Suppression of the periodontopathic microflora in localized juvenile periodontitis by systemic tetracycline

Abstract. Since recent studies have implicated Actinobacillus actinomycetemcomitans in the etiology of localized juvenile periodontitis, this investigation determined the effectiveness of subgingival debridement, topical Betadine Solution®, and systemic tetiacycline in suppressing subgingival A. actinomycetemcomitans and other microorganisms. A total of 20 deep periodontal pockets and 10 normal periodontal sites of 6 localized juvenile periodontitis patients was included in the study. Each patient was treated in 3 stages over a period of 22 weeks, and the result of treatment was monitored for an additional 38 weeks. The first stage of treatment included plaque control, as well as thorough scaling and root planing, composed of at least 6 h of debridement. No concomitant periodontal surgery was performed. In the second stage, Betadine saturated cotton gauze was inserted into the periodontal pockets for 10 min. Stage 3 involved systemic tetracycline therapy (1 g/day) for J4 days. The subgingival microflora was determined at frequent intervals by selective culturing of A. actinomycetemcomitans and Capnocytophaga and by direct microscopic examination. The clinical effect was assessed by measuring changes in probing periodontal attachment level, probing periodontal pocket depth, radiographic alveolar bone mass, and other relevant clinical parameters. Scaling and root planing reduced the total subgingival bacterial counts and the proportions of certain Gram-negative bacteria, but no periodontal pocket became free of A actinomycetemcomitans. Betadine application had little or no effect on the subgingival microflora. In contrast, tetracycline administered via the systemic route suppressed. A actinomycetemcomitans, Capnocytophaga, and spirochetes to low or undetectable levels in all test periodontal pockets. A, actinomycetemcomitans reappeared in 9 of the deep periodontal pockets after the administration of tetracycline. Most of these 9 pockets became free of detectable A. actinomycetemcomitans during the second week of tetracycline administration, whereas pockets which yielded no A. actinomycetemcomitans after tetracycline therapy became free of the organisms during the first week of tetracycline treatment. This data suggests that systemic tetracycline therapy of localized juvenile periodontitis should, as a practical rate, be continued for 3 weeks. Periodontal destruction continued in 4 deep pockets which all showed high posttetracycline A, actinomycetemcomitans counts. All 6 pockets which demonstrated a marked gain in periodontal attachment yielded no cultivable A. actinomycetemcomitans. No association was found between periodontal disease status and subgingival Capnocytophaga, spirochetes or motile rods. The present study indicates that A. actinomycetemcomitans is an important etiologic agent in localized juvenile periodontitis. Also, this study demonstrates that the effectiveness of therapy can be monitored by subgingival A. actinomycetemcomitans counts, and that periodontal A, actinomycetemcomitans infections cannot be resolved by root surface debridement alone but can be cured by systemic tetracycline therapy.     

Opsonic IgG antibody against Actinobacillus actinomycetemcomitans in localized juvenile periodontitis

Actinobacillus actinomycetemcomitans is a gram-negative bacterium frequently recovered from periodontal lesions of patients with localized juvenile periodontitis (LJP). Elevated levels of serum IgG and IgM antibodies to A. actinomycetemcomitans antigens are frequently observed in LJP patients, although the functional properties of such antibodies have not been characterized systematically. In this study, we analyzed serum from LJP subjects infected with A. actinomycetemcomitans with respect to the presence of IgG antibodies expressing opsonic, bactericidal and/or leukotoxin-neutralizing activity against this organism. The IgG fractions obtained from serum of 3 LJP patients with elevated antibody titers to A. actinomycetemcomitans contained opsonic activity against a non-leukotoxic Y4 strain, as well as for a highly leukotoxic JP2 strain. Opsonic activity required the presence of complement. The IgG fractions of pooled normal serum and serum from a fourth LJP subject with minimal ELISA-reactive IgG antibody against this organism lacked detectable opsonic activity. Leukotoxin-neutralizing IgG antibodies, although variably present, did not influence neutrophil killing of the leukotoxic JP2 strain. None of the sera tested contained bactericidal IgG antibodies capable of promoting direct complement-mediated killing of A. actinomycetemcomitans. These results indicate that LJP subjects infected with A. actinomycetemcomitans are capable of producing opsonic IgG antibodies which may facilitate neutrophil-mediated host defense against this periodontopathic organism.     

