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Objective: To arrest the advancement of periodontitis., Patient: A 17-year-old boy diagnosed with Pierre-Robin sequence at birth exhibited localized juvenile periodontitis. Severe bone loss and mobile teeth were localized in the incisors and molars, which were irregularly positioned, possibly associated with a residual scar from palatoplasty for a soft palate cleft at an early age., Conclusion: Combined orthodontic-periodontic-prosthodontic treatment arrested the advancement of the periodontitis and established a stable occlusion.

Aims: This paper reports the treatment of the periodontal component of the Papillon-Lefèvre syndrome in 2 siblings (case A, born 1974; case B, born 1976)., Method: The initial treatment, in 1982, consisted of extraction of all primary teeth, scaling and rootplaning of the erupted permanent teeth and systemic antibiotic therapy. During 15 years, continuous and intensive periodontal treatment consisted of chlorhexidine 0.2% rinses, bi-weekly professional prophylaxis, scaling and rootplaning or surgery if indicated. Systemic antibiotics often accompanied mechanical therapy after bacteriological analysis., Results: In case A, a favourable number of permanent teeth could be maintained, but in case B, all permanent teeth were lost in spite of the intensive treatment. Darkfield microscopy at different intervals revealed high numbers of spirochetes and motile rods in both siblings. Only in case A were they temporarily reduced to zero after scaling and rootplaning combined with metronidazole. Anaerobic cultering revealed high numbers of Actinobacillus actinomycetemcomitans (A.a) in both patients. In 1994, 2 years after combined amoxicillin/metronidazole therapy, no A.a could be detected in case A. In case B, A.a could still be detected and was found to be resistant to metronidazole. One year after extraction of all permanent teeth, could no A.a be detected in case B., Conclusion: Intensive periodontal treatment combined with antibiotic therapy was not able to prevent complete tooth loss in case B. In case A, the treatment was more effective, resulting in preserving a number of permanent teeth in a stable clinical situation. In these 2 cases, no attempt was made to create an edentulous period between the periodontally-diseased mixed dentition and the eruption of the remaining teeth, which may have contributed to treatment failure.

Background: Chédiak-Higashi syndrome (C-HS) is a rare congenital disease characterized by defective neutrophil function with abnormal lysosomal inclusions, neutropenia, and reduced chemotaxis. The complete syndrome includes oculocutaneous albinism with photophobia, neurologic features, recurrent infections, and enterocolitis., Methods: A 14-year-old male C-HS patient was referred to us because of serious periodontal destruction with acute inflamed gingiva and ulcers. Clinical and biological investigations were performed, leading to the diagnosis of C-HS., Results: Laboratory findings included neutropenia and hypergammaglobulinemia. Peripheral blood smears showed giant granules in neutrophils, eosinophils, and granulocytes. Bone marrow smears showed giant inclusions in leukocyte precursor cells. These granules and inclusions were characteristic of Chédiak-Higashi syndrome. Oral radiographic status showed extensive loss of alveolar bone leading, in most cases, to tooth exfoliation. Bacteria often associated with periodontitis were detected in subgingival plaque samples, including Fusobacterium nucleatum, Campylobacter rectus, Prevotella melaninogenica, Peptostreptococcus anaerobius, and Clostridium sp. Biopsies of periodontal tissues for light and electronic microscopic examinations revealed massive bacterial invasion of the epithelial tissue, epithelial cells, and connective tissue. Ultrastructural observations of periodontal polymorphonuclear leukocytes showed defective granulation, with abnormal granules not discharging their lysosomal content against engulfed bacteria. Viable dividing bacteria were found in the cytoplasm., Conclusions: In this case, early-onset periodontitis seems to be the expression of C-HS granulocyte deficiency. Periodontal treatment of these patients is often unsuccessful. This case report illustrates the importance of the dentist in initiating clinical and biological investigations in such early aggressive periodontitis in young patients.

