Transmission and colonization of Actinobacillus actinomycetemcomitans in localized juvenile periodontitis patients

Actinobacillus actinomycetemcomitans is a Gram-negative oral microorganism, which has been implicated in the etiology of localized juvenile periodontitis and in severe medical infections such as bacterial endocarditis. This study evaluated the ability of periodontal probes to transmit A actinomycetemcomitans from juvenile periodontitis lesions to healthy gingival sulci in the same patient. Localized juvenile periodontitis patients exhibiting first molar and incisor alveolar bone loss and with large numbers of A actinomycetemcomitans in deep periodontal pockets were included in this study. A periodontal probe was inserted into periodontal pockets of 6 mm or greater depth. The probe was then placed into a healthy gingival sulcus of 3 mm or less, in the same subject. Fifty-five transfers by probing were made and A actinomycetemcomitans in both the donor and recipient sites was assessed by a selective culture technique. The results indicate that periodontal probes can become contaminated with A actinomycetemcomitans from juvenile periodontitis lesions during routine dental examinations and can transfer this microorganism from infected to previously uninfected sites. However, A actinomycetemcomitans inoculated into the healthy gingival sulci did not permanently colonize these sites since the organisms were eliminated within 3 weeks.     

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)     

Actinobacillus actinomycetemcomitans in human periodontal disease. Prevalence in patient groups and distribution of biotypes and serotypes within families

Actinobacillus actinomycetemcomitans is a Gram-negative oral bacterium which has been implicated in the etiology of localized juvenile periodontitis. In this study, 403 subjects from four study groups were examined for A actinomycetemcomitans in subgingival dental plaque. Samples pooled from at least six periodontal sites were included from each subject. A actinomycetemcomitans was detected in 28 of 29 localized juvenile periodontitis patients but in only 15% of the other subjects including 28 of 134 adult periodontitis patients, 24 of 142 periodontally healthy subjects and 5 of 98 insulin dependent juvenile diabetics with varying degrees of gingivitis. A actinomycetemcomitans isolates from members of five families with localized juvenile periodontitis patients were biotyped on the basis of variable fermentation of dextrin, maltose, mannitol and xylose and serotyped by indirect immunofluorescence using serotype specific rabbit antisera. Individuals within a family all harbored A actinomycetemcomitans of the same biotype and serotype. However, even in families with individuals heavily infected with A actinomycetemcomitans, some family members did not appear to be infected with the organism. The apparent poor transmissibility of A actinomycetemcomitans between individuals may, in part, explain the overall low prevalence of localized juvenile periodontitis and the familial pattern of the disease. The high prevalence of A actinomycetemcomitans in the subgingival plaque of localized juvenile periodontitis patients, compared to the much lower prevalence in other patient groups, supports the hypothesis that A actinomycetemcomitans is an etiologic agent in this periodontal disease.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Morphological compositions of subgingival microbiota in Actinobacillus actinomycetemcomitans- associated periodontitis

Infrequent occurrence of spirochetes and rather low proportions of these organisms have been reported in localized juvenile periodontitis, where periodontal lesions often harbour large numbers of Actinobacillus actinomycetemcomitans, a suspected principal periopathogen strongly implicated in the pathogenesis of this and other forms of chronic periodontitis. We studied the association of subgingival A. actinomycetemcomitans with the morphological composition of the subgingival microbiota in a large population of patients suffering from advanced periodontitis. Subgingival plaque from the deepest pockets of every quadrant of their dentitions was sampled and pooled in 70 patients between 14 and 63 years of age, and analysed morphologically by phase-contrast microscopy. A minimum % similarity index was employed to define 4 clusters with different morphological composition of the floras. The actual proportion of A. actinomycetemcomitans was determined at 2 sites with deep periodontal pockets. All clusters harboured patients infected with A. actinomycetemcomitans. If present, in clusters predominated by motile rods or medium-sized spirochetes, the organism was found in rather low proportions (median 5.3% and 3.4%, respectively). However, the cluster with a pooled flora mainly consisting of coccoid cells revealed periodontal sites with A. actinomycetemcomitans in proportions of more than 53% (median), if the organism was present (p less than 0.01). We found a positive correlation between proportions of A. actinomycetemcomitans and cocci (R = 0.65) and negative correlations with spirochetes and motile rods (R = 0.61, R = -0.59, respectively). Cautious interpretation of subgingival plaque predominated by coccoid cells is recommended, if deep periodontal pockets and obvious signs of inflammation are present, since these pockets were found to be often infected with large numbers of A. actinomycetemcomitans.     

