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Gingival crevicular fluid matrix metalloproteinase (MMP)-7, extracellular MMP inducer, and tissue inhibitor of MMP-1 levels in periodontal disease.

BACKGROUND: During periodontal inflammation, matrix metalloproteinases (MMPs) are under the control of several regulatory mechanisms including the upregulation of expression by inducers and downregulation by inhibitors. Our study aimed to examine the levels and molecular forms of MMP-7, tissue inhibitor of MMP (TIMP)-1, and extracellular matrix metalloproteinase inducer (EMMPRIN) in gingival crevicular fluid (GCF) from patients with different periodontal diseases. METHODS: A total of 80 subjects (20 patients with generalized aggressive periodontitis [GAgP], 20 with chronic periodontitis [CP], 20 with gingivitis, and 20 periodontally healthy subjects) were included in this study. Periodontal status was evaluated by measuring probing depth, clinical attachment loss, presence of bleeding on probing, and plaque. GCF MMP-7, TIMP-1, and EMMPRIN levels and molecular forms were analyzed by enzyme-linked immunosorbent assay (ELISA) and Western immunoblot techniques using specific antibodies. RESULTS: Total amounts of GCF MMP-7 were found to be similar between the study groups. GAgP, CP, and gingivitis groups had significantly higher total amounts of GCF EMMPRIN compared to healthy subjects (P <0.008). Among the patient groups, the GAgP group had the highest total amount of GCF EMMPRIN relative to the gingivitis group (P = 0.0004). Soluble EMMPRIN existed in GCF in multiple molecular-weight species especially in periodontitis-affected GCF under non-reducing conditions, i.e., 30-, 55-, 100-, 180-, and 200-kDa species. All patient groups had significantly elevated total amounts of GCF TIMP-1 relative to the healthy group (P <0.0001). GAgP and CP groups also had a higher total amount of GCF TIMP-1 compared to the gingivitis group (P <0.0001 and P <0.0001, respectively). The GAgP group had higher GCF TIMP-1 and EMMPRIN levels compared to the CP group, but this elevation did not reach statistical significance. CONCLUSIONS: Our data indicate that MMP-7 is associated with the innate host defense in periodontal tissues. Increased EMMPRIN and TIMP-1 levels in GCF are associated with the enhanced severity of periodontal inflammation, indicating that these molecules can participate in the regulation of progression of periodontal diseases. To our knowledge, the present study demonstrated the presence of soluble forms of EMMPRIN in GCF of patients with different periodontal diseases for the first time.

Adolescent↗

FcgammaRIIB gene polymorphisms in Japanese periodontitis patients.

Human type II low-affinity receptor for immunoglobulin G (FcgammaRII) constitutes a clustered gene family consisting of FcgammaRIIA, IIB and IIC genes. FcgammaRIIB is unique in its ability to transmit inhibitory signals in B cells via immunoreceptor tyrosine-based inhibitory motif (ITIM). B-cell activation and subsequent elevated production of IgG are the immunopathological features of inflammatory disease such as periodontitis. To determine whether an association with periodontitis susceptibility exists, genetic polymorphisms of FcgammaRIIB were examined in Japanese patients with aggressive periodontitis (AGP) and chronic periodontitis (CP), and in the race-matched healthy controls (HCs). A significant difference was observed in the distribution of FcgammaRIIB-232I/T allele (exon 5) between the AGP and HC groups, with enrichment of the 232T in the AGP group (P=0.006). In addition, the FcgammaRIIB-nt 646-184A/G allele (intron 4) distribution was significantly different between the CP and HC groups, with enrichment of the nt 646-184A in the CP group (P=0.011). These results document the association of FcgammaRIIB gene polymorphisms with susceptibility to periodontitis in the Japanese.

Adolescent↗

Gingipain-specific IgG in the sera of patients with periodontal disease is necessary for opsonophagocytosis of Porphyromonas gingivalis.