This case history describes the course of disease in a 17-year-old boy with Ehlers-Danlos syndrome type III and early-onset periodontitis. Flow cytometric tests showed a reduced cell count in the specific immune system. Immunoglobulin concentrations in saliva and serum were within normal limits. Infection with T-lymphotropic viruses was excluded. The phagocytic capacity of the peripheral blood polymorphonuclear leukocytes was unimpaired. The anaerobic infection present in the early-onset periodontitis was treated with systemic antibiotic therapy and closed curettage. Following 14 days of this treatment, signs of acute inflammation subsided, and 18 months after therapy ended, a slight gain in clinical attachment was found, and bone growth was visible via radiology. However, a continuing lack of adequate oral hygiene represents a risk to the success of therapy in the long term.

The patient's problem consisted of a large diastema between the central incisors. The cost-cutting treatment plan recommended to the patient and his parents by the general dentist was to use orthodontic rubber bands to loop the teeth and close the diastema.

Localized juvenile periodontitis (LJP) causes severe alveolar bone loss and early tooth loss in adolescents and young adults. If it is not appropriately treated as an infection in association with Actinobacillus actinomycetemcomitans, treatment failure is likely. This review of clinical trials of treatment of LJP uses those trials to construct guidelines for LJP treatment.

In recent years, periodontitis has been receiving increasing attention, since it not only impairs the general state of health (loss of the teeth), but also appears to have a relationship with cardiovascular and cerebrovascular illnesses (thrombocyte aggregation, insult). Periodontitis is a very frequent, chronic recurrent, unspecific bacterial inflammation of the periodontium that arises in accumulated plaques on the teeth at the gingiva. It leads to an irreversible destruction of soft tissue followed by loss of bony substance. Three types of periodontitis can be distinguished: 1. adult periodontitis (AP), 2. rapidly progressive periodontitis (RPP) and juvenile periodontitis (JP). Periodontitis appears to have a genetic component. Additional risk factors include juvenile diabetes mellitus and smoking. The diagnosis, prevention and treatment are discussed. The basis for prevention and treatment is individual hygiene and professional dental care.

Localized juvenile periodontitis (LJP) is not commonly encountered in dental practice. Yet, when it is encountered, prompt and effective therapy is required to combat the severity of disease and its rapid progression. Failure to understand its diagnosis and etiology leads to failures in management of LJP. The clinical features, etiology, and pathogenesis of LJP are reviewed to provide the clinician with a sufficient understanding to appropriately manage or refer LJP patients.

Individuals with Down's syndrome (DS) have an increased prevalence of periodontal disease compared with otherwise normal, age-matched control groups and other mentally handicapped patients of similar age distribution. The exaggerated immune-inflammatory response of the tissues cannot be explained by poor oral hygiene alone and might be the result of an impaired cell-mediated and humoral immunity and a deficient phagocytic system. As far as the progression and severity of destruction, the oral manifestations of DS patients are consistent with the juvenile periodontitis (JP) disease pattern. The purpose of the present study was 1) to assess the periodontal clinical and microbiological status of 10 DS patients aged 20 to 31 years (mean: 26.3 years) relative to that of 11 patients with cerebral palsy (CP) aged 23 to 53 years (mean: 36 years) without defective immunological functions, and 2) to determine the effect of supragingival plaque control and oral hygiene instruction in these patient groups. Subsequent to the initial examination and a professional tooth cleaning program, clinical and microbiological parameters were monitored over a period of 12 weeks. The clinical examination included the recording of plaque index (P1), gingival index (GI), probing depth (PD), and clinical attachment level (CAL). Subgingival plaque samples were always obtained from the same pocket with the highest disease activity (deepest bleeding site at baseline examination) in each subject for a morphotype analysis by dark field microscopy and for identification and quantitation of Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Eikenella corrodens, Bacteroides forsythus, Fusobacterium nucleatum, Treponema denticola, and Campylobacter rectus by DNA probes. The results of the baseline examinations demonstrated that DS patients and patients with cerebral palsy had inflamed gingiva associated with a high amount of plaque. The mean probing depth and percentage of sites with probing depth> 4 mm corresponded to age and poor oral hygiene in CP patients. Deep pockets in DS patients demonstrated a high prevalence of periodontal disease compared with age-matched children with mental retardation and non-handicapped patients. Regarding the young age of onset, the severe destruction of periodontal tissues and pathogenesis of periodontitis in DS patients are consistent with the juvenile periodontitis disease pattern. The missing clinical benefit and alteration of the subgingival flora following supragingival plaque control in DS patients underlined the alteration in the immunological response.