Tissue localization of Actinobacillus actinomycetemcomitans in human periodontitis. I. Light, immunofluorescence and electron microscopic studies

Invasion of periodontal tissues by different bacterial morphotypes has been reported in human periodontitis; however, limited information is available as to prevalence, localization and the bacterial species involved. The present study determined prevalence and gingival localization of Actinobacillus (Haemophilus) actinomycetemcomitans in periodontal lesions of juvenile periodontitis patients. Thirty-five gingival biopsies were obtained from 12 juvenile periodontitis patients at the time of periodontal therapy. One additional control biopsy was obtained from each of two adult periodontally healthy subjects, one adult periodontitis patient and one periodontally healthy monkey (Macaca fosibolius). The biopsies were carefully processed to avoid mechanical introduction of bacteria into the tissues and were examined using light and electron microscopy. Rabbit antisera specific for the three A. actinomycetemcomitans serotypes were used for immunofluorescence microscopic localization of A. actinomycetemcomitans antigens in the gingival sections. Immunofluorescence microscopy showed A. actinomycetemcomitans specific antigens in the gingival tissues of 11 of the 12 juvenile patients examined. None of the control specimens showed evidence of A. actinomycetemcomitans antigens in the gingival connective tissue. One specimen from a periodontally healthy subject and the monkey biopsy, however, showed A. actinomycetemcomitans antigens in bacterial plaque on the surface of the crevicular epithelium. Transmission electron microscopic examination showed microcolonies of small gram-negative rods in the connective tissue, as well as single bacterial cells between collagen fibers and in areas of cell debris. In addition to these extracellular bacterial cells, evidence of bacterial cells was also found within gingival connective tissue phagocytic cells. The data from the present study suggest that the gingival tissue in juvenile periodontitis lesions harbors A. actinomycetemcomitans.     

Actinobacillus actinomycetemcomitans recovery from extracrevicular locations of the mouth

Associations between recovery of Actinobacillus actinomycetemcomitans from samples of subgingival plaque, and samples of buccal mucosa, tongue and unstimulated saliva were studied in 107 subjects. Ten subjects had gingivitis, 18 localized juvenile periodontitis, 45 rapidly progressive periodontitis and 32 adult periodontitis. Two children suffered from prepubertal periodontitis. Heterogeneity tests for associations in different study populations yielded nonsignificant results. Mantel-Haenszel's common odds ratios were 52.9, 37.2 and 19.8 for respective associations between pooled subgingival samples, and cheek, saliva and tongue samples. Significant McNemar's chi-square of 5.88, 11.25 and 16.96 for respective associations pointed to secondary occurrence of A. actinomycetemcomitans in extra-crevicular samples. Multiple linear regression yielded a significant influence of the number of deep periodontal pockets of 7 mm or more and a negative influence of the diagnosis "adult periodontitis" on the log-transformed number of colony-forming units of A. actinomycetemcomitans in samples from cheek mucosa in patients infected with the organism. Extracrevicular occurrence of A. actinomycetemcomitans seems to reflect total subgingival numbers of the organism. Especially sampling check mucosa appears to be a promising tool in the diagnosis of a periodontal infection with A. actinomycetemcomitans .     

Actinobacillus actinomycetemcomitans and clinical periodontal status in Finnish juvenile periodontitis patients

The relationship between the clinical periodontal status and the occurrence of Actinobacillus actinomycetemcomitans (A.a.) in 19 Finnish patients with localized juvenile periodontitis (LJP) was studied. Clinical examination included the Plaque Index, Gingival Index, suppuration, probing depth and bleeding on probing. The subgingival bacterial samples were taken from two diseases periodontal pockets with radiographic bone loss and two periodontal pockets exhibiting no radiographic alveolar bone loss. The results indicate that A.a. was isolated in 17 (89%) patients, in 68% of the diseased and in 32% of the control periodontal sites. Supragingival plaque, marginal gingival inflammation, gingival bleeding on probing, and suppuration were found as frequently in A.a.-positive as in A.a.-negative diseased LJP pockets. It was concluded that A.a. was frequently, but not always, detected in diseased LJP lesions. No association was found between the clinical status and the occurrence of A.a.     