Quantitative aspects of the subgingival distribution of Actinobacillus actinomycetemcomitans in a patient with localized juvenile periodontitis

Abstract The subgingival microflora in a patient with localized juvenile periodontitis was studied. Of the 97 sites investigated, 28 (29%) showed attachment loss. A correlation was found between the number of Actinobacillus actinomycetemcomitans cells and the clinical attachment level and probing pocket depth. Of the 97 test sites, 70 (73%) were positive for A. actinomycetemcomitans. Of the total number of A. actinomycetemcomitans cells isolated from this patient, more than 99% were found at sites with attachment loss, <1 % being present at sites without attachment loss. The mean percentage of A. actinomycetemcomitans was 21.2% at sites with attachment loss and 0.45% at sites without attachment loss. The distribution of Porphyromonas gingilis showed a symmetrical pattern, being present at the 1st molar and 2nd premolar sites in all quadrants and at the lower incisor sites. This species was absent at multiple sites showing overt attachment loss.     

Occurrence of Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis and Prevotella intermedia in juvenile periodontitis

Abstract The occurrence of Actinobacillus actinomycetemcomitans, Porphyromanas gingivalis and Prevotella intermedia in subgingival plaque in 24 juvenile periodontitis patients was determined using DNA probe. 36 samples of subgingival plaque from 36 pockets having ≥6 mm depth, ≥3 mm of loss of attachment, and Weeding on probing anchor suppuration were taken from 18 patients with localized juvenile periodontitis (LJP, age range 12-24 years); and 12 samples from-6 patients with generalized juvenile periodontitis (GJP, age range 23–26 years). As control, an equal numbers of samples from health sites in the same patients were studied. P. gingivalis was found in 17 of 18 LJP patients, and in 31 of 36 diseased sites in those patients. P. intermedia was found in 15 out of the 18 LJP patients and in 28 of the 36 diseased sites. A, actinomycetemcomitans was present in 7 of the 18 LJP patients, and in 9 of the 36 diseased sites, and was not found in any GJP patients. All GJP patients had P. gingivalis 1 out of 12 diseased sites) and P. intermedia (all of the diseased sites). None of the three bacterial species was detected in healthy sites of GJP patients, and were found in healthy sites in only 2 of 18 LJP patients. The high prevalence and high levels of P. gingivalis and P. intermedia found in the LJP and GJP patients studied, suggest that there are populations affected by juvenile periodontitis in which this type of periodontitis is more associated with these species than with A. actinomycetemcomitans.     

Microbiological and clinical effects of metronidazole and amoxicillin in Actinobacillus actinomycetemcomitans associated periodontitis

Abstract In this study, we evaluated the microbiological and clinical effects of mechanical debridement in combination with metronidazole and amoxicillin therapy in 48 patients with Actinobacillus actinomycetemcomitans-associated periodontitis, 3 months and at least 24 months after active treatment. The results of this study showed that 47 out of 48 patients were still negative for A. actinomycetemcomitans subgingivally, at the mucous membranes, the tonsillar area and in the saliva, 2 years after therapy. The clinical results showed that a reduction of probing pocket depth, probing attachment level, bleeding index and plaque index was not only seen in the time between baseline and 3 months after therapy, but further clinical improvement was observed between 3 and 24 months after active treatment. We conclude that combined mechanical debridement and metronidazole plus amoxicillin therapy is very effective in suppressing A. actinomycetemcomitans below cultivable levels over a long period of time, suggesting elimination of this organism, and that recolonization of A. actinomycetemcomitans seems to be a rare event. The elimination of A. actinomycetemcomitans is paralleled by a further improvement of the periodontal status of the patients, even up to 24 months after active treatment.     