Insulin-dependent diabetes mellitus (IDDM) is a risk factor for periodontitis. Depressed neutrophil chemotaxis has been demonstrated in IDDM and in early-onset periodontitis (EOP). HLA-DR antigens are associated with both IDDM and periodontitis. This investigation sought to determine an association of HLA-DR3, -DR4, and -DR53 with impaired neutrophil chemotaxis in an IDDM sample. The neutrophil chemotaxis index of 41 diabetics and 27 controls was determined by a modified Boyden chamber method, and certain class II HLA genotypes were determined by polymerase chain-reaction amplification of genomic DNA by means of sequence-specific primers (PCR-SSP). The mean chemotaxis index of the diabetics was significantly less than that of the controls (p < or = 0.02). HLA-DR3 (p < or = 0.002), -DR4 (p < 0.003), and -DR53 (p < or = 0.001) were associated with IDDM. Neutrophil chemotaxis and glucose metabolism were not significantly correlated. None of the HLA-DR alleles was associated with impaired neutrophil chemotaxis. Therefore, the neutrophil chemotaxis defect of IDDM appears to be independent of these HLA-DR-associated genes.

This study was undertaken to test the hypothesis that gingival inflammation and dental calculus are important determinants of the development and progression of early-onset periodontitis. The study sample included 156 individuals who were 13-20 years old at baseline and who were examined 2x during 6 years to assess the attachment loss, gingival state and the presence of dental calculus. 33 (21%), 62 (40%), and 61 (39%) individuals were classified as having localized, generalized, or incidental EOP, respectively. The results showed an increase in the % of teeth with overt gingivitis and subgingival calculus, and also an increase in the % of teeth showing attachment loss during the 6-year period in all classification groups. Of teeth with 0-2 mm attachment loss at the beginning of the study and which developed > or = 3 mm attachment loss during the following 6 years, there were 2x as many teeth with overt gingival inflammation, and 4x more teeth with subgingival calculus at baseline than teeth without. Gingivitis and subgingival calculus when present at both examinations resulted in a stronger association with the development of new lesions than presence of these variables at baseline. Teeth with gingivitis at baseline had a significantly higher mean attachment loss during 6 years than teeth without gingivitis (p<0.0001), and teeth with subgingival calculus at baseline had a significantly higher mean attachment loss than teeth without subgingival calculus (p<0.0001). The presence of gingivitis and subgingival calculus at baseline and 6 years later was associated with the occurrence of even higher disease progression during this period. The association between gingival inflammation and subgingival calculus and the development and progression of attachment loss during the study period in the generalized and the localized EOP groups was significantly higher than the association in the incidental EOP group. In an appreciable % of the sites in all 3 groups, however, the presence of the 2 factors was not associated with attachment loss during 6 years. The results suggest a significant association between gingival inflammation and subgingival calculus and the development and progression of early-onset periodontitis.

