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Diagnosis of source of maxillofacial infection in paediatric patients can be challenging due to difficulty in eliciting a proper history and multiple potential sources of infection. Identification and removal of the nidus of infection with decompression and institution of antibiotic therapy as per the culture-sensitivity report form the mainstay treatment of the infection. Deviation from it may result in persistence or even progression of infection, resulting in significant morbidity and mortality. In the past decade, the incidence of community-acquired methicillin-resistant Staphylococcus aureus infection in the oral cavity has seen an upward trend. This has further led to an increase in complexity in the diagnosis of maxillofacial infections. In this case, the authors want to bring to light the challenges faced in managing a paediatric patient with persistent fascial space infection even after removal of the offending tooth, which signifies the importance of managing the infection by the time-tested protocol., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2021. No commercial re-use. See rights and permissions. Published by BMJ.)

The purpose of this cross-sectional study was to investigate the effect of different forms of periodontal diseases on Oral Health-Related Quality of Life (OHRQoL). Fifty-two patients with Aggressive Periodontitis (AP) or Chronic Periodontitis (CP) were included: nine patients with Localized Aggressive Periodontitis (LAP), thirty-three patients with Generalized Aggressive Periodontitis (GAP) and ten patients with Generalized Chronic Periodontitis (GCP). Oral Health Impact Profile questionnaires (OHIP-14) were distributed after a clinical examination that measured the following periodontal parameters: tooth loss, bleeding on probing (BoP), probing depth (PD), gingival recession (REC) and clinical attachment level (CAL). The global OHIP-14 score means were 10.6 for LAP, 16.5 for GAP, and 17.5 for GCP. A statistically significant difference (p < 0.01) was observed between the LAP group and the other two groups. There was significantly less bleeding and recession in the LAP group than in the patients with the generalized forms of periodontitis. LAP, GAP and GCP have an impact on patient quality of life when measured using the OHIP-14. Patients with GAP and GCP had poorer OHRQoL than LAP patients.

Periodontal disease (PD) is generated by microorganisms. These microbes can enter the general circulation causing a bacteraemia. The result can be adverse systemic effects, which could promote conditions such as cardiovascular disease. Level A evidence supports that PD is independently associated with arterial disease. PD is a common chronic condition affecting the majority of Americans 30 years of age and older. Atherosclerosis remains the largest cause of death and disability. Studies indicate that the adverse cardiovascular effects from PD are due to a few putative or high-risk bacteria: Aggregatibacter actinomycetemcomitans , Porphyromonas gingivalis , Tannerella forsythia , Treponema denticola or Fusobacterium nucleatum There are three accepted essential elements in the pathogenesis of atherosclerosis: lipoprotein serum concentration, endothelial permeability and binding of lipoproteins in the arterial intima. There is scientific evidence that PD caused by the high-risk pathogens can influence the pathogenesis triad in an adverse manner. With this appreciation, it is reasonable to state PD, due to high-risk pathogens, is a contributory cause of atherosclerosis. Distinguishing this type of PD as causal provides a significant opportunity to reduce arterial disease., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.)

Aggregatibacter actinomycetemcomitans is a perio-pathogenic bacteria that has long been associated with localized aggressive periodontitis. The mechanisms of its pathogenicity have been studied in humans and preclinical experimental models. Although different serotypes of A. actinomycetemcomitans have differential virulence factor expression, A. actinomycetemcomitans cytolethal distending toxin (CDT), leukotoxin, and lipopolysaccharide (LPS) have been most extensively studied in the context of modulating the host immune response. Following colonization and attachment in the oral cavity, A. actinomycetemcomitans employs CDT, leukotoxin, and LPS to evade host innate defense mechanisms and drive a pathophysiologic inflammatory response. This supra-physiologic immune response state perturbs normal periodontal tissue remodeling/turnover and ultimately has catabolic effects on periodontal tissue homeostasis. In this review, we have divided the host response into two systems: non-hematopoietic and hematopoietic. Non-hematopoietic barriers include epithelium and fibroblasts that initiate the innate immune host response. The hematopoietic system contains lymphoid and myeloid-derived cell lineages that are responsible for expanding the immune response and driving the pathophysiologic inflammatory state in the local periodontal microenvironment. Effector systems and signaling transduction pathways activated and utilized in response to A. actinomycetemcomitans will be discussed to further delineate immune cell mechanisms during A. actinomycetemcomitans infection. Finally, we will discuss the osteo-immunomodulatory effects induced by A. actinomycetemcomitans and dissect the catabolic disruption of balanced osteoclast-osteoblast-mediated bone remodeling, which subsequently leads to net alveolar bone loss., (© 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Aggressive periodontitis (AgP) is thought to have a faster rate of progression than chronic periodontitis (CP). However, there is a lack of studies systematically investigating disease progression and tooth loss in AgP. A systematic search of the literature was conducted by two independent reviewers for longitudinal studies including patients with AgP (previously known as 'periodontosis', 'juvenile' or 'early-onset' periodontitis) indicating measures of disease progression. Ovid MEDLINE(®) and Embase databases were searched for at least 5-year longitudinal human studies in AgP patients. In total, 16 studies were included in the review, from an initial search of 1,601 titles. Heterogeneity was detected for disease definition and clinical data reporting; hence meta-analysis was feasible only for the objective measure 'tooth loss'. The average tooth loss for all AgP cases was 0.09 (95% C.I. = 0.06-0.16) per patient-year. The corresponding values by diagnosis were 0.05, 0.14, and 0.12 tooth loss per patient-year, respectively, for LAgP, GAgP, and un-specified AgP. For studies reporting tooth loss during the 'observational period' (excluding extractions at initial therapy), the average tooth loss for AgP was 0.09 per patient-year. High heterogeneity was detected for these analyses. In conclusion, most studies report good long-term stability of treated AgP cases.