BACKGROUND: Porphyromonas gingivalis is a primary etiologic agent of generalized aggressive periodontitis (GAgP), and gingipains, a group of cysteine proteinases, are critical virulence factors expressed by this organism. GAgP patients develop specific antibodies to gingipains; however, the function of these antibodies in the clearance of P. gingivalis infection is poorly understood. METHODS: In this study, we defined the levels of gingipain-specific antibodies in GAgP patient sera and examined the ability of gingipain-specific antibodies to facilitate opsonophagocytosis of P. gingivalis by human polymorphonuclear leukocytes (PMNs) using a fluorescent phagocytosis assay. RESULTS: GAgP patient sera possessed elevated levels of P. gingivalis-, arginine-gingipain (Rgp)A-, RgpB-, and lysine-gingipain (Kgp)-specific IgG (Kgp > RgpA > P. gingivalis > RgpB). Adsorption of GAgP sera with P. gingivalis whole organisms, RgpA, RgpB, and Kgp conjugated to sepharose beads reduced opsonophagocytosis of P. gingivalis by PMNs. CONCLUSIONS: Our studies demonstrate that GAgP patient sera possess elevated levels of P. gingivalis- and gingipain-specific IgG. Furthermore, we show that gingipain antibodies promote uptake of P. gingivalis by PMNs, and our data suggest that gingipain-specific antibodies may be important for the control of P. gingivalis infections.

Adhesins, Bacterial↗

Plasma antibody levels in periodontitis patients and controls.

BACKGROUND: A major aspect of the adaptive host response in periodontitis is the production of antibodies. Several risk and susceptibility factors for periodontitis, including smoking, age and composition of the subgingival microflora, have also been suggested to influence antibody production. AIM: The present study was conducted to investigate plasma levels of immunoglobulin (Ig) G, A and M antibodies in periodontitis patients of Caucasian European heritage in relation to disease severity, smoking, diagnosis and prevalence of periodontopathogens. METHODS: In this study, 29 patients with severe periodontitis, 51 with moderate periodontitis and 55 controls without periodontal destruction were enrolled. From the total of 80 patients, 18 were diagnosed with aggressive periodontitis and 62 with chronic periodontitis. Total IgG, IgA and IgM as well as IgG isotypes were analyzed in plasma samples. RESULTS: Levels of total IgG, IgA and IgM were not different between patients and controls; however, in periodontitis, higher levels of IgG1 and IgG2 were observed. Smoking appeared to be significantly and inversely related to antibody levels in periodontitis, in particular for total IgG and IgG2. The absence of an elevated total IgG and IgG2 in smoking patients was irrespective of severity, prevalence of periodontal pathogens and diagnosis. The elevation of total IgG and IgG1 and IgG2 in non-smoker periodontitis patients was observed in patients with moderate periodontitis and even greater in patients with severe periodontitis, but was independent whether patients were infected with Actinobacillus actinomycetemcomitans or Porphyromonas gingivalis and independent of diagnosis. Clinically, it was observed that patients who smoked had more periodontal bone loss; the current findings on antibody levels may be one of several mechanisms related to more extensive periodontal breakdown in smoker patients. CONCLUSION: The current study shows that non-smoker periodontitis patients have higher levels of total IgG and IgG2 than smoker periodontitis patients.

Acute Disease↗

Chronic periodontal disease is associated with single-nucleotide polymorphisms of the human TLR-4 gene.

Periodontitis is an inflammatory disease affecting the connective tissue surrounding the teeth leading to tooth loss. Pathogens associated with periodontitis interact with Toll-like receptors (TLRs) to induce cytokines causing and aggravating disease. We screened 197 individuals suffering from generalized periodontitis for the presence of Asp299Gly and Thr399Ile of TLR-4 as well as Arg753Gln of TLR-2 in comparison to matched controls. Single-nucleotide polymorphisms (SNPs) of TLR-4 were elevated among patients (odd's ratio 3.650, 95% CI 1.573-8.467, P < or = 0.0001), while no difference was observed for TLR-2. TLR-4 SNPs were correlated with chronic periodontitis (odd's ratio 5.562, 95% CI 2.199-14.04, P < or = 0.0001), but not with aggressive periodontitis. This observation was confirmed employing a group of periodontally healthy probands over 60 years of age. These data demonstrate that genetic variants of TLR-4 may act as risk factors for the development of generalized chronic periodontitis in humans.

