Actinobacillus actinomycetemcomitans serotypes and leukotoxicity in Korean localized juvenile periodontitis

Actinobacillus actinomycetemcomitans is though to play an important role in the pathogenesis of localized juvenile periodontitis (LJP). Preliminary data suggested that the serotype distribution of A. actinomycetemcomitans in Korea and the United States differ. This study evaluated A. actinomycetemcomitans prevalence, serotype distribution, and leukotoxicity in Korean LJP patients by culture, enzyme-linked immunosorbent assay, indirect immunofluorescence, and lactate dehydrogenase release from polymorphonuclear leukocytes exposed to A. actinomycetemcomitans. A. actinomycetemcomitans occurred in 75% of LJP lesions and 6% of normal sites with approximately equal distribution of serotype a, b, and c. Single serotypes were isolated from nine patients while three patients harbored two serotypes either in the same or different disease sites. A. actinomycetemcomitans leukotoxicity occurred in 22% isolates with a 69% prevalence. Individual sites harbored both leukotoxic and non-leukotoxic strains with no serotype association. The distribution of serotypes and leukotoxic strains of A. actinomycetemcomitans in Korean LJP patients differed from those reported in the United States. This suggests that serotype b may not be more important in the pathogenesis of LJP.     

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.     

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.     

The effect of treatment on Actinobacillus actinomycetemcomitans in localized juvenile periodontitis

Three treatment regimens including local tetracycline delivery, systemic doxycycline and surgery plus systemic doxycycline were investigated in a localized juvenile periodontitis (LJP) population. Of the investigated treatments only surgery plus systemic doxycycline for 14 days was effective in eliminating or suppressing Actinobacillus actinomycetemcomitans, an organism strongly associated with LJP lesions. While surgery plus antibiotics was the superior treatment, it appears that the possibility of reinfection or incomplete elimination of the organism exists. Careful long-term follow-up, including clinical and microbiological monitoring, is highly recommended in this periodontal population.     

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.     

Suppression of subgingival Actinobacillus actinomycetemcomitans in localized juvenile periodontitis by systemic tetracycline

Abstract The current study assessed the clinical and microbiological effects of systemic antimicrobial therapy alone in Actinobacillus actinomycetemcomitans-infected adolescents with periodontal disease. The study involved 6 localized juvenile periodontitis patients 13–18 years of age, who harbored high numbers of A. actinomycetemcomitans: in subgingival plaque samples. The periodontal lesions were microbiologically monitored by selective culture, and clinically assessed for probing pocket depth and periodontal attachment level 3 months prior to baseline, and at 3, 6, 12, and 24 months posttreatment. Tetracycline-HCl (250 mg/ QID) was prescribed until 1 week after subgingival A. actinomycetemcomitans was no longer detectable or for a maximum of 8 weeks. During 3 months prior to treatment, pocket depth was unchanged, and was then significantly reduced from an average of 7.1 mm to 5.1 mm 12 months after treatment (p - 0.02). The mean change in clinical attachment level was a gain of 1.4 mm between baseline and 12 months (p= 0.02). 3 of the 6 patients were still infected with A. actinomycetemcomitans after 8 weeks of antibiotic therapy and 4 subjects were infected at 12 months. Numbers of A. actinomycetemcomitans were still suppressed in most lesions. There was a strong association between mean numbers of A. actinomycetemcomitans in periodontal pockets and mean change in probing attachment level at any given time point. For 22 available comparisons, derived from all time points, there was a strong association (r= 0.68) between subgingival A. actinomycetemcomitans and change in probing attachment level. 8 of 9 (89%; sensitivity) individual patient time intervals with “disease” (< 1.5 mm gain in probing attachment level) were tested positive (≥ 100 CFUJ, whereas 9 of 13 (69%; specificity) individual patient time intervals with “no disease” (≥ 1.5 mm gain in probing attachment level) were A. actinomycetemcomitans negative (< 100 CPU) (p= 0.007).     