Aim: The aim of this study is to investigate the effect various dietary nutrients in aggressive periodontitis patients., Materials and Methods: A total of 85 patients were selected and divided into two groups, 45 patients are with aggressive periodontitis and 40 patients are healthy. Periodontal parameters such as oral hygiene index, Russels periodontal index and radiograph were taken. The food consumption survey was conducted in all the households of subjects both in control and experimental group. The individual of food intake of the subjects was assessed by the oral questionnaire (24 hours recall) method. The quantity of raw foods used for various preparations and volumes of cooked quantities of such preparations in terms of standardized cups were noted. Body measurements were taken on all the subjects, standing height using a height measuring rod and weight in standard weighing machine., Results: Aggressive periodontitis is seen in young individual and mostly in females; majority of the patients of both groups belongs to low socioeconomic group. Body mass index which is a refection of nutritional status of an individual indicated that chronically energy defcient subjects in experimental group appeared to be higher. The average food and nutrient intake in control group was slightly better than that of experimental group., Conclusion: The diet survey indicated marginal and negligible defciencies in aggressive periodontitis patients compared to controls, and this coupled with chronically energy defciency as indicated by body mass index, calls for a detailed study of this aspect of aggressive periodontitis. The present study indicates that nutritional infuences point to a needle of suspicion toward the etiology of aggressive periodontitis.

Introduction: The aim of this study was to examine a potential link between apoptotic biomarkers in gingival crevicular fluid (GCF) and periodontal destruction in four cases of localized aggressive periodontitis (LAP), diagnostically enhanced by cone beam computed tomography., Case Series: This study examined the GCF in four patients diagnosed with LAP (formerly localized juvenile periodontitis) at a routine periodontal examination. The LAP diseased sites had attachment loss ranging from 5-12 mm. Atotal of 62 samples of GCF were collected from diseased sites and from contralateral, matched healthy sites with minimal or no attachment loss. All samples were assayed for apoptotic markers, including Fas/FasL, DNAfragmentation, and nitric oxide. The GCF samples were analyzed utilizing enzyme-linked immunosorbent assays for DNA fragments and nitric oxide levels, whereas Western blotting was used for Fas/FasL analyses. Our results showed a significant increase in the apoptotic markers Fas/FasL and DNA fragmentation when comparing GCF from diseased versus non-diseased sites in patients with LAP., Conclusion: To our knowledge, this is the first report of apoptotic biomarkers associated with patients diagnosed with LAP. Finding significantly increased levels of these markers in localized areas may help us understand the pathophysiology associated with this specific form of periodontitis, and, furthermore, may provide a basis for a quantifiably prognostic test when attempting to treat this disease.

Background: Premature exfoliation of primary teeth is an important diagnostic event warranting urgent investigation. The majority of conditions presenting with early loss of teeth are serious and in some cases fatal., Case Report: This is a case of premature exfoliation of primary teeth in a 4-yr-old female. On presentation her teeth were mobile and there was a history of gingival bleeding when biting into food. Hair loss and fatigue were also reported. Her medical history revealed she had dry skin but was otherwise fit and healthy. Extra-oral examination was unremarkable. Dental examination revealed she had a full complement of primary teeth with unusual spacing, generalised tooth mobility, halitosis and an orange extrinsic dicolouration. Her gingivae were inflamed in the 84 region. Radiographic examination revealed severe generalised bone loss., Treatment: She received periodontal care including regular scaling, a short course of metronidazole, preventative advice and continued monitoring. She was also sequentially referred to the departments of Dermatology, Paediatric Haematology, Immunology, Oral Microbiology and Oral Pathology for further investigation. Underlying disorders known to cause premature tooth loss were ruled out., Follow-Up: Two years on, there has been early exfoliation of her 54, 51, 61, 62, 64, 71, 84 and 81 with no new progressive mobility of her remaining primary teeth., Conclusion: The commonest causes of premature tooth loss have been eliminated including Papillion-Lefevre syndrome, Chediak-Higashi syndrome, hypophosphatasia, Langerhans' cell histiocytosis, neutropenia and leukemia. Therefore, this fit and healthy 4-yr-old has an aggressive early onset periodontal condition with associated fatigue and hair loss. Diagnosis of associated systemic conditions is not straightforward in these cases and requires multi-disciplinary input.

Periodontal infections have been associated with a state of chronic inflammation. To ascertain whether severe periodontitis and its treatment are associated with oxidative stress, we recruited 145 cases (periodontitis) and 56 controls in a case-control study. A further pilot intervention study of 14 cases (periodontal therapy) was performed. Blood samples were taken at baseline (case-control) and 1, 3, 5, 7, and 30 days after treatment (intervention). Diacron-reactive oxygen metabolites (D-ROM), anti-oxidant potential, C-reactive protein (CRP), interleukin-6, and lipid profiles were determined with high-sensitivity assays in serum. Patients with severe periodontitis exhibited higher D-ROM levels (P < 0.001) and lower total anti-oxidant capacity (P < 0.001) compared with healthy control individuals. These findings were independent of age, gender, smoking habits, ethnicity, and standard lipids differences. D-ROM levels were positively correlated with CRP (R = 0.4, P < 0.001) and clinical periodontal parameters (R = 0.20, P < 0.05). Acute increases of D-ROM (P < 0.01) were observed following periodontal therapy. Analysis of these data suggests a positive association between severe periodontitis and oxidative stress.