Adult↗

A functional interleukin-1 beta gene polymorphism is associated with chronic periodontitis in a sample of Brazilian individuals.

BACKGROUND: Interleukin-1 beta (IL-1 beta) is a potent inflammatory mediator and an important polymorphism in the locus +3954 (C/T) of the human IL1 B gene has been shown to affect the levels of this cytokine. This functional polymorphism has been associated with the establishment of inflammatory diseases, including periodontal disease, in European, Asian and North American populations. OBJECTIVE: The aim of this study was to investigate the association between the IL1 B (+3954) gene polymorphism and the occurrence of different clinical forms of periodontitis in a sample of Brazilian individuals. METHODS: This study employed a cross-sectional design involving individuals from the State of Minas Gerais in the south-eastern region of Brazil. Genomic DNA was obtained from oral swabs of 129 individuals and amplified using the polymerase chain reaction (PCR) with specific primers flanking the locus +3954 of IL1 B. PCR products were submitted to restriction endonuclease digestion and analyzed by polyacrylamide gel electrophoresis, to distinguish alleles T and C of the IL1 B gene, allowing for the determination of the genotypes and detection of the polymorphism. RESULTS AND CONCLUSIONS: The chronic periodontitis group displayed a higher percentage of the T allele (28%) when compared to the aggressive periodontitis group (10.7%, chi(2)=5.24, p=0.02, OR=0.31, CI=0.11--0.88) and to control group (8.7%, chi(2)=7.11, p=0.007, OR=0.24, CI=0.08--0.73). Our data suggested that the polymorphism in the locus +3954 of IL1 B gene could be a risk factor for chronic periodontitis in a sample of Brazilian individuals.

Adolescent↗

[Judicious use of antibiotics in dental practice].

With the discovery of penicillin and entrance into the antibiotic era, the capability of dentists to treat dental infections have changed dramatically. Many antibacterial agents have developed since, but bacterial resistance using diverse mechanisms, have increased concomitantly. Since antimicrobial agents are frequently needed in dentistry, their judicious use is of prime importance. Dental infections can be divided to two main groups according to the origin of the infection. First, odontogenic infections (acute dento-alveolar abscess) originating from the dental pulp are most commonly caused by gram-positive anaerobic or facultative bacteria. Systemic antibiotic should be given concomitantly with drainage of the dento-alveolar abscess, debridment of the root canal of the infected tooth, and placement of inta-canal antimicrobial medication such as calcium hydroxide. Penicillin G, penicillin V (Rafapen) or amoxycillin (moxypen) are the first line systemic antimicrobial agents. In case of no improvement within 2-3 days, second line regimens such as amoxycillin-clavulanate (augmentin), cefuroxime (zinnat) or penicillin and metronidazole are recommended. In patients allergic to penicillin, clindamycinn (dalacin) is preferred over macrolides. The second group of infections originates from the periodontal apparatus, and is caused usually by gram-negative anaerobes bacilli, sometimes with Actinobacillus actinomycetemcomitance (Aa). Systemic antibiotics are only infrequently indicated in this situation, and always accompanied by scaling, root planning and curettage of the infected root and gingiva. In regenerative or post surgical periodontitis, augmentin, metronidazole or metronidazole in combination with penicillin or amoxycillin augmentin are recommended. In aggressive periodontitis the most common pathogen is Aa and therefore tetracycline, augmentin, or metronidazole and amoxicillin are recommended. In necrotizing ulcerative gingivitis, which is caused usually by fusiform bacilli and spirochetes, metronidazole or augmentin are appropriate. In patients with periodontal disease who are allergic to penicillin can be treated with a macrolides.

Aggregatibacter actinomycetemcomitans↗

Distribution of Bacteroides forsythus genotypes in a Japanese periodontitis population.