Collagenase activity in gingival crevicular fluid of patients with juvenile periodontitis

The nature and origin of collagenases in gingival crevicular fluid of juvenile periodontitis patients was investigated. Gingival crevicular fluid collected from deep untreated periodontal pockets of juvenile periodontitis patients was found to contain only vertebrate collagenase (EC 3.4.24.7) activity that cleaved soluble type-I and -III collagens into 3/4 and 1/4 length fragments, as analyzed by SDS-polyacrylamide gel electrophoresis. Type II collagen was degraded at a markedly slower rate. This substrate specificity is indicative of collagenases produced by fibroblasts, epithelial cells and macrophages. We have previously found that collagenase in gingival crevicular fluid of adult periodontics patients appears to be mainly derived from polymorphonuclear leukocytes (PMN). The reasons for the apparent difference in collagenase source between the groups were investigated. We examined whether the pathogen characteristic for juvenile periodontitis, Actinobacillus actinomycetemcomitans, can release collagenase from normal human PMNs. All 10 A. actinomycetemcomitans strains tested, freshly isolated from the subgingival plaque of juvenile periodontitis patients, caused release of collagenase from PMNs in vitro. These results suggest that the lack of normally functioning PMNs in the periodontium of juvenile periodontitis patients may result in a colonization of bacteria that activate the resident periodontal cells to produce increased amounts of collagenase.     

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.     

Activity of metronidazole and its hydroxy metabolite against clinical isolates of Actinobacillus actinomycetemcomitans

The in vitro susceptibility of Actinobacillus actinomycetemcomitans to metronidazole and its hydroxy metabolite was determined by the agar dilution method with 73 A. actinomycetemcomitans strains, recent clinical isolates from 13 patients with localized juvenile periodontitis. The minimal inhibitory concentrations (MICs) for 50% and for 90% of the isolates were, respectively, 16 μg/ml and 32 μg/ml of metronidazole, and 4 μg/ml and 8 μg/ml of the hydroxy metabolite. Although the MICs of the hydroxy metabolite were lower than those of the parent compound, the presently used dosage of metronidazole in treatment of periodontal diseases may not result in sufficiently high drug levels in gingival crevice fluid or in plasma to inhibit all A. actinomycetemcomitans strains. However, the known synergistic and additive effects of these compounds may increase the clinical efficacy of metronidazole in the treatment of periodontal infections associated with A. actinomycetemcomitans.     

Tetracycline inhibition identifies the cellular origin of interstitial collagenases in human periodontal diseases in vivo

Mammalian interstitial collagenases (E.C.3.4.24.7) are considered as key initiators of collagen degradation in periodontal diseases. However, the cellular sources of collagenases present in gingival crevicular fluid have not been completely clarified. Resident fibroblasts and epithelial cells as well as infiltrating neutrophils and monocyte/macrophages are potential sources of the enzymes. We have recently found significant differences in tetracycline inhibition between human neutrophil and fibroblast interstitial collagenases. To address the cellular source of collagenase present in gingival crevicular fluid in 2 distinct periodontal diseases, we studied the tetracycline inhibition of collagenase in gingival crevicular fluid of patients with localized juvenile periodontitis and adult periodontitis. Gingival crevicular fluid samples were collected from deep (greater than 5 mm) periodontal pockets and assayed for collagenase in the presence of 0-1000 microM doxycycline as well as a chemically modified tetracycline devoid of antimicrobial activity (4-de-dimethylaminotetracycline). The drug concentration required to inhibit 50% of collagenase activity (IC50) in localized juvenile periodontitis gingival crevicular fluid was 280 microM for doxycycline and 470 microM for 4-de-dimethylaminotetracycline. Significantly lower values, 10-20 microM, were obtained for collagenase in gingival crevicular fluid of patients with adult periodontitis. We propose that systemic tetracycline levels are efficient inhibitors of collagenase in gingival crevicular fluid in affected sites of patients with adult periodontitis but not of patients with localized juvenile periodontitis and that the fibroblast type interstitial collagenase is the predominant collagenase type in gingival crevicular fluid in affected sites of patients with localized juvenile periodontitis and the neutrophil collagenase in adult periodontitis gingival crevicular fluid.(ABSTRACT TRUNCATED AT 250 WORDS)     