The distribution and transmission of Actinobacillus actinomycetemcomitans in families with localized juvenile periodontitis

Abstract. The prevalence and distribution of A. actinomycetemcomitans in families where at least one family member (proband) suffered from localized juvenile periodontitis was investigated. 25 probands with localized juvenile periodontitis (LJP) and their 78 close family members were screened for the presence of A. actinomycetemcomitans. Among these 25 families, 10 contained at least one additional family member colonized with oral A. actinomycetemcomitans. Genomic DNA from subgingival A. actinomycetemcomitans strains from each of the probands and their family members were amplified and characterized by the polymerase chain reaction (PCR) using a single primer known to distinguish A. actinomycetemcomitans strains. The PCR products from each strain were separated by electrophoresis on a 1% submarine agarose gel containing ethidium bromide and visualized by UV light transillumination. The studies showed that 41.2% of the parents and 58% of the siblings in this LJP-based population harbored the bacterium. Comparison of the PCR generated amplitypes showed that there was a wide distribution of amplitypes among the probands and immediate relatives. No clear transmission paths were observed in this specific population.     

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.     

Occurrence of Bacteroides gingivalis, Bacteroides intermedius and Actinobacillus actinomycetemcomitans in severe periodontitis in relation to age and treatment history

A total of 242 subjects including 138 untreated severe periodontitis patients and 104 patients with refractory periodontal disease, previously treated for severe periodontitis, were examined for the occurrence of Actinobacillus actinomycetemcomitans, Bacteroides gingivalis and Bacteroides intermedius. Pooled subgingival samples of representative periodontal lesions were used for anaerobic cultivation on blood agar and for the enumeration of A. actinomycetemcomitans on selective TSBV medium. 97% of the untreated patients were infected with one or more of the test micro-organisms. In this patient group, the occurrence of A. actinomycetemcomitans, B. gingivalis and B. intermedius was 54%, 48% and 63%, respectively. The prevalence of A. actinomycetemcomitans positive patients appeared to be age related and decreased with increasing age. Likewise, the number of patients solely infected with A. actinomycetemcomitans decreased with increasing age. The prevalence of B. gingivalis infected patients appeared to increase with increasing age. These phenomena were not observed in the refractory periodontitis patients. The occurrence of A. actinomycetemcomitans, B. gingivalis and B. intermedius in the refractory periodontitis group was 55%, 27% and 59%, respectively. A statistical significant difference in the prevalence of B. gingivalis was found between the untreated and the refractory periodontitis patients. In both patient groups, the relative proportion of A. actinomycetemcomitans was significantly higher in subjects with this bacterium as the sole indicator micro-organism than in patients who, besides being infected with A. actinomycetemcomitans, were also infected with black-pigmented Bacteroides species. Furthermore, in comparison with untreated patients, unsuccessfully treated patients solely infected with A. actinomycetemcomitans had on average a lower number but also a higher mean % of this bacterium.(ABSTRACT TRUNCATED AT 250 WORDS)     

Distribution of Actinobacillus actinomycetemcomitans in localized juvenile periodontitis plaque: an electron immunocytochemical study

The use of an indirect electron immunocytochemical labelling procedure for labelling Actinobacillus actinomy cetemcomitans (serotype b) in ultrathin sections of pure bacterial cultures and in localized juvenile periodontitis-derived plaque is described. Optimal labelling was obtained after fixation with 2.5% glutaraldehyde, embedding in glycol methacrylate and labelling with highly diluted absorbed rabbit anti-A. actinomycetemcomtians γ-globulin followed by incubation with diluted goat anti-rabbit γ-globulin conjugated with horseradish peroxidase. and subsequent histochemical visualization of the peroxidase. These labelling conditions were used to determine that no cross reactions existed with commonly found plaque bacteria. Two of 5 labelled plaque specimens were positive for this A. actinamycetemcomitans serotype. In one specimen large numbers of labelled bacteria were located only in the most apical portion of the plaque layer. In another specimen labelled cells were scattered throughout the plaque. Control experiments using normal rabbit γ-globulin were all negative.     