Bacteroides forsythus is an important pathogen in periodontal diseases and has been associated with advanced and refractory periodontitis. The difficulties associated with culturing this species have meant that the distribution and pathogenic mechanisms of B. forsythus remain unclear. In this study, the arbitrarily primed polymerase chain reaction (AP-PCR) method was used to investigate the genotype distribution of B. forsythus in a Japanese periodontitis population, as well as the relationship between AP-PCR genotypes and periodontal status. B. forsythus reference strain, ATCC 43037T and 137 clinical bacterial isolates from 64 subjects were separated into 11 distinct AP-PCR genotypes using a single randomly-sequenced primer, 5'-CCGGCGGCG-3' (A-05). The majority (80.9%) of B. forsythus strains examined belonged to AP-PCR genotypes I, II, III and IV (accounting for 39.7%, 20.6%, 10.3% and 10.3%, respectively). Types I and III primarily consisted of isolates from chronic periodontitis subjects (80.8% and 85.7%, respectively), while Types II and IV consisted mainly of isolates from aggressive periodontitis subjects (85.7% and 100%, respectively). Except for three subjects who harbored two different B. forsythus genotypes in the oral cavity, all subjects only infected with one genotype intraindividually. These results demonstrate that the AP-PCR method is useful for genotypic analysis of B. forsythus. This species showed a genetic diversity among the investigated population. A clonal nature of B. forsythus infection is suggested. Furthermore, different AP-PCR genotypes of B. forsythus appear to be associated with different types of periodontitis.

Acute Disease↗

The Fc gamma receptor genotype as a severity factor for chronic periodontitis in Japanese patients.

BACKGROUND: Functional polymorphisms of immunoglobulin G (IgG) Fc receptors (Fc gamma R) have been shown to be associated with generalized aggressive periodontitis (GAgP) or recurrence of chronic periodontitis (CP) in Japanese patients. The purpose of this study was to evaluate whether Fc gamma R polymorphisms are also associated with severity of CP. METHODS: Fifty Japanese non-smoking patients with severe CP and 39 Japanese non-smoking patients with moderate CP were identified according to established clinical criteria, including measurements of probing depth (PD), clinical attachment level (CAL), and alveolar bone loss (BL). Fc gamma R genotypes for 3 bi-allelic polymorphisms (Fc gamma RIIa-R/H131, Fc gamma RIIIa-158V/F, Fc gamma RIIIb-NA1/NA2) were determined in these CP patients and 64 race-matched, non-smoking healthy controls by means of allele-specific polymerase chain reactions. RESULTS: There was a significant over-representation of Fc gamma RIIIa-158V allele in severe CP patients compared to moderate CP patients (odds ratio 2.03, 95% confidence interval [CI] 1.03-4.01, chi 2 = 4.86, P = 0.028). In addition, we found a strong association between CP severity and Fc gamma R composite genotype comprising Fc gamma RIIIa-158V plus Fc gamma RIIIb-NA2 (severe CP versus moderate CP: odds ratio 4.69, 95% CI 1.52-15.10, chi 2 = 9.35, P = 0.002; severe CP versus healthy controls: odds ratio 4.10, 95% CI 1.62-10.59, chi 2 = 11.13, P = 0.0009). Moreover, CP patients positive for the composite genotype exhibited more severe signs of periodontitis than composite genotype-negative individuals (positive versus negative; mean PD: 3.8 mm versus 3.2 mm, P = 0.005; mean CAL: 4.5 mm versus 3.7 mm, P = 0.005; mean % BL: 37.6% versus 29.9%, P = 0.008). CONCLUSION: Our results document the Fc gamma RIIIa-158V allele and possibly Fc gamma RIIIb-NA2 to be associated with severity of CP in Japanese patients.

Adult↗

Gingival crevicular fluid matrix metalloproteinase-13 levels and molecular forms in various types of periodontal diseases.