Neutropenia is an absolute decrease in the number of circulating neutrophils in the blood which results in susceptibility to severe pyogenic infections. Various oral findings such as periodontitis, alveolar bone loss and ulceration may be seen in neutropenic patients. A case is presented of a 6 year old girl with chronic, probably congenital, severe neutropenia with frequent respiratory tract infections, recurrent oral ulcerations and significant periodontal break-down resembling prepubertal periodontitis. She was given granulocyte-colony stimulating factor (G-CSF) treatment which resulted in an increase in granulocyte count within two weeks and resolution of the neutropenic ulceration. It is suggested that G-CSF together with dental care regimens is a promising treatment model in chronic severe neutropenia cases presenting with oral manifestations.

Juvenile periodontitis is a form of periodontitis characterised by a pattern of rapid vertical loss of alveolar bone around the permanent first molars and incisors. In this hospital based retrospective study of juvenile periodontitis in Ibadan, 34 cases in the age range 17-34 years were seen over a period of five years. The mean age was 23.2 years. Diagnosis was made on accepted clinical and radiological parameters. The findings showed a low prevalence of 1.56%, (64.7% of localised juvenile periodontitis, 35.3% of generalised juvenile periodontitis). There was a 2:1 female to male relationship and the oral hygiene status of the subjects was fairly good in most instances. Remarkable symmetrical pattern and relationship was observed. The age of onset or age at presentation was 17 years contrary to reports from other studies which revealed circumpubertal age of onset.

The presence of systemic disease in patients requiring periodontal therapy creates challenges for management. Alteration of treatment plans, with emphasis on physician consultation and preventive periodontal care, is frequently needed to minimize the impact of periodontal disease on the systemic condition. Conversely, detection and treatment of systemic disorders may impact upon the status of the periodontium and the success of periodontal therapy. The goal of holistic patient management is facilitated by a free flow of information between the patients and their medical and dental health care providers.

A case is presented that demonstrates successful management of a maxillary canine with dens invaginatus (Oehlers' type 3 invagination) with associated chronic periradicular periodontitis and a vital pulp. Debridement and obturation of the invaginated space resulted in resolution of the associated periradicular radiolucency. Pulp vitality was retained after endodontic treatment of the invagination.

There is a group of periodontal diseases affecting children and young adults that is characterized by onset prior to age 35, often with a rapid rate of periodontal destruction. Although a wide variation in patterns of presentation exist, these diseases can be described under the broad categories of (a) early onset periodontitis (juvenile periodontitis), (b) necrotizing ulcerative gingivitis/periodontitis, (c) periodontitis associated with systemic diseases. A discussion of each of these categories is followed by two case reports which illustrate possible clinical presentations of these diseases.

Recent data indicate that smoking is an important risk factor for the development of periodontitis. Smoking is also known to reduce serum immunoglobulin G (IgG) levels. Interestingly, patients with the localized form of early-onset periodontitis (LJP) have elevated levels of serum IgG2, and those who smoke are not clinically different from nonsmoking LJ subjects. In contrast, patients with the generalized form of early-onset periodontitis (G-EOP) who smoke have more extensive destruction than their nonsmoking counterparts. Given the effects of smoking on EOP and the association of IgG2 with less severe disease, we hypothesized that smoking might reduce serum IgG2 and that this might be most apparent in G-EOP. We therefore examined the effects of smoking on serum IgG subclass concentrations in race-matched groups: LJP, G-EOP, and age-matched periodontally healthy controls (NPs). Smoking status was established from serum cotinine levels, and serum IgG subclass concentrations were determined by using radial immunodiffusion. The data indicated that the effects of smoking were remarkably selective with respect to both IgG subclass and race. Smoking did not appear to have any effect on the concentration of IgG1 or IgG3 in either black or white subjects. In contrast, smoking was associated with depressed serum IgG2 concentrations in both white NP and G-EOP subgroups. Serum IgG2 levels in black subjects did not appear to be depressed by smoking, with the single striking exception of the black G-EOP subgroup which also had depressed serum IgG4 levels. The results here confirm that smoking has effects on serum immunoglobulin levels, but the effects were both race and serum IgG subclass specific. Furthermore, the periodontal diagnosis of EOP subjects appeared to be important, as indicated by the fact that IgG2 and IgG4 levels were reduced in smoking black G-EOP subjects whereas the IgG2 and IgG4 levels in black LJP and NP subjects were not reduced by smoking.

