Juvenile Periodontitis Patients Research Articles

DGKα in Neutrophil Biology and Its Implications for Respiratory Diseases.

Diacylglycerol kinases (DGKs) play a key role in phosphoinositide signaling by removing diacylglycerol and generating phosphatidic acid. Besides the well-documented role of DGKα and DGKζ as negative regulators of lymphocyte responses, a robust body of literature points to those enzymes, and specifically DGKα, as crucial regulators of leukocyte function. Upon neutrophil stimulation, DGKα activation is necessary for migration and a productive response. The role of DGKα in neutrophils is evidenced by its aberrant behavior in juvenile periodontitis patients, which express an inactive DGKα transcript. Together with in vitro experiments, this suggests that DGKs may represent potential therapeutic targets for disorders where inflammation, and neutrophils in particular, plays a major role. In this paper we focus on obstructive respiratory diseases, including asthma and chronic obstructive pulmonary disease (COPD), but also rare genetic diseases such as alpha-1-antitrypsin deficiency. Indeed, the biological role of DGKα is understudied outside the T lymphocyte field. The recent wave of research aiming to develop novel and specific inhibitors as well as KO mice will allow a better understanding of DGK’s role in neutrophilic inflammation. Better knowledge and pharmacologic tools may also allow DGK to move from the laboratory bench to clinical trials.

Pattern of juvenile periodontitis in Lagos University Teaching Hospital Dental Centre

Objective: The aim of the survey was to study the pattern of juvenile periodontitis patients that presented at the Lagos University Teaching Hospital Dental Centre from November 1999 to March 2004. Methods: Through review of case files of patients, twenty six juvenile periodontitis patients, within the age range of 18 and 30 years were identified and their dental records reviewed. Results: There were 11 males and 15 females, giving a male female ratio of 0.73:1. Overall, the maxillary and mandibular incisors were the most missing tooth type (47.54%), particularly in the 20 - 24 year age group. Comparatively, more incisors were missing in females compared to males. Conversely, tooth mobility was more common in males; 60% of severely mobile teeth were seen in males. These patients were found to have poor facial aesthetics. Conclusion: Given the late presentation of juvenile periodontitis found in the study, it is recommended that check-ups of patients at the dental clinics for early diagnosis of juvenile periodontitis and regular check-ups to prevent the rapid progression of this condition in juveniles should beKeywors: juvenile, periodontitis, Lagos University Teaching HospitalJournal of Community Medicine and Primary Health Care 2005, 17(1): 51-54

Patterns of Presentation of Periodontal Conditions seen in Juvenile Periodontitis Patients In Lagos

Patterns of Presentation of Periodontal Conditions seen in Juvenile Periodontitis Patients In Lagos

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.

Immunolocalization of Inducible Nitric Oxide Synthase in Localized Juvenile Periodontitis Patients

Immunolocalization of Inducible Nitric Oxide Synthase in Localized Juvenile Periodontitis Patients

Immunolocalization of Inducible Nitric Oxide Synthase in Localized Juvenile Periodontitis Patients

Localized juvenile periodontitis (LJP) is associated with a destruction of periodontal tissues and the presence of Actinobacillus actinomycetemcomitans ( AA ). Lipopolysaccharide (LPS) from AA was found to induce a significant macrophage production of nitric oxide (NO). Increased nitric oxide synthase (NOS) activity was found to be negatively correlated with the neutrophil chemotactic response. The aim of this study was to determine the occurrence and distribution of inducible NOS (iNOS) in human gingival tissue from LJP patients. The distribution of iNOS was assessed by monoclonal antibody against iNOS. Cellular markers (CD 3, CD 20, and CD 68) were used to determine the cellular origin of iNOS. The immunostaining revealed the appearance of iNOS in inflamed compared to noninflamed gingival tissues. Macrophages expressed high levels of iNOS that may cause some damage to the periodontal tissues. This study suggests that iNOS activity in macrophages may modify abnormalities of neutrophil function.

The in vivo expression of the collagenolytic matrix metalloproteinases (MMP-2, -8, -13, and -14) and matrilysin (MMP-7) in adult and localized juvenile periodontitis.