BACKGROUND: The purpose of this study was to evaluate the levels, molecular forms and activation degree of matrix metalloproteinase-13 (MMP-13) in the gingival crevicular fluid (GCF) of patients with periodontal diseases and to correlate these findings with periodontal clinical parameters. METHODS: Sixty one subjects participated in this study as healthy (n = 18), gingivitis (n = 17), aggressive periodontitis (AgP; n = 15) and chronic periodontitis (CP; n = 11) groups. Clinical measurements and GCF samples were obtained from each subject. The molecular forms of MMP-13 in GCF samples were analyzed by Western immunoblotting method. Differences among the groups were assessed using non-parametric statistical analysis. RESULTS: In the CP group, levels of 29-30 kDa fragment of MMP-13, total MMP-13, and activated form of MMP-13 were significantly higher than in the healthy, gingivitis and AgP groups. GCF levels of all molecular forms of MMP-13 in AgP group were similar to those of healthy and gingivitis groups. Total and activated MMP-13 levels were positively correlated with all clinical parameters. 29-30 kDa fragment levels of MMP-13 were also positively correlated with papillary bleeding index and plaque index. CONCLUSION: These results indicate that elevated GCF MMP-13 levels may play an important role in the pathogenesis of CP. These data demonstrate, for the first time, pathologically activated and elevated MMP-13 in GCF.

Acute Disease↗

Neutral proteases in crevicular fluid as an indicator for periodontal treatment intervention.

PURPOSE: To longitudinally determine if early therapeutic intervention, based on a positive neutral protease activity (NPA) assay score could effectively arrest the progress of periodontal disease destruction. MATERIALS AND METHODS: 63 periodontal sites which had previously undergone probing attachment loss were identified from among 31 previously treated adult periodontitis patients who were monitored during periodontal maintenance for an average of 3 yrs. Clinical levels of gingival inflammation and attachment levels and NPA assay data were collected at the beginning of each maintenance visit. When a site tested negative with the assay, routine Supportive Periodontal Therapy (SPT) was followed during the same appointment, while sites exhibiting a positive NPA score received more aggressive periodontal treatment. RESULTS: During the study period, 51 of 63 sites displayed at least one positive NPA score. Our protocol of administering periodontal treatment rendered at the visit showing a positive NPA score revealed that only 1 of the 51 sites lost > or = 1 mm attachment during the study period. The remaining 50 positive assay sites showed an overall gain of > or = 1 mm of probing attachment over the course of the study. 12 of 63 sites consistently tested negative for neutral protease enzyme activity and remained stable, although 9 of these sites exhibited bleeding on probing (BOP) at least once during this study. Initial group mean probing attachment measurements were 5.6 mm for NPA negative and 5.7 mm for NPA positive sites.

Adult↗

[Importance of periodic follow up of periodontal diseases for the maintenance of periodontal health and the longevity of dental restoration].

The major objective of the author's investigation was to determine if the progression of attachment loss, the recurrence of active phase of periodontitis and development of new carious lesions can be controlled and prevented in individuals with prior history of aggressive periodontitis provided full mouth reconstruction and maintained at a proper level of oral hygiene. The results of a group on regular periodontal recall program were compared with the five years dental and periodontal findings on a matched group of patients having not been on regular maintenance program. The well maintained group of patients' annual recall data did not vary markedly. In five years basically the same amount of attachment apparatus was maintained. The reexamination of the non recall group at the end of the fifth year shoved a total deterioration of dentition due to the progression of periodontal disease and attachment loss. Especially those of rapidly progressing periodontitis cases shoved 70 to 100% attachment loss. This comparative study attempted to outline the insufficiency of our former dental philosophy of patient management and follow up. Authors emphasize the importance of the follow up, and maintenance of a very high level.

Adult↗

Experimentally induced periodontitis in beagle dogs causes rapid increases in osteoclastic resorption of alveolar bone.