The human periodontal diseases are a complex group of disorders that span the entire length of the human life cycle. They are infective in nature, but are mediated by host parasite interactions that are influenced not only by the nature of the pathogens present but also by a variety of underlying immunological and connective tissue anomalies. Thus, on occasion they may reflect systemic disorders that have previously been undiagnosed. As such abnormalities frequently present in childhood or adolescence, knowledge of the potential implications of this broad group of diseases is important. This paper reviews the current classification of childhood periodontal disease and outlines the clinical presentation and management of the more common disorders.

The group of periodontal diseases known as the early-onset periodontal diseases are defined by the age of onset of periodontal destruction, distribution of lesions, association of disease with specific microbial infections, and identification of characteristic alterations, in the host response. Significant progress has recently been made in our understanding of the etiology of juvenile and rapidly progressive periodontitis. Considerable evidence points to a familial pattern of disease; both localized and generalized forms of disease may be observed in the same family. The exact mode of inheritance remains unclear, and disease may be the result of a complex interplay between genetically determined alterations of the host response and a specific bacterial challenge. Both neutrophil function and immunoglobulin response are altered and appear to be characteristic of an immunologic hyperresponsiveness. Bacterial colonization by Actinobacillus actinomycetemcomitans (serotype b) and/or Porphyromonas gingivalis appears to be the primary initiator of disease. Evidence suggests that lesion distribution may be a function of the nature of the infecting agent and the characteristics of the immune response.

The findings of a recent study show that smoking was more prevalent in a group of patients with generalized early-onset periodontitis and adult periodontitis than in patients with localized juvenile periodontitis or healthy periodontium. In patients with generalized early-onset periodontitis, smoking had a significant effect on periodontal attachment loss; these patients had significantly more teeth with affected sites and a greater mean loss of attachment than patients who did not smoke. Thus, the risk of smoking could greatly accelerate tooth loss in this relatively young group of individuals who are already at high risk for progressive periodontal attachment loss.

A case of Papillon-Lefèvre syndrome that has been managed successfully for six years is reported. Papillon-Lefèvre syndrome is a rare form of early onset periodontitis that occurs at a rate of 1-3 per million. Diagnostic features include palmar-plantar hyperkeratosis and rapid periodontal destruction. Although the etiology of this syndrome is unknown, current theories on the nature of the underlying defect fall into three main categories: anatomical, bacterial and host response. Historically, Papillon-Lefèvre syndrome was thought to lead to the inevitable loss of both the primary and permanent dentitions. However, a recently proposed treatment involving antibiotic coverage, extraction of the primary dentition and a period of edentulism has been shown to be effective in maintaining the permanent dentition. Since treatment may begin prior to the eruption of the permanent dentition, early recognition of Papillon-Lefèvre syndrome is critical. Any young patient who exhibits palmar hyperkeratosis should be examined carefully for periodontal breakdown. Since the number of cases available for study is limited, referral of such individuals to University dental clinics may allow for a more specific analysis of immune or bacterial factors that may lead to a better understanding of this disease.

Hypophosphatasia, an inheritable metabolic disorder affecting calcification, has been shown to have various oral manifestations. Recently, it was suggested that it may serve as a predisposing factor in the pathogenesis of early-onset periodontitis. The present study was designed to examine the frequency of hypophosphatasia among patients with juvenile periodontitis and rapidly progressive periodontitis. Eighteen patients, nine females and nine males (age 19-37 years, mean 23.2 years), were included in this study. Venous blood and urinary samples were collected and assayed for alkaline phosphatase and urinary phosphoethanolamine. Mean alkaline phosphatase levels (109 +/- 35 IU/L) were within the normal limits for all patients except one who exhibited slightly lower than normal values. Urinary phosphoethanolamine, a typical marker of hypophosphatasia, was absent from all specimens, which rules out the possible diagnosis of such disorder in these patients. Until more information is available, the role of hypophosphatasia as a predisposing factor in early-onset periodontitis is yet to be established.