The JP2 clone of Aggregatibacter actinomycetemcomitans is strongly associated with aggressive periodontitis. To obtain information about colonization dynamics of the JP2 clone, we used PCR to examine its presence in 365 Moroccan juveniles from whom periodontal plaque samples were collected at baseline and after one and two years. Periodontal attachment loss was measured at baseline and at the two-year follow-up. At baseline, 43 (12%) carriers of the JP2 clone were found. Nearly half (44 %) of these were persistently colonized with the clone. The relative risk for the development of aggressive periodontitis, adjusted for the concomitant presence of other genotypes of A. actinomycetemcomitans, was highest for individuals continuously infected by the JP2 clone (RR = 13.9; 95% CI, 9.0 to 21.4), indicating a relationship between infectious dose and disease, which further substantiates the evidence for the JP2 clone as a causal factor in aggressive periodontitis.

Introduction: Teaching of biomedical knowledge lays the foundations for the understanding and treatment of diseases. However, the representation of pathophysiological explanations in the management of clinical cases differs for various levels of medical expertise and different theories have been proposed to explain this phenomenon. The present study investigated for the first time how biomedical knowledge is used in clinical reasoning in dental medicine., Materials and Methods: In an experimental study 20 experts in the field of Periodontology and 61 students of different levels of training produced written pathophysiological explanations after having studied three different clinical cases. By comparing the written protocols to a visualised expert-made 'canonical' explanation the concepts used in the pathophysiological explanation were counted and classified as well as the links between concepts., Results: The statistical analysis by MANOVA showed significant differences between third- and fourth-year students, students of intermediate expertise level (fifth-year) and experts for various parameters qualifying concepts or links of the written pathophysiological explanations. The participants of intermediate expertise level produced a high rate of concepts and links; however, characteristic findings for knowledge encapsulation in the different levels of expertise were not evident. The analysis showed that the design of the clinical cases and of the canonical explanations significantly influenced the outcomes., Conclusion: The present study demonstrated the pathophysiological representations of clinical cases in dental students and experts to be different from other medical disciplines. It could be assumed that this observation is based on different contents for teaching of practical skills and diagnostic procedures in dental compared with medical education.

Objective: To investigate 7 short chain fatty acids (SCFA) concentrations in gingival crevicular fluid (GCF) of aggressive periodontitis (AgP) and to analyze the relationship between levels of SCFA and AgP clinical parameters., Methods: GCF was collected from 152 sites of 38 AgP patients and 56 sites of 14 healthy subjects. Formic acid, succinic acid, acetic acid, lactic acid, propionic acid, butyric acid and isovalerianic acid were detected by high performance capillary electrophoresis., Results: The concentrations of succinic acid, acetic acid, lactic acid, propionic acid, butyric acid and isovalerianic acid in GCF were significantly higher in AgP patients than in healthy group, while formic acid was lower in GCF of AgP group compared with healthy group. Correlation analysis showed that formic acid was negatively correlated with bleeding index (BI), probing depth (PD) and attachment loss (AL), while BI was positively correlated with succinic acid, acetic acid, lactic acid, propionic acid and butyric acid; PD and AL were positively correlated with succinic acid, acetic acid, propionic acid, butyric acid and isovalerianic acid., Conclusions: The elevation of succinic acid, acetic acid, propionic acid, butyric acid and isovalerianic acid concentrations in GCF may be related with AgP destruction condition, while formic acid concentration was reduced.

Implant therapy in partially edentulous patients has proven to be a predictable procedure with a high implant survival rate. The success rate in patients with a history of aggressive periodontitis, however, is still unclear. A Medline/PubMed search was conducted to identify and summarize articles published in English and reported on the survival of implants in aggressive, rapidly progressive, or juvenile periodontitis patients. Our search revealed only 9 articles, 4 of which were case reports. Although available evidence is weak, it suggests good short-term survival of implants placed in periodontally well-maintained aggressive periodontitis patients. Bone loss around implants in aggressive periodontitis patients, however, appears to occur more frequently than it does in chronic periodontitis patients or periodontally healthy individuals. A summary and critical analysis of the aforementioned articles is presented.

Background: Periodontitis is a loss of supporting connective tissue and alveolar bone around teeth, and if it occurs in an aggressive form it can lead to tooth loss before the age of 20 years. Although the cause of periodontitis in general remains elusive, a particular clone (JP2) of the gram-negative rod Aggregatibacter (Actinobacillus) actinomycetemcomitans is considered a possible aetiological agent of the aggressive form in adolescents living in or originating from north and west Africa, where the disease is highly prevalent. We did a population-based longitudinal study of adolescents to assess the role of the JP2 clone in the initiation of aggressive periodontitis., Methods: A total of 700 adolescents from public schools in Rabat, Morocco, were enrolled in the study. We used PCR to detect A actinomycetemcomitans in plaque samples (taken from molar and incisor sites) and to differentiate between the JP2 clone and other non-JP2 genotypes of the bacterium. 18 individuals were found to already have periodontitis and were excluded. The 682 periodontally healthy adolescents (mean age 12.5 years; SD 1.0) were classified according to their A actinomycetemcomitans carrier status at baseline. After 2 years, 428 (62.8%) individuals returned for re-examination, which included recording of periodontal attachment loss measured from the cemento-enamel junction to the bottom of the periodontal pockets of all teeth present., Findings: Individuals who carried the JP2 clone of A actinomycetemcomitans alone (relative risk 18.0; 95% CI 7.8-41.2, p<0.0001) or together with non-JP2 clones of A actinomycetemcomitans (12.4; 5.2-29.9, p<0.0001) had a significantly increased risk of periodontal attachment loss. A much less pronounced disease risk was found in those carrying non-JP2 clones only (3.0; 1.3-7.1, p=0.012)., Interpretation: The JP2 clone of A actinomycetemcomitans is likely to be an important aetiological agent in initiation of periodontal attachment loss in children and adolescents. Co-occurrence of non-JP2 clones of A actinomycetemcomitans reduces the risk of development of periodontitis, suggesting competition for the ecological niche between the JP2 and non-JP2 clones of this species.