Antigenic components of Actinobacillus actinomycetemcomitans lipopolysaccharide recognized by sera from patients with localized juvenile periodontitis

The dominant antigen of Actinobacillus actinomycetemcomitans recognized by high-titer sera from patients with localized juvenile periodontitis is the serotype antigen located in the O-side chains of lipopolysaccharide. Whether such sera contain antibodies reactive with other epitopes in lipopolysaccharide, as is the case for patients with rapidly progressive periodontitis, remains unknown. We prepared and characterized by gas liquid chromatography lipopolysaccharide, lipid A, core carbohydrate with no or few O-side chains (core) and high-molecular-mass carbohydrate-rich in O-side chains (oligosaccharide) from A. actinomyce-temcomitans ATCC 43718 (serotype b, Y4). Using enzyme-linked immunosorbent assay (ELISA), sera from 36 patients with localized juvenile periodontitis were surveyed using whole-cell sonicate as plate antigen. The seven highest titer sera were selected for further study. Specific IgG antibody binding was observed to intact lipopolysaccharide and to all the lipopolysaccharide fractions. The mean titers were highest for intact lipopolysaccharide (138.8 ELISA units), and lipid A (122 ELISA units), followed by the core fraction (81 ELISA units) and the oligosaccharide fraction (69.5 ELISA units). ELISA inhibition revealed that the core fraction at a concentration of 10 micrograms/test well inhibited antibody binding to A. actinomycetemcomitans lipopolysaccharide by a mean value of 56.7%. To further characterize antibody binding to the core fraction, ELISA inhibition was performed using as inhibitor the core carbohydrate fraction of the Re mutant of Salmonella minnesota, which is known to contain only alpha-keto-3-deoxyoctonate residues and phosphate. This fraction at 10 micrograms/test well inhibited binding of antibodies from 6 of 7 test sera with a mean value of 49.2%. Thus, sera from patients with localized juvenile periodontitis contain antibodies that bind to the O-side chains of lipopolysaccharide, as has been previously reported, but they also contain antibodies that bind to lipid A and to lipopolysaccharide core polysaccharide epitopes, specifically to alpha-keto-3-deoxyoctonate moieties. The humoral immune response to A. actinomycetemcomitans in patients with localized juvenile periodontitis is more complex than previously reported and is very similar to that of patients with rapidly progressive periodontitis.     

Serum immunoglobulin G responses to various Actinobacillus actinomycetemcomitans serotypesinayoung ethnographically heterogeneous periodontitis patient group

Sera from young patients with periodontal diseases have been shown to often contain highly elevated antibody levels to Actinobacillus actinomycetemcomitans. in particular serotype b. Such responses were reportedly predominated by antibodies of the immunoglobulin G2 (IgG2) subclass. The aim of this study was to investigate an ethnically diverse group of 14 early-onset periodontitis and 15 rapidly progressive periodontitis patients for the occurrence of elevated antibody titers against the five known A. actinomycetemcomitans serotypes, and to compare the patient's IgG subclass response profiles. Enzyme-linked immunosorbent assays were used to measure both total IgG and subclass specific IgG titers. Twenty-four subjects had markedly elevated total IgG levels against at least one serotype. The frequencies of high responses against serotypes a, b, c, d and e were 7, 11, 6, 4, and 4, respectively. Elevated antibody responses were predominated by IgG2, regardless of the serotype to which the response was directed. The serotype specificity of the host responses was further investigated by competitive binding studies with serotype-specific monoclonal antibodies. Twelve sera were found to contain antibodies capable to strongly inhibit the binding of monoclonal antibodies against a single serotype; four other sera had antibodies against epitopes of two, and one serum against those of three serotypes. The findings document broad serotype diversity in an ethnically heterogeneous group of patients and indicate that strong antibody responses to A. actinomycetemcomitans are predominated by IgG2 regardless of the serotype of the infective agent.     