This study was undertaken to observe osteoclast differentiation related to inflammatory progression in aggressive periodontitis induced in beagle dogs by ligature of the gingival sulcus. To monitor osteoclastic activity, we used histochemical methods (staining for tartrate-resistant acid phosphatase [TRAP]) to visualize osteoclasts and their TRAP-positive precursors and biochemical methods (ELISA assay of pyridinium crosslinks) to detect bone matrix degradation products in gingival crevicular fluid (GCF), serum, and urine. For histochemical study, tissue specimens were prepared from 3 adult female beagle dogs induced with experimental periodontitis by silk ligature placement below the gingival margin of mandibular molars ligated for 3, 7, and 21 days. For biochemical study for pyridinoline measurement, the 24 mandibular molars of 4 male beagle dogs were ligated. GCF, urine, and serum were collected at day 0 and at 3, 7, 14, and 21 days after ligation. In the early inflammatory phase of ligature-induced periodontitis (day 3), TRAP+ mononuclear and TRAP+ multinucleated cells were present in the gingival connective tissue, and active bone-resorbing cells were found in excavated lacunae at the alveolar crest, but osteoclasts were not infiltrating the periodontal ligament during this early phase. During later stages of the inflammatory process (7 and 21 days), osteoclasts appeared at both the gingival and ligament side of the alveolar bone. Osteoclastic bone resorption appeared to be more severe on the bone surface at the gingival side than on the bone surface of the periodontal ligament side. Measurement of pyridinoline significantly increased in GCF and urine 3 days after ligation. The results suggested that bone at the crest of the alveolar bone is rapidly resorbed within 3 days of inducing experimental periodontitis.

Acid Phosphatase↗

Variation in periodontal diagnosis and treatment planning among clinical instructors.

Consistency in clinical decision making may be necessary for reliable assessment of student performance and teaching effectiveness, yet little has been done to examine variation in periodontal diagnosis and treatment planning among dental school faculty. The purpose of this investigation was to examine variation among faculty in diagnosis and management of common periodontal diseases. Twenty-seven clinical instructors (periodontists, general dentists, dental hygienists, and first- and second-year periodontal graduate students) reviewed three web-based cases and answered a brief questionnaire focusing on radiographic interpretation, periodontal diagnosis, and treatment planning. Response rates for the three cases ranged from 62 percent to 70 percent. Clinical instructors' rating of percent bone loss in the majority of cases varied between three descriptive categories for the same tooth. Greater consistency in periodontal diagnosis was noted within the graduate student group as compared to periodontal and dental hygiene faculty groups. Diagnoses offered for one of the three patients varied between gingivitis and chronic and aggressive periodontitis. Six to nineteen different treatment plans (many with subtle differences) were submitted for each of the three cases. Inter-rater variation was qualitatively more prevalent than intra-rater variation. To our knowledge, this is the first study to document substantial variation among instructors in radiographic interpretation, diagnosis, and treatment planning for common periodontal diseases. Qualitative judgments speculating on the impact of variability among dental school faculty on student performance and patient care can be made but as yet remain unknown. Consistent use of accepted practice guidelines and greater consensus-building opportunities may decrease variation among faculty and enhance dental education.

Adult↗

Total proteoglycan and chondroitin-4-sulfate levels in gingiva of patients with various types of periodontitis.

BACKGROUND: The aim of the present study was to investigate the total proteoglycan (PG) and chondroitin-4-sulfate (C4S) levels in gingival tissue samples obtained from patients with aggressive periodontitis (AgP) and chronic periodontitis (CP) before therapy (baseline) and 1 month after completion of non-surgical periodontal therapy. METHODS: Gingival tissue samples were obtained from 10 AgP and 10 CP patients before initiation of treatment (baseline) and 1 month after non-surgical periodontal treatment. The control group comprised 10 systemically and periodontally healthy subjects. Total PG and C4S levels were determined by biochemical techniques. PG levels were analyzed using a modified Bitter and Muir method. C4S assay was carried out using chondroitin sulphate lyase AC and chondroitin-6 sulphate sulphohydrolase enzymes. The results were tested statistically using parametric tests. RESULTS: The clinical periodontal parameters demonstrated significant decreases in the periodontitis groups (P<0.05) after treatment, and there was no significant difference between AgP and CP groups at baseline and after treatment (P>0.05). At baseline, total PG and C4S levels in both of the periodontitis groups were significantly lower than that of the control group (P<0.05). One month after the non-surgical periodontal treatment, total PG levels in the periodontitis groups were comparable to the control group (P>0.05), whereas C4S levels in the AgP group were significantly lower than the other study groups (P<0.05). In the CP group, total PG and C4S levels increased significantly (P = 0.001 and P = 0.006, respectively) after non-surgical periodontal treatment, but they did not increase in the AgP group (P>0.05). CONCLUSION: The significant increases observed in total proteoglycan and chondroitin-4-sulfate levels after non-surgical periodontal treatment in the CP group but not in the AgP group may suggest that healing patterns differ between the two periodontitis types in terms of PG and C4S composition of extracellular matrix.