Systemic diseases affecting the host response as primary immunodeficiencies or secondary defects caused by lack of nutrients or changes in the local tissues are very often accompanied by early-onset prepubertal periodontitis. Local treatment in combination with systemic antibiotics may in milder forms improve the situation, but in many cases the success is questionable and premature loss of teeth occurs. Since the genetic basis of many of the diseases has been identified, future developments permit the correction of at least some of these defects by gene therapy.

Regional hemodynamics, bioelectric activity of masticatory muscles, and compactness of mandibular bone were studied by the rheographic method for measuring periodontal bloodflow, by electromyography, and echo-osteometry in 52 volunteers after 4-week regular chewing of Dirol chewing gum. Congestive hyperemia develops in periodontal tissues; functional activity of masticatory muscles and compactness of mandibular bone are normal.

The periodontal pathogen Actinobacillus actinomycetemcomitans produces a leukotoxin that is considered a primary virulence factor in localized juvenile periodontitis (LJP). Select strains of the bacterium contain a 530-bp deletion in the promoter region of the leukotoxin gene operon which results in enhanced transcription of the leukotoxin. DNA hybridization and polymerase chain reaction (PCR) were used to examine genetic variants of A. actinomycetemcomitans in 24 LJP-susceptible children from 21 families having a history of the disease and 34 control children from non-LJP families. A significant association was found between the detection of variants that had a deletion in the leukotoxin promoter region, indicative of a high level expression leukotoxin genotype, and conversion from a healthy periodontal status to disease. Subjects harboring A. actinomycetemcomitans of this genotype were more likely to convert to LJP than those subjects who had variants containing the full length leukotoxin promoter region (odds ratio = 22.5; 95% C.I., 2.84 < 206.66) [corrected]. These findings support the concept that highly virulent strains or clonal types of periodontal pathogens play a major role in the initiation of periodontal disease in susceptible hosts.

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.

Actinobacillus actinomycetemcomitans has been associated with different forms of periodontitis, particularly with localized juvenile periodontitis (LJP). The bacterium possesses several virulence factors which have been shown to interact with the host immune system. Among these factors, leukotoxin, surface antigens (serotype) and bacteriophages have been suggested directly or indirectly to influence the course of infection. However, few studies have been able to show associations between these factors and periodontal disease, alone or in combination. Thus, the purpose of the present study was to investigate possible correlations between periodontal disease status and selected virulence factors (serotype, presence of bacteriophages, and the presence of a 530 bp deletion in the promoter region of the leukotoxin gene). 36 subjects took part in the study. Serotype c was the most frequently found serotype among periodontally affected subjects, although serotypes a and b were also present. 27 out of 36 strains harbored bacteriophages, and there was strong evidence that some of the bacteriophages were different from the previously characterized phi Aa phage. A. actinomycetemcomitans containing the F-fragment phage were more frequently associated with periodontal disease. Five strains, all serotype b, 3 from LJP patients and 2 from healthy subjects, showed a 530-bp deletion in the promoter region of the leukotoxin gene.

Objectives: This manuscript attempts to critically review current literature regarding the natural history, aetiology and pathogenesis of the common periodontal diseases to affect children and adolescents. The logic behind the emergence of a new classification in the early 1990s is explained and potential problems with the interpretation of such systems outlined., Data Sources: The manuscript focuses upon recent developments, reported in the international periodontal literature, aimed at unraveling the molecular basis for this group of diseases. The concept of one disease type progressing with time to another disease within the same individual is discussed, and early data presented that indicate the possibility of microbial transmission from deciduous to permanent dentition's within a subject., Conclusions: It is concluded that differing classification systems for adolescent and childhood periodontal diseases may lead to confusion within the dental profession, unless the clinical and molecular basis for such diseases is fully understood. Further advances in basic research using molecular biology tools should assist in our understanding of the aetiopathology at a molecular level and hopefully lead to the development of new treatment strategies.