Genetic factors were recognized as possible predisposing factors in the etiopathogenesis of prepubertal periodontitis (PP). Consequently, the present work was carried out to determine the possible mode of inheritance and if there were any associated chromosomal aberrations in cases with PP. The study included 3 families with probands manifesting PP (the families included 18 individuals). Pedigree analysis was carried out as well as chromosomal analysis. The results pointed out to the possibility of new mutations arising due to various environmental factors (including the use of pesticides and their handling), in addition to a possible autosomal recessive inheritance. Chromosomal analysis showed no association between a certain chromosomal aberration and PP. An interesting finding was that a girl proband proved to be Xo female, i.e. a case of Turner's syndrome. This could be considered the first report of Turner's syndrome with PP.

The present investigation was carried out 1) to identify subjects with juvenile periodontitis (JP) in a group of schoolchildren from a community with a high prevalence of periodontal diseases and with no access to preventive dental care, and 2) to study the clinical features of the disease and the progression pattern during a period of 1 yr, and the relationship of JP to clinical periodontal parameters. The periodontal condition of a group of 502 Iraqi schoolchildren (260 girls and 242 boys) was assessed radiographically and clinically at baseline. Children showing > or = 3 mm arc-shaped angular radiographic bone loss at the proximal surfaces of two or more first molars and who showed clinical attachment loss at the same sites were regarded as JP patients. A second group of children with no signs of JP were randomly chosen from the study material. One year later, the JP and the non-JP groups were re-examined radiographically and clinically to assess plaque, gingivitis and presence of calculus. The results showed that nine children (1.8%) had JP. The ratio of girls to boys was 3.5:1, and of localized to generalized forms 2:1. Mesial surfaces of first molars were more often affected than distal surfaces. Clinical assessments showed a more profound loss than was depicted radiographically. All JP patients exhibited evidence of periodontal disease progression during the following year. There were no differences between JP and non-JP children with respect to gingival inflammation, dental plaque, or calculus deposits on teeth.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypophosphatasia is a congenital disease characterized by defective bone mineralization, deficiency of alkaline phosphatase (ALP) activity, increased excretion of the phosphoethanolamine (PEA) in the urine, and premature loss of the deciduous teeth. A male hypophosphatasia patient (aged 15 years 6 months) with premature exfoliation of the deciduous teeth was referred to our hospital because of severe periodontal destruction in the permanent dentition. Blood and urine tests as well as oral and periodontal examinations were performed. Serum antibody titers against 7 periodontopathic bacteria by the enzyme-linked immunosorbent assay (ELISA), monocyte and neutrophil chemotaxis measurements, and cellular immunity tests were also performed. Low levels of ALP in serum and PEA in the urine were found. Monocyte and neutrophil chemotaxis exhibited normal values. Slightly depressed CD2+, CD3+, and CD4+ and slightly elevated activity of NK cells were found. An elevated level of serum antibody to Porphyromonas gingivalis was observed. Oral radiographic examination showed a mirror pattern of alveolar bone loss which is similar to that seen in localized juvenile periodontitis. Periodontal treatment of this patient was carried out for 4 years. The severely affected sites, the lower right and left first molars and the upper right first molar, had to be extracted. However, the other sites were well maintained. The serum IgG level against P. gingivalis was decreased after 4 years of periodontal treatment. Infection with P. gingivalis was suspected to be associated with the destruction of this patient's hypophosphatasia, but other dental abnormalities such as abnormal enamel, dentin, and cementum formation may also have contributed to the periodontal pathology.