Periodontal inflammation is characterized by irreversible degradation of periodontal ligament collagen fibers leading to loss of tooth attachment. Cultured gingival keratinocytes and fibroblasts express, in vitro, various matrix metalloproteinases (MMPs) which can degrade fibrillar collagens. We hypothesized that several MMPs are also synthesized in vivo by sulcular epithelium, and analyzed the collagenolytic MMPs (MMP-2, -8, -13, and -14) and matrilysin (MMP-7) in gingival tissue specimens and gingival crevicular fluid from adult and localized juvenile periodontitis patients by in situ hybridization, immunohistochemistry, and Western immunoblotting. MMP-2, -7, -8, and -13 were expressed in gingival sulcular epithelium. MMP-7 and -13 were also located in fibroblasts and macrophages, and MMP-8 in neutrophils. MMP-8- and -13-positive cells/mm2 were higher in periodontitis gingiva when compared with healthy control tissue (p < 0.01). In periodontal diseases, gingival sulcular epithelium expresses several, rather than a single, collagenolytic MMPs, and this proteolytic cascade is evidently responsible for the tissue destruction characteristic of adult and juvenile periodontitis.

Proximal caries in juvenile periodontitis patients.

Caries is recognized as the prevalent proximal dental disease in adolescents, while proximal bone loss is minimal to non-existent in this population. Adolescents demonstrating an inverse disease pattern, i.e., minimal caries and active periodontitis, could provide powerful clues with regard to both diseases. However, data are inconsistent. This study was designed to clarify this relationship by comparing proximal caries prevalence in a juvenile periodontitis (JP) group to a matched non-periodontally diseased control group. Two groups (cases [JPs] and control patients [CPs]) were matched for age, sex, and race and evaluated for decayed, missing, filled teeth and surfaces (DMFS) by radiographic analysis. Statistical analysis was performed by ANOVA and Student t test. The study consisted of four phases. Phase I was based on data from a previous study that failed to include race in the analysis. Thus, the original 23 JP patients (mostly African-Americans from New York City) were rematched for race as well as sex and age with CPs from Newark, NJ. The effect of water fluoridation (found in NYC) was evaluated in Phase II by matching the 23 original CPs (mostly Caucasian from NYC) with 23 CPs from NJ. Since differences were seen, we rematched our original JPs from NYC with a new set of race-matched CPs from NYC (Phase III). Finally, 13 JP patients from the University of Medicine and Dentistry of New Jersey (UMDNJ) were matched with CPs from NJ (Phase IV). Phase I and III indicated that JP patients had significantly less proximal caries than their matched CPs (P < or =0.05). Phase II confirmed the role of fluoride in caries reduction. Phase IV (NJ sample) supported our previous data and suggested that JP patients had less proximal caries than CPs (P < or =0.05). JP patients had significantly less proximal caries than their matched CPs when groups were balanced and radiographic evaluations were performed. In-depth studies of JP patients could provide important clues about both caries and periodontal disease etiology and pathogenesis.

Lipoxin A(4) analogues inhibit leukocyte recruitment to Porphyromonas gingivalis: a role for cyclooxygenase-2 and lipoxins in periodontal disease.

The potential involvement of the inducible cyclooxygenase isoform (COX-2) and the role of novel lipid mediators were investigated in the pathogenesis of periodontal disease. Crevicular fluids from localized juvenile periodontitis (LJP) patients contained prostaglandin (PG)E(2) and 5-lipoxygenase-derived products, leukotriene B(4), and the biosynthesis interaction product, lipoxin (LX)A(4). Neutrophils from peripheral blood of LJP patients, but not from asymptomatic donors, also generated LXA(4), suggesting a role for this immunomodulatory molecule in periodontal disease. To characterize host responses of interest to periodontal pathogens, Porphyromonas gingivalis was introduced within murine dorsal air pouches. In the air pouch cavity, P. gingivalis elicited leukocyte infiltration, concomitant with elevated PGE(2) levels in the cellular exudates, and upregulated COX-2 expression in infiltrated leukocytes. In addition, human neutrophils exposed to P. gingivalis also upregulated COX-2 expression. Blood borne P. gingivalis gave significant increases in the murine tissue levels of COX-2 mRNA associated with both heart and lungs, supporting a potential role for this oral pathogen in the evolution of systemic events. The administration of metabolically stable analogues of LX and of aspirin-triggered LX potently blocked neutrophil traffic into the dorsal pouch cavity and lowered PGE(2) levels within exudates. Together, these results identify PMN as an additional and potentially important source of PGE(2) in periodontal tissues. Moreover, they provide evidence for a novel protective role for LX in periodontitis, limiting further PMN recruitment and PMN-mediated tissue injury that can lead to loss of inflammatory barriers that prevent systemic tissue invasion of oral microbial pathogens.