We studied the pattern of progression of early-onset periodontitis and the change in the extent and severity of the periodontal condition in adolescents who were followed for 6 years. In a national survey of the oral health of U.S. children, 14,013 adolescents were examined clinically in 1986/1987 to assess the periodontal attachment loss of teeth. Individuals with early-onset periodontitis within this population were identified and classified into localized juvenile periodontitis (LJP), generalized juvenile periodontitis (GJP), and incidental attachment loss (IAL) groups. Ninety-one subjects, 13 to 20 years old at baseline, were examined 6 years later. They included 51 males and 40 females; and 72 Blacks, 6 Hispanics, and 13 Whites. They were clinically re-examined and then reclassified according to their periodontal status at follow-up. The severity and extent of these diseases continued to increase during the study period. In teeth that were affected at baseline, the lesions had progressed to include deeper portions of the periodontium, and more of the teeth unaffected at baseline exhibited periodontal attachment loss at follow-up, thus changing the disease characteristics and the basis for the clinical classification. Of the individuals classified with LJP at baseline, 62% continued to have LJP 6 years later and 35% developed GJP. Of those classified with GJP initially, all but two (82%) continued to have GJP at follow-up. Among the IAL group, 28% of subjects developed LJP or GJP, and 30% were reclassified in the no attachment loss group. Molars and incisors were the teeth most often affected in all three groups. The mean change in attachment loss over 6 years in the LJP, GJP, and IAL groups was 0.45, 1.12, and 0.13 mm, respectively. The present findings demonstrate the limitations of the currently used morphological criteria in the classification of early-onset periodontitis. The findings also suggest that the difference between LJP and GJP is in the number and type of teeth involved, and that the two classifications progress similarly, with some cases of LJP developing into GJP.

Pathogenic bacteria constitute the primary extrinsic agent in the etiology of early onset periodontitis. However, the risk of developing periodontal disease is not equal for all individuals, suggesting host factors are involved in determining an individual's disease susceptibility. In this report, a case of an otherwise healthy female, who exhibited prepubertal periodontitis (PPP) at age 10, juvenile periodontitis (JP) at age 13, and rapidly progressive periodontitis (RPP) at age 29 years, is presented. Microbial, immunological, and genetic features of the case are presented. PPP, JP, and RPP are considered distinct disease entities, albeit with similar pathology and pathogenesis, yet all were manifest sequentially in the same individual. This report presents the idea that certain individuals are predisposed to early-onset periodontal diseases and the early identification of risk factors is important in the management of these individuals.

Frequent bleeding on probing (BOP) has been considered a risk factor for recurrence of periodontitis. In the present study, 29 patients with Actinobacillus actinomycetemcomitans-associated periodontitis were enrolled in a carefully performed recall system. At 6 sites per tooth, periodontal probing depth (PPD), gingival index (GI), plaque index (PlI) and BOP was assessed 6 weeks, 6 months, 1 and 2 years after comprehensive therapy. Professional toothcleaning and subgingival scaling at sites with PPD > or = 5 mm and BOP was carried out every 2nd or 3rd month. Subgingival samples from 2 sites, a pooled subgingival sample, cheek mucosa, saliva and tongue samples were selectively cultivated for A. actinomycetemcomitans after 2 years. Following active therapy, 8% sites had a PPD of > or = 4 mm, whereas 21% sites bled on probing. After 2 years, respective figures were 12 and 27%. During maintenance, frequent BOP (> or = 3 times at 4 visits) had a predictive value of 0.133 to indicate an increase in PPD of > or = 2 mm and a negative predictive value of 0.947. The predictive value of no bleeding to indicate a stable site was 0.972, the negative predictive value 0.078. There was evidence for heterogeneity of associations between increase in PPD of > or = 2 mm and > or = 3 times BOP among patients (chi 2(28) = 41.45, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Localized juvenile periodontitis (ljp) is an early onset form of periodontal disease characterized by unique localization to first molars and incisors and a high prevalence of neutrophil abnormalities, particularly chemotaxis. The intracellular transduction mechanisms that follow receptor-ligand coupling on the neutrophil surface and lead to chemotaxis are not clearly established. Chemotaxis and phagocytosis are modulated by a variety of receptors and involve several activation pathways; the role of intracellular calcium as a presumptive second messenger and mediator of these events is well established. The putative effector mechanisms for the chemotactic receptor of neutrophils also include the possible activation of a phospholipase, protein kinase C, methyltransferase, or adenylate cyclase. In normal neutrophils, a phosphoinositide pathway initiated by phospholipase C, which results in the activation of protein kinase C via diacylglycerol and the generation of IP3, has been implicated. In order to better understand the stages of neutrophil transduction, fluorescent probes were used to monitor neutrophil calcium changes. Chlorotetracycline (CTC) was used as an indirect probe of intracellular membrane-bound pool of calcium stores, and Quin-2 was used to monitor cytosolic free calcium levels of FMLP stimulated normal and LJP neutrophils. The results indicate that the early phase of the calcium response affiliated with the release of intracellularly sequestered calcium appears intact in LJP neutrophils, as the CTC fluorescence changes were similar to control values. The second phase of the calcium response, associated with membrane channel activation and an influx of extracellular calcium, appeared compromised in the neutrophils of the LJP population.(ABSTRACT TRUNCATED AT 250 WORDS)

We compared salivary epidermal growth factor (EGF) concentrations in patients with juvenile periodontitis (JP) and periodontally healthy controls. In initial screening of 45 JP patients and a group of healthy controls, significantly higher salivary EGF concentrations were measured in the JP patients. Subsequently, 17 JP patients who had high EGF concentrations in some of their salivary samples were chosen, and a group of age- and sex-matched controls was selected. We then examined their EGF concentrations and EGF secretion rates under standardized conditions in stimulated and unstimulated saliva and studied the expression of EGF receptor (EGF-R) in their gingival tissues. The results showed that the mean EGF concentration (pmol/ml) was slightly higher in JP patients than in controls. However, the difference was statistically significant only in stimulated saliva and when calculated per milligram salivary protein. When EGF release was measured as the rate of EGF secretion (pg/min), significantly higher values were observed in JP patients than in controls both in unstimulated and stimulated saliva. Immunofluorescence microscopy (IF) of gingival samples from JP patients and their controls revealed no quantitative or qualitative differences in the expression of EGF-R. Our results demonstrate the complex nature of salivary EGF release. The elevated rate of salivary EGF secretion in JP patients may be associated with the pathogenetic mechanisms of juvenile periodontitis.