The gingival immune response to Actinobacillus actinomycetemcomitans in juvenile periodontitis.

The established and advanced lesions of juvenile periodontitis-localized form (JP) are predominated by B-lymphocytes and plasma cells. Local immune processes may participate in protective or immunopathologic roles in the pathogenesis of this disease. Actinobacillus actinomycetemcomitans (A.a.) is implicated as a primary etiologic agent in JP. An in vitro gingival explant culture system was utilized to study the specificity of immunoglobulins produced by diseased JP tissues. A dot-immunobinding assay demonstrated that 46% of the supernatant fluids (SF) from explant cultures of diseased tissues (n = 39) were positive for the presence of antibody to A.a. Y4, while 61% of autologous JP sera (n = 39) tested positive. For rapidly progressive (RP) and adult periodontitis (AP) SF, 50% and 40% were positive for A.a. Y4, respectively. Seventeen percent of SF from healthy tissue were positive for A.a. Y4. There was no significant difference between JP SF reactivities to A.a. Y4 when compared to reactivities of SF from AP and RP patients. Only 10% of JP SF were positive for Porphyromonas asaccharolytica, a non-oral control microorganism. The de novo biosynthesis of antibody in JP tissue, reactive with A.a. Y4, was demonstrated with Staph Protein A isolated 14C-labeled IgG (SPAG) and the use of a dot-immunobinding assay and autoradiography. The in vitro gingival tissue explant culture system described provides a useful model for the study of the synthesis and specificity of localized immunoglobulins produced by diseased tissues of JP patients.     

Localized juvenile periodontitis and Actinobacillus actinomycetemcomitans in a Brazilian population

Localized juvenile periodontitis (LJP) has been used as a model for studying periodontal disease, and its prevalence is considered to be higher in third-world countries (0.3–8%) than in industrialized countries (0.1%). Mostly, the disease has been associated with Actinobacillus actinomycetemcomitans ( A.a. ) but lack of association has also been reported. The aim of this study was to identify LJP patients in geographically different Brazilian populations and assess the presence of A.a. in their periodontal lesions. 7843 children, 12–19–years of age, from the cities of Rio de Janeiro, Votorantim and Belo Horizonte were screened, and LJP patients were identified by strict clinical and radiographical criteria. A final LJP prevalence of 0.3%, with a 99% confidence interval between 0.16%) to 0.47%, was found. The prevalence in the subpopulations varied between 0.1–1.1% in the different areas. Subgingival bacterial samples were obtained from the oral cavity of 25 patients and their family members. 80% of these patients, 39.5% of their family members, 35.3% of their parents, and 43.9% of all siblings were culture positive for A.a. All but one of the families had at least one member in addition to the patient who was culture positive for A.a. In 3 families, >1 member showed radiographic and clinical signs of LJP. 30% of non-LJP subjects coming from one of the areas with higher LJP prevalence harbored A.a. We conclude that LJP is highly associated with A.a. in this Brazilian population.     

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.     

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 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.     

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.     

IgG antibody response of localized juvenile periodontitis patients to the 29 kilodalton outer membrane protein of Actinobacillus actinomycetemcomitans