Probe-specific DNA fingerprinting applied to the epidemiology of localized juvenile periodontitis

Although Actinobacillus actinomycetemcomitans has been recognized as a primary etiological agent in localized juvenile periodontitis, questions remain concerning the source of infection, mode of transmission, and relative virulence of strains. DNA fingerprinting analysis, using a randomly cloned chromosomal DNA fragment as a probe, revealed that previously characterized strains of A. actinomycetemcomitans displayed significant restriction site heterogeneity which could be applied to the typing of clinical isolates of this bacterium such that individual strains or variants could be traced within subjects from localized juvenile periodontitis families. Hybridization data derived from an analysis of bacterial isolates obtained from families participating in an ongoing longitudinal study of the disease showed that a single individual could be infected with more than one strain or variant of A. actinomycetemcomitans and that various members of the same family could harbor different strains or variants of the bacterium. In several cases the clinical isolates were matched to characterized laboratory strains by comparing hybridization patterns generated by digestion of the DNA with several restriction enzymes in independent reactions. Thus, probe-specific DNA fingerprinting of A. actinomycetemcomitans will permit us to determine if particular strains or variants are frequently associated with sites of periodontal destruction. Attention could then be focused on determining the virulence properties of those strains or variants that have in vivo significance.     

Characterization of tetracycline resistance in Actinobacillus actinomycetemcomitans

Comparison of susceptibility data for Actinobacillus actinomycetemcomitans has been difficult because of the lack of standard susceptibility testing conditions. In this study, minimum inhibitory concentration to tetracycline was evaluated by comparing different media, air conditions and incubation times. Ten of 22 (45%) A. actinomycetemcomitans isolated from periodontally diseased sites grew on media supplemented with 4 μg per ml of tetracycline, but minimum inhibitory concentrations ranged from 0.125 to 8 μg/ml depending on the media and condition used. The best results were obtained with brain heart infusion agar (Difco Laboratories, Detroit MI) incubated in 5% CO₂ for 48 h. Eighteen (82%) of the A. actinomycetemcomitans isolates hybridized with the Tet B determinant. The Tet B determinant was transferable between A. actinomycetemcomitans isolates as well as a Haemophilus influenzae recipient and appears to be associated with conjugative plasmids.     

Ultrastructure of the subgingival microflora in juvenile periodontitis

abstract — The ultrastructure of the subgingival deposits on the root surfaces of teeth affected by juvenile periodontitis was studied on 12 teeth from nine individuals, 15–30 years of age. The deposits consisted of either microbial masses associated with a pellicle, or of a cuticular material almost free of bacteria. Gram-negative rods and filaments were the predominant microorganisms. "Corncob" configurations consisting of filamentous bacteria surrounded by Gram-positive cocci, and "bristle brush" formations comprising corncobs surrounded by long rods were observed in the superficial layer of the plaque. Spirochetes and flagellated rods constituted a major segment of the microflora. The present data indicate that the deep pockets in juvenile periodontitis harbor a sparse but relatively characteristic microbial population.     

Serum neutralizing activity against Actinobacillus actinomycetemcomitans leukotoxin in juvenile periodontitis

A relatively high incidence of infection by Actinobacillus actionomycetemcomitans can be shown in subgingival plaque samples obtained from patients with juvenile periodontitis. These organisms possess a potent leukotoxin(s) which rapidly destroys isolated human polymorphonuclear leukocytes (PMNs) and monocytes. If such leukotoxins operate in vivo, they could deprive the gingival crevice area of an essential antibacterial defense mechanism. We have found that sera from juvenile periodontitis patients consistently (greater than 90%) contain antibodies which neutralize Actinobacillus actinomycetemcomitans leukotoxin(s). On the other hand, sera from normal individuals or patients with other types of periodontal disease usually amplified rather than inhibited the leukotoxic reaction. Many patients with juvenile periodontitis have demonstrable defects in PMN or monocyte chemotaxis and this may place them at risk to gingival infection by Actinobacillus actinomycetemcomitans. The immune response against these organisms could be a crucial determinant in the course of juvenile periodontitis. While this disease is relatively rare, it does cause immeasurable emotional, physical and economic hardship for patients and their families. The identification of Actinobacillus actinomycetemcomitans as a potential pathogen in this disorder may eventually lead to specific forms of therapy to prevent and eliminate infection by this organism in these patients.     