The present study was performed to investigate the factors associated with disease progression in localized juvenile periodontitis (LJP) patients by longitudinal monitoring of microbiological changes. Following a 9-month period, 9 LJP patients were divided into 2 groups based upon attachment loss, progressing and non-progressing. Both groups received scaling, root planing, and modified Widman flaps. Clinical and microbiological data were obtained at baseline, following the observation period, and at 6 and 12 months post-treatment. At 6 and 12 months post-treatment significantly more cocci were persistent in the non-progressing group than in the progressing group. Actinobacillus actinomycetemcomitans was also more frequently isolated in the progressing group than in the non-progressing group initially and following the 9-month observation period. Also after treatment, A. actinomycetemcomitans recolonized earlier in the progressing group than in the non-progressing group. These studies suggest that A. actinomycetemcomitans may play a role in disease progression in LJP; however, they do not eliminate the possibility that other organisms may also play a role, since A. actinomycetemcomitans was not detected in all of the patients in whom disease progressed.

Adherence is a major pathogenicity factor for many bacteria. The aim of this study was to measure the adherence potential of Actinobacillus actinomycetemcomitans (A.a.) for buccal epithelial cells (BEC). In the second part of the study, the inhibitory potential of saliva on adherence between A.a. and BEC was tested. Saliva specimens were obtained from three groups of subjects: a group of normal subjects (NS), a group of subject with localized juvenile periodontitis (LJPS) and a group of subjects with adult periodontitis (APS). Clinical strains of A.a. showed a major adherence potential for BEC (25.5 A.a./BEC). In contrast, reference strains of bacteria appeared to possess a much lower potential for adherence (12.6 A.a./BEC). Saliva samples taken from from the LJPS and APS group had a high inhibitory adherence potential, since in each of these groups a reduction of 60.9% and 66.7% respectively, was observed in the number of bacteria adhering to BEC.

Fifty-one subjects (16-61 years old) with evidence of prior destructive periodontal disease were monitored clinically and immunologically at bi-monthly intervals for up to 5 yr. Periodontal disease activity, determined as new attachment loss, was detected in 33 of these subjects. Only 4 of 51 subjects failed to show an elevated serum antibody level to any of the 18 subgingival species tested. The antibody level threshold established for periodontally healthy subjects was exceeded most often in diseased subjects with serum antibody to Actinobacillus sp., P. gingivalis, E. corrodens, C. concisus, F. nucleatum and P. intermedia in that order. In general, most serum antibody levels to subgingival species remained relatively consistent for periods as long as 5 yr. However, major increases and decreases in antibody could be detected to at most one or two species in individual subjects. In addition, prolonged, steady increases and decreases in antibody to specific species could be detected in certain subjects. These findings suggest that major changes occurring in serum antibody may reflect fluctuations in the nature of the infection. Differences were observed in the antibody level to specific species when subjects were divided into subsets on the basis of clinical criteria. These included high levels of antibody to A. actinomycetemcomitans Y4 in LJP and RPP subjects and to A. actinomycetemcomitans 29523 in LJP and GJP subjects.

Early onset periodontitis is a group of familial diseases that are not yet clearly defined by etiologic mechanisms, although some risk factors have been recognized. The disorders include a localized form of juvenile periodontitis (JP), and a more generalized form (GP). In a family study, 39 sibships (116 individuals, aged 13-48) were evaluated for clinical indices, neutrophil chemotaxis, and serum antibodies to A. actinomycetemcomitans (Aa). Of 77 siblings, 41 were healthy at examination. In 14 sibships, all affected persons had JP; 14 other sibships had all affected individuals with GP; and 11 had at least one sib with each form. For probands with decreased chemotaxis, 71% of affected sibs and 36% of clinically healthy sibs had decreased chemotaxis. For Aa seropositive probands, 83% of affected siblings and 65% of currently healthy sibs were also seropositive. The associations of disease with these risk factors were stronger in JP-only sibships. Some affected sibs had neither risk factor, while many currently healthy sibs had 1 or both. While these 2 factors demonstrate population association with disease, neither fits the pattern expected within families to clearly suggest a causal mechanism. The assessment of within and among family variability remains the best approach for recognition of possible causal mechanisms and sources of heterogeneity.

The complement-dependent phagocytic functions of polymorphonuclear leucocytes (PMNL) in peripheral blood from 15 patients with localized juvenile periodontitis (LJP), 13 with generalized juvenile periodontitis (GJP) and 52 with adult periodontitis (AP), and from 30 normal subjects as controls were measured by flow cytometry. Heparinized blood was collected and incubated with fluorescent microspheres, and erythrocytes were removed. By means of single-cell analysis the percentage of phagocytosing cells (% phagocytosis) and the mean number of microspheres phagocytosed by one PMNL (degree of phagocytosis; d-phagocytosis) were measured. Some but not all patients with LJP (53%) and GJP (46%) showed consistently low % phagocytosis and d-phagocytosis. On the other hand, only 6% of AP patients and no healthy subjects showed a reduction of PMNL phagocytosis. Phagocytosis was unchanged after initial periodontal treatment in all subjects, suggesting the depression of PMNL phagocytosis may not be a transient phenomenon associated with periodontal status. Furthermore, PMNLs from the LJP patients that showed depressed phagocytic function exhibited depressed phagocytic responses with either autologous or normal plasma, while control PMNLs with either normal or the patients' plasma showed normal responses. These results suggested that the depressed phagocytic responses in LJP patients could be due to cell-associated defect(s) on the PMNL.