Adult↗

Clinical effects of scaling and root planing on untreated teeth.

OBJECTIVE: The aim of this report is to examine whether scaling and root planing (SRP) in one area of the mouth may affect periodontal improvement in untreated areas in the same patient, possibly through systemic effects of treatment. MATERIAL AND METHODS: Twenty patients diagnosed with generalized aggressive periodontitis were randomized into treatment (n=11) and no treatment (n=9) groups. Within the treatment group, three quadrants were treated by SRP at week 0, 3, 12, and 24, while a single experimental quadrant remained untreated throughout the study. The outcome for all teeth was assessed using clinical parameters, subtraction radiography, and pathogenic bacteria levels in the subgingival flora over the 24-week study period. RESULTS: Compared with sites in no treatment patients, the treated sites in the treated patients showed a 1 mm decrease in probing depth (PD) (p<0.01) and a 0.5 mm increase in bone height (p<0.01) by 24 weeks. In untreated sites within treated subjects, however, PDs tended to improve (p=0.09) but at a reduced rate compared with treated sites. The levels of Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Tannerella forsythensis (Bacteroides forsythus) remained unchanged in untreated sites while levels of Prevetolla intermedia and Treponema denticola tended to decrease as compared with controls but did not reach significance. CONCLUSIONS: This study indicates that untreated sites in treated periodontitis patients show a trend towards clinical improvement and exhibit reductions in some but not all periodontopathic bacterial species tested.

Adolescent↗

Fcgamma receptor polymorphisms in relation to periodontitis.

OBJECTIVES: Evidence suggests functional relevance for polymorphisms in FcgammaR in relation to inflammatory and infectious diseases. The present aim was to investigate genetic polymorphisms in three FcgammaR in relation to susceptibility and severity of periodontitis. MATERIAL AND METHODS: The study population consisted of 68 periodontitis patients and 61 controls (Northern European Caucasian background, mean ages 44 and 42 years, respectively). Among the patients, 12 subjects were diagnosed with aggressive periodontitis (AgP) and 56 individuals were diagnosed with chronic periodontitis (CP). Radiographic bone levels were scored for all teeth in the patients. Subjects were typed for the following genes (alleles): FcgammaRIIa (R131 or H131), FcgammaRIIIa (V158 or F158) and FcgammaRIIIb (NA1 or NA2). RESULTS: Hardy-Weinberg equilibrium criteria were fulfilled for the different genotypes at the three genes investigated. The frequency of the FcgammaRIIIa-V158 allele in the patient population (53%) was higher than in the control group (39%) (OR 1.73 [1.06-2.85], p=0.034). The V158 carriage rate in AgP was even higher (63%). The frequency of the FcgammaRIIa-H131 allele in the total periodontitis population was 58%; for AgP this was 79%, compared with 51% in the control population (OR 3.68 [1.29-10.5], p=0.013). Also, the frequency of the FcgammaRIIa-H/H131 genotype was significantly higher in AgP patients than in controls (OR 9.07 [1.29-63.56], p=0.026, adjusted for smoking status and other potential confounders). Moreover, patients with the FcgammaRIIa-H/H131 genotype had more severe radiographic bone loss than patients with the other FcgammaRIIa genotypes. CONCLUSION: The current study of relative small sample size suggests that the FcgammaRIIa-H/H131 genotype may be a putative susceptibility and severity factor, and the FcgammaRIIIa-V158 allele a putative susceptibility factor for periodontitis in Northern European Caucasians. These results need further verification and the biological importance of these findings needs further investigation.

Acute Disease↗

[Classification of aggressive form of periodontal diseases].

An attempt at objective evaluation of currently used classifications of periodontal diseases is made. The first classification of aggressive forms of periodontitis was offered in 1983. Classifications of 1982, 1992, 1999, and 2001 also reflect the clinical forms of atypical periodontitis.

Gingivitis↗