The presence of phage-infected Actinobacillus actinomycetemcomitans in localized juvenile periodontitis patients

Electron microscopy revealed 2 different types of bacteriophages isolated from Actinobacillus actinomycetemcomitans colonizing exclusively diseased sites in 4 patients with localized juvenile periodontitis (LJP). All sites infected with phage were undergoing periodontal destruction, as judged from consecutive routine radiographs. The phages isolated had a wide host range as assessed from their ability to infect a series of reference strains of A. actinomycetemcomitans. A 5th patient harboured non-infected A. actinomycetemcomitans in a surgically treated site which had undergone no bone destruction during the last 12 months. The present findings suggested that the pathogenic potential of A. actinomycetemcomitans in LJP may increase due to phage infection.     

Inhibition of Actinobacillus actinomycetemcomitans leukotoxicity by bacteria from the subgingival flora

Actinobacillus actinomycetemcomitans produces a pore-forming leukotoxin that lyses human polymorphonuclear leukocytes and monocytes. Certain proteolytic bacteria may coexist with A. actinomycetemcomitans in periodontal pockets. We aimed therefore to examine whether oral bacteria can modify the leukotoxicity of A. actinomycetemcomitans. A total of 55 strains representing 45 bacterial species of the subgingival flora were tested. Each strain was incubated with the highly toxic strain of A. actinomycetemcomitans HK 1519 and the leukotoxic activity of the suspension against human polymorphonuclear leukocytes was determined from the activity of the lactate dehydrogenase released upon lysis of the leukocytes. Porphyromonas gingivalis, Prevotella intermedia, Prevotella nigrescens, Prevotella melaninogenica and Prevotella loeschii inhibited the leukotoxicity of A. actinomycetemcomitans cells as well as the activity of leukotoxin purified from the same strain. The bacterial strains without the ability to block leukotoxic activity also failed to destroy pure leukotoxin even after 5 h of incubation. The proteolytic degradation of leukotoxin by P. gingivalis was mainly dependent on the activity of the enzymes R- and K-gingipains. P. intermedia and P. nigrescens also degraded the leukotoxin by enzymes. The results imply a role of the periodontal microflora in modifying the virulence of A. actinomycetemcomitans by destroying its leukotoxin.     

Comparative antibody titers to Actinobacillus actinomycetemcomitans in juvenile periodontitis, chronic periodontitis and periodontally healthy subjects

Abstract Circulating antibody levels to four strains of Actinobacillus actinomycetemcomitans (Aa) were determined by means of an indirect immunofluorescent technique in three groups of 21 subjects each, including one with juvenile periodontitis (JP), one with chronic periodontitis (CP) and one free of periodontal disease (N). Mean levels of antibody to Aa were significantly elevated in the JP group as compared to the CP and N groups with respect to strains Y4, 29522 and 29524, but not strain 29523. Since strains Y4, 29522 and 29524 contain a leukotoxin that is missing from strain 29523, the results suggest that the leukotoxin could account for the difference in the immune response among the three groups of subjects. Varying the end-point considered to represent positive fluorescence did not significantly affect the results, although discrimination among the three groups appeared to be somewhat better at lower intensities of fluorescence. Because of wide variations in antibody titers recorded in individual subjects, elevated levels of antibody to certain strains of Aa may not be useful as a primary diagnostic test for JP, but may be of value in confirming an otherwise uncertain clinical diagnosis.     