Hypoxic stimulation was added to local therapy of periodontitis in 26 adolescents with the initial manifestations of this condition. Analysis of the results has shown that hypoxic stimulation enhanced the body adaptive and compensatory potentialities, was conductive to recovery of the disordered oxygen metabolism and normalization of the regional hemodynamics and periodontal microcirculation.

We studied the periodontal disease progression and the relationship between some forms of destructive periodontitis in a group of Brazilian adolescents with high prevalence of periodontal destruction, and evaluated the adequacy of reducing data by limiting the measurement of disease to first molars and by aggregating and pooling site-scores into subject-level scores. Over a period of 3 years 222 adolescents were examined annually by bite-wing radiographs. Individuals displaying arc-shaped bone lesions adjacent to greater than or equal to 2 first molars were diagnosed as juvenile periodontitis (JP) patients, while those with greater than or equal to 1 first molars showing vertical lesions were regarded as periodontal risk subjects. Teenagers with greater than or equal to 2 first molars exhibiting longitudinal bone loss were defined as high-risk patients. At the ages of 13 and 16 years, 3 (1.3%) and 4 (1.8%) subjects had JP, while 12 (5.4%) and 28 (12.6%) were regarded as periodontal risks; 8 (3.6%) subjects were assigned to the high-risk group; 4 (1.8%) 13-year olds had greater than or equal to 1 first molars missing; hence, no loss of posterior teeth occurred over a period of 3 years. Analyzing the data at the site-level revealed progressive loss and little fluctuation in the alveolar bone height in the high-risk group, and a more pronounced bone loss at the mesial than at the distal surfaces. Simpler data sets were constructed by aggregating some of the site-scores or by pooling these into subject-level scores.(ABSTRACT TRUNCATED AT 250 WORDS)

Juvenile periodontitis (JP) is a disease characterized by severe gingival infections. PMN from some JP patients exhibit abnormal chemotactic responsiveness when challenged with the synthetic formyl peptide, FMLP. While investigating PMN function in JP, we found a patient in whom abnormal PMN chemotactic responses to FMLP were associated with a defective population of PMN formyl peptide receptor(s) (FPR). JP PMN failed to respond chemotactically when challenged with FMLP, but exhibited normal chemotactic responses upon exposure to purified human C5a. Furthermore, JP PMN were capable of degranulating and generating superoxide anion radicals as well as normal PMN upon exposure to FMLP. Binding studies demonstrated that JP PMN had a diminution in the number of high-affinity FPR. Studies in which FPR was radiolabeled by chemical cross-linking demonstrated that JP PMN FPR exhibited the same molecular weight and N-linked glycosylation as normal PMN FPR. JP PMN FPR, however, was more resistant to papain cleavage than normal PMN FPR. Autoradiograms obtained from 2D-PAGE of normal and JP PMN FPR demonstrated decreased amounts of FPR isoforms in JP PMN.

An aggressive form of localized juvenile periodontitis (LJP) in a 12-year old West African female is reported. The case was treated with scaling, root planing, debridement, and tetracycline therapy, which resulted in complete resolution of the disease, including elimination of periodontal inflammation, regeneration of lost periodontal structures, and spontaneous repositioning of teeth that had pathologically migrated. A hopelessly involved mandibular right first molar was successfully replaced by an incompletely developed maxillary third molar tooth bud whose roots and pulp structure continued to develop after autotransplantation. It is suggested, that LJP can be successfully treated without periodontal surgery and that the potential for repair in LJP cases is apparently greater than what one can anticipate in adult forms of periodontitis.

Seven juvenile periodontally diseased patients were evaluated for clinical, microbiologic and local or systemic host factors. Three patients showed the localized from of periodontitis clinically and radiographically and by deep periodontal pockets associated with the molars and incisors. Four were in the generalized froms, in which in most cases all teeth were affected. The results in both diseased froms on the predominant cultivable subgingival microflora, the composition of which was not different from that in adult periodontitis, consisted of significantly increased proportions of Gram-negative anaerobic rods, Bacteroides sp. and B. gingivalis, Haemophilus sp. and H. actinomycetemcomitans were detected in 1/3 of the localized and 2/4 of the generalized periodontitis. They were of no value in distinguishing activity that enhanced disease in the generalized from. Elevated serum IgG responses were noted with B. gingivalis. No markedly functional abnormalities of neutrophils from peripheral blood have been demonstrated, however it might function with systemic factors, like an insulin-dependent diabetes. Morphologic characteristics of the oral and periodontal tissue in localized periodontitis were that the pattern of destruction was confined to specific teeth groups characterized by extensive the bucco-lingual width ratio of the dental crown to alveolar bone width. These observations indicate that the generalized form of juvenile periodontitis lesions were associated not only with the presence of subgingival bacteria, but also with conditions such as local morphologic and systemic or constitutional factors, individual variation in relation to destructive and protective aspects of the defense mechanisms.