SERUM ANTIBODI-IMUNOGLOBULIN-G-SUBKLAS SPESIFIK TERHADAP NON-LEUKOTOKSIK ACTINOBACILLUS ACTINOMYCETEMCOMITANS

Serum specific IgG subclass antibodies to non-leukotoxic strains of Actinobacillus actinomycetemcomitans (Aa) NCTC 9710 and NCTC 10979 were quantified by radioimmunoassay. Samples were taken from sera of 10 patients with Juvenile Periodontitis (JP) and 10 from healthy periodontal individuals as control. The results show that JP patients had higher IgG 2 antibody levels to Aa NCTC 9710 (ABT 50 = 620) than the other IgG subclasses (IgG 1 = 300, IgG 3 = 370, and IgG 4 = 500). The JP patients had also higher IgG 2 antibody levels to Aa. NCTC 10979 (600) when compared with the other IgG subclasses (IgG 1 = 300, IgG 3 = 500, and IgG 4 = 400). Whilst, the control gorup had lower IgG subclass antibody level as compared with the JP group. In conclusion, the JP patients had an elevation of IgG 2 subclass antibodies to non-leukotoxic Actinobacillus actinomycetemcomitans.

Absence of an especially toxic clone among isolates of Actinobacillus actinomycetemcomitans recovered from army recruits.

Actinobacillus actinomycetemcomitans is a major periodontal pathogen which is associated with early-onset and adult periodontitis. The organism has been shown to be widely distributed among dentate, healthy individuals as well. It has been demonstrated that A. actinomycetemcomitans shows great genetic diversity. An especially virulent clone of the organism (JP2-like) with a specific 530-base pair (bp) deletion in the promoter region of the leukotoxin gene has been isolated from localized juvenile periodontitis patients and related subjects of African and African-American origin. The aim of the present study was to examine the presence of this specific clone employing specific oligonucleotide primers in a polymerase chain reaction among 51 isolates of A. actinomycetemcomitans recovered from 201, 18- to 25-year-old recruits with no or minor periodontal disease. In addition, clinical isolates from 37 periodontitis patients were analyzed as well as reference strains ATCC 29524, NCTC 9710, Y4 and JP2. Primers amplifying a specific 285-bp amplification product in the ltxA region of the leukotoxin gene and a specific 547-bp amplification product of 16 S rRNA were used to genetically confirm identification of the organisms. Primers amplifying sequences in the leukotoxin promoter region were used to identify the deletion. Species specific primers definitively identified all A. actinomycetemcomitans isolates. No isolates from army recruits or the reference strains displayed the deletion in the leukotoxin promoter region. However, in the periodontitis group, a 24-year-old individual from Ghana with localized juvenile periodontitis was identified with an intraoral infection with highly toxic A. actinomycetemcomitans (JP2-like). Present results confirm previous observations of absence of a highly toxic clone of A. actinomycetemcomitans among periodontally healthy and diseased Caucasians as well as a possible presence in localized juvenile periodontitis in individuals of African origin.

Actinobacillus actinomycetemcomitans serotype e--biotypes, genetic diversity and distribution in relation to periodontal status.

Actinobacillus actinomycetemcomitans isolates from 356 individuals were screened for identification of serotype e in order to investigate its distribution in relation to periodontal status. From subjects with serotype e, 1-6 isolates per subject (n = 61) were genotyped using arbitrarily primed-polymerase chain reaction (AP-PCR) and apaH gene polymerase chain reaction-restriction fragment-length polymorphism (PCR-RFLP) analysis to determine the genetic heterogeneity within the serotype. Furthermore, one serotype e strain per subject was tested for fermentation of 8 carbohydrates for biotyping. Among patients with adult periodontitis (n = 219), localized juvenile periodontitis (n = 55) and other forms of early-onset periodontitis (n = 18) serotypes b, a and c, respectively, were the most frequently detected serotypes. Non-periodontitis subjects (n = 64) were predominantly colonized with serotype c. Serotype e was found in 30 (14%) adult periodontitis patients, 2 (11%) early-onset periodontitis patients and in 5 (8%) non-periodontitis individuals, but in none of the 55 localized juvenile periodontitis patients. AP-PCR distinguished 3 and apaH gene PCR-RFLP analysis 2 genotypes among the 61 A. actinomycetemcomitans serotype e isolates, one genotype per subject. The AP-PCR genotypes 1 and 3 represented the apaH genotype 1 and the AP-PCR genotype 2 the apaH genotype 2. On the basis of variable fermentation of galactose and xylose, 3 biotypes among A. actinomycetemcomitans serotype e were established. Contrary to the absence of A. actinomycetemcomitans serotype e in localized juvenile periodontitis patients, its detection frequency was comparable among other forms of periodontitis and periodontal health. Clinical serotype e isolates form at least 2 genetic types and 3 biotypes.