Periodontitis in the primary dentition associated with Actinobacillus actinomycetemcomitans infection and leukocyte dysfunction

2 siblings, aged 5 years (girl) and 7 years (boy), with periodontitis in the primary dentition were studied. Actinobacillus actinomycetemcomitans was isolated from the gingival pockets of both children. The titers of IgG antibodies against A. actinomycetemcomitans were elevated, and the polymorphonuclear leukocytes had a decreased capacity to ingest IgG-coated latex particles. Other functions of the polymorphonuclear leukocytes were normal. After antibiotic therapy and for the 7-year-old boy, debridement of the gingival pockets A. actinomycetemcomitans was no longer detectable in the gingival pockets, and the phagocytic capacity of the polymorphonuclear leukocytes was normalized. After 2 1/2 years, A. actinomycetemcomitans was found again in the gingival pockets of the boy, and once more his polymorphonuclear leukocytes had a decreased capacity to ingest IgG-coated latex particles. The antibiotic therapy was repeated and 6 months later, the number of A. actinomycetemcomitans was very low and the phagocytic capacity of the polymorphonuclear leukocytes was back to normal. This case report suggests that A. actinomycetemcomitans may be involved in the etiology of periodontitis in the primary dentition, possibly by triggering a phagocytic dysfunction of polymorphonuclear leukocytes.     

Actinobacillus actinomycetemcomitans and Bacteroides intermedius in human periodontitis: age relationship and mutual association

This study examined age relationships and mutual interrelationships between cultivable Actinobacillus actinomycetemcomitans and Bacteroides intermedius in 1624 periodontitis patients, 15 to 89 years of age. Each subject contributed a pooled subgingival sample, obtained from 3 deep periodontal pockets with paper points. A. actinomycetemcomitans occurred with higher prevalence (74%) and mean recovery (7% in culture-positive patients) in patients less than 25 years old than in adult and geriatric patients (prevalence about 31%; mean recovery about 1%). The organism was detected in 85% of localized juvenile periodontitis patients. B. intermedius was recovered from 45% of the study subjects, averaged about 7% of total isolates in positive patients, and showed no predilection for any age group. As determined from predicted and observed values for A. actinomycetemcomitans and B. intermedius, occurring alone and in combination, no synergistic or antagonistic relationships between the organisms could be delineated with respect to subgingival colonization. The therapeutic implication of these findings is discussed.     

Tissue localization of Actinobacillus actinomycetemcomitans in human periodontitis. II. Correlation between immunofluorescence and culture techniques

Recent immunohistological studies have suggested that Actinobacillus actinomycetemcomitans is present in the gingival tissues in juvenile periodontitis lesions. The present study examined tissue bound A. actinomycetemcomitans by bacterial culture and immunohistological demonstration of antigen in tissue. A total of 14 periodontitis lesions were examined. Eleven biopsies were obtained from gingiva adjacent to A. actinomycetemcomitans infected pockets, while the remaining three control biopsies were obtained from gingiva adjacent to pockets where subgingival A. actinomycetemcomitans infection could not be detected. Each biopsy was hemisected, one half was used for immunofluorescence microscopic examination while the other half was processed for culture of A. actinomycetemcomitans. The latter section was surface-disinfected, repeatedly washed and then minced to release bacteria from within the tissues. Aliquots from the serial washings and the minced tissue suspension were cultured on medium selective for A. actinomycetemcomitans. Surface disinfection and serial washings gradually decreased cultivable A. actinomycetemcomitans in the washings aliquots. Following tissue disruption, an increase in colony-forming units of A. actinomycetemcomitans was seen from eight of the 11 test biopsies. This bacterium could not be detected in washings or minced tissue suspensions from the control biopsies obtained from lesions in which subgingival A. actinomycetemcomitans was previously not detected. A positive correlation was seen between the presence of A. actinomycetemcomitans antigens in the gingival biopsies and; (1) A. actinomycetemcomitans colony-forming units released from the minced tissues (r = 0.90, p = 0.000), as well as; (2) the colony-forming units from the periodontal pocket (r = 0.62, P = 0.017).(ABSTRACT TRUNCATED AT 250 WORDS)     