Patients suffering of parodontosis and hypertensive disease (stage II) revealed an increase of the microcirculatory blood vessels of the periodontal tissues and correspondingly a deterioration of circulation in the region of the microcirculatory bed, a reduction of the stability of microcirculatory blood vessels of the periodontal tissues. After a single use of a 0.25% clophelin solution in the form of applications the pathologically elevated arterial pressure decreased and the tone of the periodontal tissue vessels reduced as well, the rheographic index increased, the stability of blood vessels of the microcirculatory bed increased. The author recommends the use of hypotensive agents in the complex treatment of changes of the periodontal tissues in patients with hypertensive disease.

To test the hypothesis that localized and generalized juvenile periodontitis is one disease entity, the localization of bone loss was measured from orthopantomograms of 88 patients with untreated juvenile periodontitis. Linear regression analysis showed a significant correlation between the age of the patient and the number of teeth with bone loss. Similarly, a correlation was found between the Gingival Bleeding Index scores, the age of the patient, and the number of affected teeth. It is concluded that juvenile periodontitis, known to be genetically controlled, is a disease entity which starts as a localized form with affected first molars and/or incisors and develops, if not treated, gradually to the generalized form of the same disease, which resembles the adult periodontitis.

An in vivo assay was recently developed to monitor the crevicular leucocyte response to chemotactic agents, e.g., casein and N-formyl peptides. This method was used to monitor humans with little or no gingival disease (C group), gingivitis (G group), chronic periodontitis (CP group) and localized juvenile periodontitis (LJP group). Casein (0.2 microliters, 2 mg/ml) was placed into an isolated gingival crevice of each subject with a calibrated wire loop and the time recorded (t = 0). Leucocytes were counted in crevicular washes (10 microliters) 15 minutes later and every 5 minutes thereafter up to t = 50 minutes. This protocol was repeated for the crevice of an adjacent tooth except that the crevicular fluid flow response to the chemotactic challenge was monitored. The C, G and CP subjects showed a similar pattern of response to the chemoattractant with a single "peak" of leucocytes at approximately t = 25 minutes. However, the peak cell count was much greater in the G and CP groups than in the C group. LJPs showed an abnormal pattern with two leucocyte peaks, one at approximately 25 minutes and the other at 45 minutes. Both peaks tended to be higher than the single peak seen in Cs but were significantly lower than that in Gs or CPs, even at similar levels of inflammation. In addition, the peak leucocyte response (to casein) in LJPs did not increase with increasing leucocyte counts in the unchallenged (resting) crevice, whereas a positive relationship was seen in the other groups of subjects. These data suggest that this new assay may provide important diagnostic information on in vivo neutrophil migration in the gingival crevice and on susceptibility to periodontal disease.

Patients suffering from periodontitis or periodontosis were selected for the study. Further subdivision of these groups was based on the presence or absence of herpes and/or adenoviruses in their oral lymphocytes and epithelial cells. The phagocytic and bactericidal activities of oral leukocytes isolated from the same individuals were compared with virus carriage. In the periodontitis group, 60.5%, and in the periodontosis group 61.5% of patients carried viruses, while this was established only in 21.1% of control cases. On the other hand, emigration and sulcular gathering of the less viable polymorphonuclear leukocytes was elevated but their phagocytotic activity was decreased among periodontitis patients. Bactericidal capacity was significantly lowered among those subjects who carried viruses in their cells, as compared with virus-free persons, especially in the periodontitis group. The functions of the polymorphonuclear leukocytes accumulated in the sulcus gingivalis may be modified by mediators released from the virus-carrying cells. These mediators could achieve a greater concentration locally, and the damaged leukocytes would not be able to eliminate the microbes continuously so that the accumulation of bacterial products, among them endotoxins, could lead to periodontal inflammation.

The purpose of the present study was to investigate the clinical differences between individuals highly susceptible and individuals insusceptible to periodontal breakdown. The susceptible group consisted of 7 patients with a diagnosis of juvenile periodontitis. The insusceptible group consisted of 7 individuals selected on the basis of age (52 years or older), presence of at least 18 teeth, no evidence of extractions due to periodontal breakdown, no loss of attachment, shallow pockets, gross amounts of plaque and no history of interdental cleaning. Results showed that the susceptible group had more bleeding, less plaque and deeper pockets than the insusceptible group. Since the 2 groups seem to behave differently with regard to bleeding upon probing and amount of plaque, bleeding/plaque ratios were calculated. Testing showed a highly significant difference between the 2 groups. The same results were obtained if only sites with shallow pockets were included in the analysis. On the basis of these results, it is hypothesized that a high value of the ratio between bleeding and plaque may act as a prognostic indicator for periodontal breakdown.

The authors emphasized in parodontosis patients functional alterations of hypothalamic centres with phagocytosis-stimulatory, vasomotor and neurotrophic functions and disturbances of the functional relationship between the hypothalamus (H), the ascendent reticular formation (RF) and the cerebral cortex (CC). Stimulatory therapy of this areas, especially by direct stimulation of the H improves the hypothalamic functions, the relationship between H and the RF and all the clinical status of parodontosis patients. In rabbits with experimental parodontosis have been found functional and histological alterations in cerebral cortex, and especially in hypothalamus, together with lesions in the hypothalamo-posthypophyso-neurosecretoric system, in the anterior pituitary (P) cells (for ACTH, TSH and FSH) as well as in zona fasciculares of the adrenal cortex (AC). This data, together with findings of other authors, prove that parodontosis is a diencephalopathy involving a whole system: CC-H-P-AC.