Active cytomegalovirus infection in human periodontitis.

This study used the reverse transcription polymerase chain reaction method to determine mRNA transcription of subgingival human cytomegalovirus (HCMV) in six adult and three localized juvenile periodontitis patients. The oligonucleotide primers targeted the major capsid protein gene to determine active HCMV infection. HCMV major capsid protein transcript was detected in deep periodontal pockets of two adult and two localized juvenile periodontitis patients but not in any shallow periodontal sites. The findings suggest that active HCMV replication can occur in periodontal sites. Further studies are necessary to establish whether periodontal reactivation of HCMV correlates with the initiation or progression of destructive periodontal disease.

Variable serum immunoglobulin G immune response to genetically distinct Eikenella corrodens strains coexisting in the human oral cavity.

This study examined the variable serum immunoglobulin G (IgG) levels to genetically distinct autologous Eikenella corrodens strains by enzyme-linked immunosorbent assay (ELISA). Twenty subjects, including 10 adult periodontitis patients, 5 juvenile periodontitis patients and 5 periodontally healthy subjects were examined. Each subject was colonized by 2-8 genetically distinct E. corrodens strains. The serum IgG levels to autologous E. corrodens within individuals were significantly different in 7 adult periodontitis patients, 4 juvenile periodontitis patients and a periodontally healthy subject. Poor correlation was found in diseased subjects between serum IgG levels to autologous strains and to reference strains ATCC 23834 or FDC 373. Four adult periodontitis patients and two juvenile periodontitis patients exhibited significant serum IgG levels to autologous E. corrodens strains (two standard deviations above the mean for periodontally healthy subjects); two of these six diseased subjects exhibited low serum IgG levels to reference strains and would have been classified as low immune responders if only reference strains had been used in ELISA. This study showed the importance of using autologous E. corrodens strains in the assessment of serum IgG immune responses to this organism.

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

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 Actinobacillus actinomycetemcomitans (A. actinomycetemcomitans), 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 LJP patients. CAL was measured at 4 different sites around all present teeth and assessed as a % of teeth with at least 1 site moderately > or = 2 < 5 mm) or severely (> or = 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.

Opsonization of Actinobacillus actinomycetemcomitans by immunoglobulin G antibodies to the O polysaccharide of lipopolysaccharide.

Sera of localized juvenile periodontitis (LJP) patients colonized by Actinobacillus actinomycetemcomitans serotype b often contain markedly elevated levels of immunoglobulin G (IgG) antibodies to serospecific determinants in the O polysaccharide of lipopolysaccharide (LPS), as well as to outer membrane proteins of this species. IgG antibodies in LJP sera are known to opsonize A. actinomycetemcomitans for subsequent phagocytosis and killing by human neutrophils. The objective of this study was to determine whether outer membrane proteins or serospecific determinants in LPS are the primary target for opsonic IgG antibodies in LJP sera. An A. actinomycetemcomitans serotype b O-polysaccharide affinity column was constructed and subsequently used to purify LPS-specific IgG antibodies from LJP serum. The affinity-purified anti-LPS IgG antibodies were enriched in content of IgG2 (66.2%, compared with 37.0% in the total IgG fraction) and were immunospecific for A. actinomycetemcomitans serotype b LPS. In an opsonophagocytic assay using neutrophils from donors who were homozygous for the H131 allotype of Fcy receptor IIa (CD32), it was found that LPS-specific IgG antibodies exhibited substantially greater opsonic activity toward A. actinomycetemcomitans serotype b than an LJP IgG fraction that was depleted of LPS-reactive antibodies but contained antibodies against outer membrane proteins of this species. The results of this study indicate that serospecific determinants in the O polysaccharide of A. actinomycetemcomitans serotype b are a principal target for opsonic antibodies in sera of LJP subjects.

Antibody reactive with Actinobacillus actinomycetemcomitans leukotoxin in early-onset periodontitis patients.