The description of a unique population with a very high prevelance of localized juvenile periodontitis

Abstract. The reported prevalence of localized juvenile periodontitis (LJP) amongst teenagers and young adults varies greatly. The etiology of LJP has been related to Actnobacillus actinomy cetemcomitans Aa$ and it has also been suggested that there may be a transmission of Aa within families resulting in the familial distribution of the disease. This study describes the high prevalence of LJP in adolescents, 12–20 years of age, from a group of nuclear families living and functioning in a closed, closely knit community. The survey was carried out on a population of teenagers that had attended the same school and their siblings. All students attending that school and their siblings were examined. They were given a periodontal examination and a questionnaire relating to their demographic details and their personal oral hygiene habits. The periodontal examination was limited to the incisors and first molar teeth. Plaque index (PII), gingival index (GI), the presence or absence of bleeding on probing (BOP), probing pocket depth (PPD) and recession ere measured. All patients having at least two of the examined sites with probing pocket depth ≥5 mm or one site ≥6 mm were considered as possible sufferers from LJP and had a full mouth periapieal radiographic survey carried out using a paralleling technique to confirm the diagnosis. At the sites with probing pocket depth ≥5 mm, a Shei ruler was used to measure the $$ of the root coronal to the alveolar bone. A cut off point of ≥20mm was used as a measure of true bone loss confirming the clinical diagnosis of LJP 86 individuals from 30 families comprised the population of interest There were 44 males and 42 females with a mean age of 14.7±2.3. Of the 86 individuals examined, 33 individuals from 15 families were diagnosed as having LJP (38.4%). None of the individuals examined showed any evidence of the generalized form of juvenile periodontitis. The mean age of the LJP patients was 15±23 yrs. with a 1:1.75 male to female ratio. Except for 2 pairs of families with genetic tics, no familial connections could be traced between the different nuclear families affected by LJP despite repeated and intensive questioning. There were no significant differences in the PII and the GI between the groups while the LJP group had significantly higher BOP. PPD and PAL than the non-LJP group. These finding strongly suggest an environmental influence in the etiologu of the disease.     

Microbiological and clinical effects of surgical treatment of localized juvenile periodontitis

Since Actinobacillus actinomycetemcomitans appears to be a key etiologic agent in localized juvenile periodontitis, this study determined the effectiveness of different treatment modalities in suppressing A. actinomycetemcomitans in localized juvenile periodontitis lesions. A total of 25 deep periodontal lesions from 7 patients with localized juvenile periodontitis were included in the study. The test periodontal lesions either received scaling and root planing alone, scaling and root planing together with soft tissue curettage, or modified Widman flap surgery. Subgingival A. actinomycetemcomitans were enumerated using selective culturing. Clinical measurements included changes in probing periodontal attachment level, probing periodontal pocket depth, gingival index, plaque index, and digital subtraction of standardized serial radiographs. The microbiological and clinical effects of treatment were monitored over a period of 16 weeks. All periodontal lesions studied demonstrated high numbers of A. actinomycetemcomitans prior to treatment. Scaling and root planing alone did not markedly change the subgingival A. actinomycetemcomitans counts, nor any of the clinical parameters studied. In contrast, soft tissue curettage as well as modified Widman flap surgery suppressed A. actinomycetemcomitans to undetectable levels immediately after therapy in more than 80% of the lesions studied. A total of 5 periodontal lesions exhibited gain of probing periodontal attachment after subgingival curettage or Widman flap treatment; 3 of these sites revealed no detectable A. actinomycetemcomitans, and the remaining 2 sites harbored only low levels of A. actinomycetemcomitans. 5 periodontal lesions which lost probing attachment after treatment all demonstrated high numbers of subgingival A. actinomycetemcomitans. Changes in alveolar bone, assessed by digital subtraction of serial radiographs, correlated with changes in probing periodontal attachment level, confirming the clinical results. The present study revealed a close relationship between post-treatment A. actinomycetemcomitans levels and the clinical response to treatment, which supports the concept that A. actinomycetemcomitans is an important organism in the etiology of localized juvenile periodontitis. This study also showed that a substantial suppression of subgingival A. actinomycetemcomitans cannot be achieved by periodontal scaling and root planing alone, but can be accomplished by surgical removal of periodontal tissues.(ABSTRACT TRUNCATED AT 400 WORDS)     