The prevalence and severity of periodontal diseases in young people are significant. Recent progress in understanding the etiology and pathogenesis of periodontal diseases in this group of patients has allowed significant improvement in periodontal classifications. Actinobacillus actinomycetemcomitans characteristically is the major pathogen involved; black-pigmented anaerobic rods and other organisms can also be important. Treatment of periodontitis should focus on meticulous plaque control and eradication of periodontal pathogens, possibly by means of systemic or topical antimicrobial therapies.

Although prepubertal periodontitis (PP) is often associated with the Papillon-Lefèvre (PLS), the etiopathogenetic mechanism in this disease has not been clarified as yet. A three and half year old female with leukocyte chemotaxis deficiency and decrease of T-lymphocytes is presented. The immunohistochemical evaluation of neutrophils showed a reduction of myeloperoxidase content, whereas ultrastructural studies revealed no particular change. The possible role of such a deficiency in the pathogenesis of the periodontal lesion is discussed.

Hypophosphatasia is an inherited disorder characterized by defective bone mineralization, deficiency of alkaline phosphatase (ALP) activity, increased excretion of phosphoethanolamine (PEA) in the urine and premature loss of the deciduous teeth. A male hypophosphatasia patient aged 15 years 6 months, with premature exfoliation of the deciduous teeth and manifesting severe periodontal destruction in the permanent dentition, was examined. Antibody titers against seven strains by the enzyme-linked immunosorbent assay (ELISA), monocyte and neutrophil chemotaxis studies and cellular immunity tests were performed. Low levels of ALP in serum and PEA in the urine were found. Radiographic examination showed a similar pattern of alveolar bone loss to that of the localized juvenile periodontitis. Suppressed monocyte and neutrophil chemotaxis were not detected. Slightly depressed CD2+, CD3+ and CD4+ and slightly elevated activity of NK cells were found. An elevated level of antibody to Porphyromonas gingivalis was observed and this antibody titer was decreased by periodontal treatments. The affected sites of the patient showed resistance to conventional periodontal therapy. P. gingivalis was estimated to associate as an important pathogen in the etiology of periodontal destruction in this hypophosphatasia patient in addition to the dental abnormalities such as abnormal enamel, dentin, or cementum formation.

The microbiology of periodontal diseases as well as associations between certain microorganisms and types/stages of periodontal diseases are discussed and the ecology and the composition of the subgingival plaque are included in this discussion, too. Furthermore, the possible role of microorganisms associated with periodontal diseases, their pathogenic mechanisms and their virulence factors are treated in the present article. Periodic upsets of the host-parasite equilibrium seem to be responsible for the bursts of disease progression. Several plaque hypotheses (specific, non-specific, opportunistic) have been proposed as likely models to explain the nature of periodontal infections and diseases. However, none of these theories is widely accepted at the moment. Therefore, we suggest that further investigations concerning the complex bacterial interactions and the manner in which the host responds to the mass and the composition of the dental plaque must be carried out in the future.

Local factors may contribute to acute exacerbations of the periodontal disease, however, their pathological basis is systemically established. The more bacteria and bacterial products get into the periodontal tissue the more serious is destruction. Host's resistance controls composition of the subepithelial bacterial flora. Under condition of defective phagocyte function bacteria, otherwise occurring rarely in the pocket, multiply quickly and penetrate the periodontal pocket epithelium. Specific immune defence can stop them only in the subepithelial conjunctive tissue causing its destruction. Juvenile periodontitis goes with defects of granulocyte function and an aggressive pocket flora. These patients need antibiotics taken systematically, removing of the infected pocket epithelium and regular recalls. Care of patients with adult periodontitis is limited to good oral hygiene.