Levels of serum IgG antibody to the 29 kilodalton outer membrane protein of A. actinomycetemcomitans Y4 in sera of periodontally healthy subjects and localized juvenile periodontitis patients were determined using an enzyme-linked immunosorbent assay (ELISA). The 29 kDa protein was isolated by solubilization of an octylglucoside-NaCl insoluble fraction by incubation at ambient temperature in 20 mM sodium phosphate, pH 7.5, containing 1% sodium dodecyl sulfate. The isolated protein migrated on SDS-polyacrylamide gels with an apparent molecular mass of 29 kDa following incubation in sample buffer at ambient temperature. However, the protein migrated with an apparent molecular mass of 34 kDa following incubation in sample buffer at 100 degrees C for 10 minutes. Geometric mean IgG antibody titers to the 29 kDa protein were significantly higher in sera from LJP subjects than in sera obtained from periodontally healthy subjects. Twenty-two of 35 LJP sera (63%) had antibody titers greater than 2 standard deviations from the mean titer of the periodontally healthy group. Among LJP subjects, elevated antibody titers to the 29 kDa protein were found primarily in subjects greater than or equal to 18 years of age, with the highest titers seen in patients 18 to 21 years of age. The results of this study indicate that the humoral response of LJP subjects to A. actinomycetemcomitans includes the production of IgG antibodies which recognize the major outer membrane proteins of this organism.     

Antigens of Actinobacillus actinomycetemcomitans identified by immunoblotting with sera from patients with localized human juvenile periodontitis and generalized severe periodontitis

Sonicated whole cell extracts and outer membrane proteins from this bacterium were analysed using sera from 31 young patients with localized juvenile periodontitis, 55 young adults with generalized severe periodontitis and from 31 healthy control subjects. The sonicate contained 13 major bands (14-78 kDa); a greater proportion of sera from patients with generalized periodontitis reacted with 40 and 70 kDa antigens when compared with sera from localized juvenile periodontitis and controls. In contrast, a lower proportion of sera from localized juvenile periodontitis reacted with the 29 kDa antigen when compared with severe periodontitis and controls. The outer membrane proteins contained four main antigens of 19, 24, 35 and 67 kDa, which reacted with sera from all three groups. Although, so far, the findings do not allow discrimination between the two diseases, antibody responses to the 29, 40 and 70 kDa antigens of A. actinomycetemcomitans may help in the assessment of severity of the disease in patients with periodontitis.     

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.     

Attachment loss and serum antibody levels against autologous and reference strains of Actinobacillus actinomycetemcomitans in untreated localized juvenile periodontitis patients

Abstract Immunological data have been suggested to be a potential tool in the diagnosis, classification and monitoring of periodontal diseases. However, the role of circulating antibodies in periodontal patients is poorly understood. Patients suffering from localized juvenile periodontitis (LJP) are often reported to show high titers of serum IgG antibodies against Aetinobaeillus actinomycetemcomitans (A. actinomycetemcotnitans), but several affected patients do not. Most studies use well-known reference strains of the bacterium for testing against the patients' sera. The aim of the present investigation was to study the relationship between serum IgG antibody levels to autologous A. actinomycetemcomitans strains and clinical attachment loss (CAL). In addition, we wanted to assess the patients’serum titers against 4 well-known reference strains of the bacterium as well as their general potential immunoglobulin response. Intravenous blood samples were taken from 23 LJP patients and 10 healthy individuals, and autologous A. actinomycetemcomitans strains were cultured from 18 of the L.JP patients. CAL was measured at 4 different sites around ail present teeth and assessed as a % of teeth with at least 1 site moderately ≥2<5 mm) or severely (≥5 mm) involved. An enzyme-linked immunosorbent assay (ELISA) was performed to evaluate the serum titers of IgG antibodies to A. actinomycetemcomitans antigens. No significant correlation was found between serum IgG antibody titers to autologous strains and CAL. However, there was a trend that low responders had more moderately affected teeth than had high responders and patients with undetectable A. actinomycetemcomitans levels, which is in agreement with a hypothetically protective role of the antibodies. The total counts of immunoglobulin assessed in all participants showed that the predominant class was IgG and the reference group displayed significantly less (p<0.05) IgG and IgG1 counts than the LJP patients. Both the reaction pattern against reference and autologous strains varied widely. We conclude that the specific antibody response against A. actinomycetemcomitans shows a weak correlation to clinical attachment levels in LJP patients.