Diagnosis and treatment of localized juvenile periodontitis

An actinomycetemcomitans can cause localized juvenile periodontitis and certain types of adult periodontitis. Optimal treatment of periodontal disease caused by this microorganism requires systemic antibiotic therapy in addition to mechanical debridement of the infected gingival tissues. Laboratory techniques are available to assist the practitioner in identifying this microorganism in dental plaque samples.     

Differential regulation of innate immune response genes in gingival epithelial cells stimulated with Aggregatibacter actinomycetemcomitans

Background and Objective:  The gingival epithelium provides the first line of defense against colonization by periodontal pathogens, both as a physical barrier and by the production of inducible innate immune mediators such as β-defensins and pro-inflammatory cytokines. The gram-negative bacterium Aggregatibacter actinomycetemcomitans is implicated in the pathogenesis of localized aggressive periodontitis, although the bacterium is found widely in the healthy population. We hypothesized that gingival epithelial cell-derived innate immune mediators triggered in response to A. actinomycetemcomitans infection may play an important role in increased susceptibility to infection.
Material and Methods:  Primary cultures of human gingival epithelial cells were cultured in the presence of A. actinomycetemcomitans . Total mRNA was examined for the presence of innate immune markers using RT-PCR.
Results:  We show here that the mRNA levels of human β-defensin 2 and interleukin-8 are elevated by live cultures of a clinical isolate of A. actinomycetemcomitans in cultured gingival epithelial cells from healthy individuals, but not by A. actinomycetemcomitans lipopolysaccharide. Cells from a patient with localized aggressive periodontitis, however, did not respond to this bacterial stimulation. In contrast, the pro-inflammatory cytokine interleukin-19 was induced in cells from both localized aggressive periodontitis and healthy subjects. Examination of Toll-like receptors and associated adapter molecules indicated lower levels of Toll-like receptor 2 mRNA in the localized aggressive periodontitis patient-derived cells compared with cells from healthy subjects.
Conclusion:  These results suggest that a differential expression of innate immune response genes to A. actinomycetemcomitans in the gingival epithelium could be an underlying factor of susceptibility to localized aggressive periodontitis.     

Microbiological and clinical effects of surgery plus doxycycline on juvenile periodontitis

It was previously determined that surgery plus the antibiotic doxycycline were effective in eliminating or suppressing Actinobacillus actinomycetemcomitans (Aa), an organism strongly associated with disease in localized juvenile periodontitis (LJP). Eight patients with LJP participated in this surgical study. Patients were reexamined three and 12 months following therapy. The results of this study strongly suggest that surgery plus doxycycline effectively eliminate Aa from periodontal pockets. This elimination results in clinical improvement and attachment gain at three and 12 months following surgery. Further destruction was seen in individuals who continued to harbor high levels of Aa.     

Metronidazole plus amoxycillin in the treatment of Actinobacillus associated periodontitis

The potential use of an adjunctive therapy of metronidazole plus amoxycillin for the subgingival elimination of Actinobacillus actinomycetemcomitans in periodontitis patients was investigated. 22 patients participated in this study, 11 with localized juvenile periodontitis (LJP) and 11 with rapidly progressive periodontitis (RPP). 14 patients had received periodontal treatment in the past. All patients were subgingivally infected with A. actinomycetemcomitans. After mechanical subgingival debridement in combination with the antibiotic treatment, elimination of A. actinomycetemcomitans was achieved in all patients but one. With this one exception, clinical improvements were observed in all patients, resulting in reduced pocket probing depths as well as in a significant reduction in bleeding on probing. Re-examination of 16 patients after 9-11 months revealed that A. actinomycetemcomitans was still undetectable and further clinical improvement was observed. It was concluded that the combination of metronidazole plus amoxycillin is a valuable adjunct to mechanical therapy in A. actinomycetemcomitans associated periodontal infections.