The objective of this study was to determine whether a relationship exists between antibody reactive with the Actinobacillus actinomycetemcomitans leukotoxin and the severity of periodontal disease. Serum concentrations of antibody reactive with the leukotoxin were determined for 119 early-onset periodontitis patients and 59 non-periodontitis subjects using limiting dilution analysis on Western blots. Immunoglobulin G (IgG) antibody reactive with the A. actinomycetemcomitans leukotoxin ranged from undetectable to 29 micrograms/ml (mean = 3.13 +/- 0.97 micrograms/ml for the generalized early-onset periodontitis and 2.17 +/- 0.86 micrograms/ml for the localized juvenile periodontitis patients vs 0.32 +/- 0.24 ng/ml for 59 non-periodontitis controls), and the dominant subclass was IgG1. Analysis of the relationship between antibody reactive with A. actinomycetemcomitans sonicate, A. actinomycetemcomitans leukotoxin and attachment loss patterns indicates that seropositive generalized early-onset periodontitis patients had decreased attachment loss compared with patients lacking this antibody. The statistical relationship appeared to be stronger for the sonicate than the purified leukotoxin. These data suggest that antibody reactive with A. actinomycetemcomitans leukotoxin may be protective in early-onset periodontitis, but given that the sonicate appeared better than the leukotoxin alone, it is not likely that leukotoxin is the only antigen of importance to host defense.

The Distribution of Actinobacillus actinomycetemcomitans and Some Gram Negative Anaerobic Rods in Periodontitis

Periodontitis is the most common form of periodontal disease initiated and sustained by the composition of microbial dental plaque. The purpose of this investigation was to determine the frequency of Actinobacillus actinomycetemcomitans and.some Gram negative anaerobic rods including Porphyromonas gingivaiis, Prevotella intermedia, and Fusobacterium species in subgingival plaque samples from different forms of periodontitis. The study population comprised 24 subjets, 8 of whom had adult peridontitis (AP) , 9 rapidly progressive periodontitis (R PP) , and 7 juvenile periodontitis (JP). A total of 96 periodnontal sites were examined microbiologically. Subgingival plaque samples were taken from representative affected sites with at least 5 mm pocket depth from each quadrant. Samples were cultured on supplemented blood agar for Gram negative rods and selettive agar (TSBV) for A. actinomycetemcomitans. Total isolates and colony types were determined by examining the surface growth on plates incubated anaerobically for 5- 7 days. All were identified by analysis of colony morphology and pigmentation Gram staining characteristics, biochemical procedures and using api 20 A strips. A , actinomycetemcomitans was not detected in AP patients, whereas it was higher in JP (25%) than in R PP (2.7%) patients. On the other hand, the number of sites infected with P, gingivalis and P. intermedia were higher in AP (34.3%, 40,6% respectively) and R PP (25%, 19.4% respectively) than in JP (14,8%, 14.8% respectively) patients. There were no differences in the frequencies of Fusobacterium s pp. between AP, R PP, and JP groups (53.1 %, 58,3%, 50% respectively). Although A. actinomycetemcomitans. P. gingivallis, and P, intermedia are included in the various types of periodontitis microflora, their incidence and proteins seem to be different, which is of critical importance for disease initiation, progression, treatment and maintenance program.

Chymotrypsin-like enzyme secretion is stimulated in cultured epithelial cells during proliferation and in response to Actinobacillus actinomycetemcomitans.

A chymotrypsin-like enzyme was partially purified from culture medium of epithelial cells of human skin, human gingiva and porcine periodontal ligament by aprotinin-affinity chromatography. The enzyme levels from all three cell types were low in quiescent cultures but increased markedly when the cells were allowed to proliferate. The biphasic elution profile of the enzyme from the affinity column closely matched that of alpha-chymotrypsin and the protein comigrated with it on polyacrylamide gels at 27,000 ML. Synthetic substrate tests of purified fractions showed strong chymotrypsin-like but no trypsin-like or elastase-like activity. Inhibition of protease activity and pH optimum in the range of 7.5-8.0 were consistent with chymotrypsin-like enzymes. Secreted activity was found to be significantly increased by phorbol myristate acetate treatment in a time-course that differed from that of elastase-like activity. Keratinocyte growth factor and epidermal growth factor but not transforming growth factor-beta increased the chymotrypsin-like activity in a concentration-dependent manner. The enzyme secretion by epithelial cells was strongly elevated by exposure to 5 of 6 Actinobacillus actinomycetemcomitans strains isolated from plaque samples of juvenile periodontitis patients. These results indicate that chymotrypsin-like enzymes are secreted by proliferative phenotypes of normal epithelial cells. This enzyme may, therefore, play a role in epithelial physiology and in cell response to certain pathogenic bacteria.

Association between HLA antigens and early onset periodontitis

HLA-A, B, C and DR antigen frequencies were determined in a group of patients with juvenile periodontitis and rapidly progressive periodontitis. In juvenile periodontitis patients, HLA-A24 and DR4 were found at a significantly higher level than in the control group, and in rapidly progressive periodontitis patients, A9 and DR4 were found at a significantly higher level than the control group. The presence of these antigens gives evidence as to the susceptibility of various forms of early onset periodontitis.