This paper reviews the literature on prepubertal periodontitis (PP) according to the definition and the classification of PP by Page. The generalized form of PP (G-PP) defined by Page was identified as the oral manifestation of a systemic disease called leukocyte adhesion deficiency (LAD) and thus the pathogenesis is known at the molecular level. On the other hand, the localized form of PP (L-PP) is a disease defined by clinical criteria and its pathogenesis is not known at the molecular level. The reported prevalence of L-PP differs widely in reports, according to the methodology and population studied. However, it seems to be at least 0.84% or greater. Potential periodontal pathogens that have been associated with L-PP include the following bacteria: Actinobacillus actinomycetemcomitans (A.a.), Bacteroides intermedius, Bacteroides gingivalis, Capnocytophaga sputigena, and Eikenella corrodens. Suggested contributing factors have included PMN or monocyte chemotactic defects and cementum defects. There is no unique pattern of bone loss in L-PP; however, there may be a type of periodontitis that affects all deciduous teeth, in the absence of LAD. L-PP may lead to localized juvenile periodontitis (LJP) or generalized juvenile periodontitis (GJP). Histiocytosis X, hypophosphatasia and mild forms of blood dyscrasias may have minimal or no clinical signs and symptoms except for alveolar bone loss. Therefore diseases known to be associated with alveolar bone loss must be definitively excluded in prepubertal children until the pathogenesis of L-PP at the cellular and molecular levels is understood and L-PP can be definitively diagnosed either as a distinct disease entity or entities.

Since periodontal diseases are mainly of bacterial origin, the use of antibiotics could seem justified for their treatment. Numerous studies, however, have shown that these drugs are not a first choice treatment for acute and chronic periodontitis. Chemotherapy can represent a valuable adjunct to routine mechanical debridement, particularly for adult recurrent periodontitis, juvenile periodontitis and rapidly progressive periodontitis. Furthermore, prophylactic chemotherapy should be provided for patients at risk with systemic diseases, notably when congenital or acquired valvular heart defects are present. For the treatment of adult recurrent periodontitis, the most appropriate systematic drugs are, presently, tetracyclines or imidazoles. Juvenile periodontitis can be treated with the help of tetracyclines and rapidly progressive periodontitis with imidazoles. As for high risk patients, the use of various penicillins is mandatory. A decision to use antibiotics must be made only after due consideration of their potential disadvantages. One should also remember that the possible positive or negative effects of antibiotics upon the host defence mechanisms are for the moment unknown.

The role of the neutrophil as a primary protective cell in the pathogenesis of periodontal disease has been well established. In this paper, the role of receptor modulation on the neutrophil surface is discussed as a possible mechanism for neutrophil functional abnormalities. Using localized juvenile periodontitis (LJP) as a model, the direct inhibition of neutrophils by bacterial products is discussed as a possible mechanism for local neutrophil dysfunction. In both disease processes, neutrophil receptor modulation plays a central role.

Human serum antibody responses to antigens from a suspected oral pathogen, Actinobacillus actinomycetemcomitans (Aa), were studied. IgG and IgM isotype antibodies to four antigen preparations, sonicate antigen (SA), leukotoxin (LT), group carbohydrate (LG), and lipopolysaccharide (LPS), were determined using an ELISA. An ELISA inhibition technique was developed to show that human serum antibodies reacting with the LT, LG, or LPS materials were binding to different antigenic moieties in each preparation. Cross-sectional studies of serum IgG antibodies showed that patients with localized juvenile periodontitis (LJP) had a greater frequency of occurrence and a higher level of antibodies to the SA (82%), LT (70%), and LG (62%) antigens compared to all other diseased (11-46%) or normal (4-13%) groups. Serum IgM antibodies to LPS were increased in LJP, generalized juvenile periodontitis, and adult periodontitis patients compared to all other groups. Therefore, while both IgG and IgM antibodies were found against various Aa antigens, the detection of IgG antibodies was most clearly associated with the specific disease classification of LJP. Blocking studies suggested that the human serum responses were specific for the Aa antigens and that the LT, LG, and LPS comprise major antigenic determinants on the organisms to which human serum antibody reacts.