T-cell-receptor gene usage of Actinobacillus actinomycetemcomitans-reactive periodontal CD4+ T cells from localized juvenile periodontitis patients and human peripheral blood leukocyte-reconstituted NOD/SCID mice

We investigated the variable Valpha and Vbeta gene usage of Actinobacillus actinomycetemcomitans-reactive periodontal CD4+ T cell receptors (TCR) from: (i) four A. actinomycetemcomitans-infected localized juvenile periodontitis (LJP) patients, (ii) four groups of A. actinomycetemcomitans-inoculated NOD/SCID mice engrafted with individual LJP-derived HuPBL and (iii) HuPBL samples of four LJP patients and two healthy control subjects, by quantitative PCR analyses. The results show that: (i) the majority of the TCR genes (82.5% of Valpha and 91.1% of Vbeta) used by periodontal CD4+ T cells in A. actinomycetemcomitans-inoculated HuPBL-engrafted NOD/SCID mice overlap with those used by local periodontal T cells in LJP patients, (ii) although A. actinomycetemcomitans-reactive periodontal CD4+ TCR repertoire is relatively widespread, there are a few dominant genes shared by the LJP patients, suggesting a limited number of antigens or epitopes commonly recognized and (iii) A. actinomycetemcomitans likely lacks superantigenic characteristics. These results suggest A. actinomycetemcomitans-associated human CD4+ T cell repertoire established in HuPBL-NOD/SCID mice provides a useful approach to study specific aspects of immune-parasite interactions in the periodontium.     

A double-blind trial of tetracycline in the management of early onset periodontitis

Abstract The aim of the study was to evaluate the adjunctive effect of systemic tetracycline (250 mg qds for 14 days) in sequential root planing and surgical phases of treatment in a randomised, double-blind controlled trial. 38 patients who were under 26 years of age. in good general health and with localised (15 test/15 control) or generalised (4 test/4 control) early onset periodontitis completed the non-surgical phase. Data were analysed by ANOVA using baseline covariates and transformations where appropriate. Improvements in probing depth, probing attachment level and bleeding on probing were significantly better in the group treated with adjunctive tetracycline. at 3 months post-treatment. 26 patients (13 test/13 control) subsequently completed the surgical phase (modified Widman flap surgery with adjunctive tetracycline or placebo as before) and were re-examined at 6 months and 12 months. In the test group, 58% of the originally affected teeth required surgery compared to 75% in the control group. Surgery produced further reductions in mean probing depths but no further gains in probing attachment. There were no further statistically significant differences between test and control groups for any of the clinical measures, although the tetracycline group appeared to maintain an advantage. In conclusion, systemically administered tetracycline is a useful adjunct in the management of early onset periodontitis. particularly in non-surgical treatment.     

A case of localized juvenile periodontitis: treatment and 3 years follow-up with superimposable radiographs

Abstract A 17-year-old male patient with localized juvenile periodontitis was treated by subgingival instrumentation with full thickness flap on the lower molars, combined with a 3-week course of systemic tetracycline, and a programme of supervised oral hygiene. The treatment was rapidly followed by dramatic clinical and microbiological improvement. However, despite good oral hygiene, gingival inflammation recurred at regular intervals. It was necessary to maintain the clinical results by periodic subgingival instrumentation with an ultrasonic sealer. Healing of alveolar bone was monitored in the lower 1st molar regions over 3 years by using superimposable radiographs. Quantitative analysis of bone density performed with a high-resolution digitalisation technique showed a considerable improvement 1 year after therapy. However, continuous remodelling, probably related to variations in inflammation, occurred during the 3 postoperative years.