Genes and gene polymorphisms associated with periodontal disease.

The scientific literature during the last ten years has seen an exponential increase in the number of reports claiming links for genetic polymorphisms with a variety of medical diseases, particularly chronic immune and inflammatory conditions. Recently, periodontal research has contributed to this growth area. This new research has coincided with an increased understanding of the genome which, in turn, has permitted the functional interrelationships of gene products with each other and with environmental agents to be understood. As a result of this knowledge explosion, it is evident that there is a genetic basis for most diseases, including periodontitis. This realization has fostered the idea that if we can understand the genetic basis of diseases, genetic tests to assess disease risk and to develop etiology-based treatments will soon be reality. Consequently, there has been great interest in identifying allelic variants of genes that can be used to assess disease risk for periodontal diseases. Reports of genetic polymorphisms associated with periodontal disease are increasing, but the limitations of such studies are not widely appreciated. While there have been dramatic successes in the identification of mutations responsible for rare genetic conditions, few genetic polymorphisms reported for complex genetic diseases have been demonstrated to be clinically valid, and fewer have been shown to have clinical utility. Although geneticists warn clinicians on the over-enthusiastic use and interpretation of their studies, there continues to be a disparity between the geneticists and the clinicians in the emphasis placed on genes and genetic polymorphism associations. This review critically reviews genetic associations claimed for periodontal disease. It reveals that, despite major advances in the awareness of genetic risk factors for periodontal disease (with the exception of periodontitis associated with certain monogenetic conditions), we are still some way from determining the genetic basis of both aggressive and chronic periodontitis. We have, however, gained considerable insight into the hereditary pattern for aggressive periodontitis. Related to our understanding that it is autosomal-dominant with reduced penetrance comes a major clinically relevant insight into the risk assessment and screening for this disease, in that we appreciate that parents, offspring, and siblings of patients affected with aggressive periodontitis have a 50% risk of this disease also. Nevertheless, we must exercise caution and proper scientific method in the pursuit of clinically valid and useful genetic diagnostic tests for chronic and aggressive periodontitis. We must plan our research using plausible biological arguments and carefully avoid the numerous bias and misinterpretation pitfalls inherent in researching genetic associations with disease.

Aggressive Periodontitis↗
PubMed2001

Failure to detect an association with IL1 genotypes in European Caucasians with generalised early onset periodontitis.

OBJECTIVES: In order to elucidate the genetic background to EOP it is useful to investigate associations with genetic polymorphisms of immune response genes, whose products play a r le in the inflammatory process. The aim of this study was to examine IL1A and IL1B genetic polymorphisms in unrelated European white Caucasian patients with generalised early-onset periodontitis (GEOP). MATERIAL AND METHODS: Polymerase chain reaction (PCR) amplification of the ILIA (-889) gene and IL1B (+3953) gene (56 patients, 56 controls) was carried out and PCR products subjected to restriction fragment length polymorphism (RFLP) analysis. RESULTS: There were no significant differences between patients and controls for any of the genotype or allele frequencies investigated (p = 1.0). Smoking status was also included as a covariate but this did not alter the results. Furthermore, expression of the composite genotype described by Kornman and coworkers was also investigated in these subjects. No significant differences were found between patients and controls whether smoking was included as a covariate or not. CONCLUSION: The lack of any association between the IL1 polymorphisms and GEOP, in the population presented here, brings into doubt the usefulness of these candidate genes as markers of susceptibility to this form of periodontitis.

Adolescent↗
PubMed2001

Changes in subgingival microflora and humoral immune response following periodontal therapy.

OBJECTIVES: To investigate the effect of scaling and root planing (SRP) on the microflora and humoral immune response in adult periodontitis. MATERIALS & METHODS: Clinical measurements, subgingival plaque samples, gingival crevicular fluid and sera were taken from 4 sites in 28 adult periodontitis patients before and after SRP. Polymerase chain reaction was used to determine the presence of A. actinomycetemcomitans, P. gingivalis, B. forsythus, P. intermedia, and T. denticola. ELISA was used to investigate the systemic and local antibody titres to these organisms, and thiocyanate dissociation for the determination of serum antibody avidity. RESULTS: SRP produced a good clinical improvement. On a subject basis there was little significant change in the microflora. However, on a site basis, there were significant reductions in P. intermedia, B. forsythus and T. denticola. There was little change in systemic and local antibody titres following SRP, although there was a significant reduction in antibody avidity to P. gingivalis and P. intermedia CONCLUSION: Post-therapy clinical improvement was associated with a reduction in bacterial prevalence, but statistical significance was only reached at a site level and this microbial reduction was not significant for all organisms. No significant post-therapy effects on the humoral immune response were noted other than a reduced antibody avidity to P. gingivalis and P. intermedia. The lack of a clear pattern in the humoral immune response may reflect a failure of the host response to produce adequate levels of biologically functional antibodies, and complex interactions between the subgingival flora and the host response.

Adult↗