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Papillon-Lefevre Syndrome (PLS) is an inherited autosomal recessive disorder presenting with Palmar plantar Keratoderma and Juvenile Periodontitis leading to early loss of both the dentitions. Two cases of PLS in a family with a history of consanguineous descent are presented.
The prevalence and distribution of Haemophilus actinomycetemcomitans (H.a.) were studied in 3292 specimens of subgingival plaque on the four subgingival aspects of all teeth of the dental arch, 150 specimens from the mucosal surface (tongue and cheek) and 30 saliva specimens in 30 subjects. The sample population of 30 subjects was subdivided into three groups: 10 normal subjects, 10 subjects with localised juvenile periodontitis (SLJP) and 10 subjects with adult chronic periodontitis (SACP). The prevalences of H.a. in subgingival areas of each group mentioned were 30%, 90% and 60% respectively. Scores for prevalence obtained with other types of specimens proved to be lower except for saliva specimens which appear to be a less representative marker of subgingival prevalence of H.a.. Histograms for the distribution of H.a. revealed a predominance of this microorganism on the proximal surface of molar teeth in the three groups of patients. Only the SLJP also exhibited a high prevalence on the proximal aspect of the incisor teeth. The wide distribution of H.a. in all of the clinical groups studied suggests that this bacterium is not a good marker of periodontal disease and that it is necessary to define the most characteristic phenotypes and genotypes.
The development of periodontal treatment based on knowledge of the aetiology and pathogenesis of the diseases is reviewed. Emphasis is laid on the role of microorganisms and especially on the significance of their immunological interactions with the host. It is concluded that, despite increasing knowledge of the pathogenesis, microbiology and immunology of periodontal diseases, the methods of treatment have not changed essentially during the past 30 years. Oral hygiene instruction, scaling and root planing are still the methods of choice.
Periodontal diseases are caused by specific bacteria in the periodontal pocket. Despite the vast complexity of the flora on the teeth and the more than 300 types of bacteria that may be found in the mouth, studies have been able to narrow the list of pathogens to a small group of suspected bacteria. It is not clear, however, how much of the destruction of periodontal tissue is caused by the direct effects of the bacteria and how much by indirect effects mediated by the host's reaction to the bacteria.
The nature of increased luminol-enhanced chemiluminescence (CL) in peripheral polymorphonuclear neutrophils (PMN) in juvenile periodontitis is of pathophysiological interest and may serve as a model for tissue damage caused by granulocytes. Activation of PMNs by opsonized Staphylococcus aureus was compared with that of Actinobacillus actinomycetemcomitans and Bacteroides gingivalis, regarded as being more specific for juvenile periodontitis. The CL was higher in the PMNs from the patients, independently of bacteria and mode of opsonization (autologous serum or gamma-globulin). Fc-gamma-RIII assessed on the washed fragments from peripheral PMNs was significantly (p < or = 0.005) lower in the patients with juvenile periodontitis than in their pair-matched healthy controls, while the content of fibronectin was higher (p < or = 0.032). However, when Fc-gamma-RIII and fibronectin were studied in fresh PMNs by flow cytometry no difference could be found between the two groups. The increased generation of CL of peripheral PMNs found in patients with juvenile periodontitis seems to be independent of humoral factors and of bacterial species and may be related to the properties of the PMN cell membranes.
OBJECTIVE: Our aim was to compare the periodontal conditions in a group of juvenile idiopathic arthritis (JIA) patients with those in a control group of healthy subjects (CTR). MATERIAL AND METHODS: Thirty-two patients with JIA and 24 controls were selected. The measurements used to diagnose periodontal disease included plaque and bleeding scores, probing depths (PDs) and clinical attachment loss (CAL). Laboratory indicators of JIA activity included the erythrocyte sedimentation rate (ESR) and capsule-reactive protein (CRP). The Mann-Whitney test was used to evaluate the data (alpha = 0.05). RESULTS: The mean ages were 15.9 (+/- 2.7) years and 14.7 (+/- 2.3) years for groups JIA and CTR, respectively. The median ESR was 42 mm/h 13 mm/h in the CTR group (p = 0.032) and the median CRP was 1.9 and 0.4 mg/l, respectively (p = 0.001). The prevalence of patients with a proximal attachment loss of 2mm or more in the JIA group was 25% and in controls it was 4.2%. The mean percentages of visible plaque and marginal bleeding were similar in the JIA (54 +/- 22 and 30 +/- 16, respectively) and CTR groups (44 +/- 18 and 29 +/- 11, respectively). The mean percentages of sites with PD > or = 4 mm were significantly higher in the JIA group (3 +/- 4.7) than in the CTR group (0.4 +/- 1.7) (p = 0.012). The mean percentages of sites with proximal CAL > or = 2 mm were 0.7 (+/- 1.4) in the JIA group and 0.001 (+/- 0.2) in the CTR group (p = 0.022). CONCLUSION: Adolescents with JIA present more periodontal attachment loss than healthy controls, in spite of similar plaque and marginal bleeding levels.
Accelerated periodontal tissue destruction in patients with labile insulin-dependent diabetes mellitus (DM) and localized juvenile periodontitis (LJP) has been suggested to be related to functional abnormalities of neutrophils. We have recently found that collagenase in gingival crevicular fluid (GCF) of adult periodontitis patients is primarily derived from neutrophils and that neutrophil collagenase activity is more sensitive to inhibition by tetracyclines than collagenase produced by fibroblasts. This study is to characterize the cellular sources, activation and inhibition of collagenase in GCF of DM patients and to compare it with collagenase in LJP GCF. We found differences which may have therapeutic implications. Specific doxycycline inhibition tests revealed that GCF collagenase in DM is derived from neutrophils, whereas the enzyme in LJP originates primarily from fibroblasts. Oxidant, sodium hypochlorite, activated efficiently GCF collagenase of DM but not LJP patients. In contrast, plasmin activated LJP GCF collagenase but not that of DM patients. In GCF of DM patients 50-60% of collagenase existed in an active form, whereas in LJP GCF, the enzyme was almost completely in a latent form. The results suggest that collagenase in GCF of periodontitis patients with labile DM is primarily derived from neutrophils and that tetracycline therapy may be an effective adjunct in treatment aimed at controlling the periodontal breakdown in these patients. On the other hand, in LJP the anti-collagenase property of tetracyclines may be less important for control of periodontal tissue destruction because of the tetracycline-resistance of fibroblast collagenase.
OBJECTIVE: The aim of this study was to examine the longitudinal association of selected non-immune anti-microbial host factors (peroxidases, lysozyme and lactoferrin) to the localized juvenile periodontitis (LJP) disease status. MATERIALS AND METHODS: Peroxidases, lysozyme and lactoferrin were quantitated from seven patients with LJP before and after periodontal therapy. Analyses were performed from simultaneously collected samples of peripheral blood polymorphonuclear leukocytes (PMNs), gingival crevicular fluid (GCF from diseased sites) and paraffin-stimulated whole saliva. Similar assays were done also from seven periodontally healthy controls. RESULTS: During untreated phase of LJP myeloperoxidase, lysozyme and lactoferrin concentrations were remarkably elevated in peripheral blood PMNs, also reflected in their high concentrations in GCF. All these values normalised with respect to healthy controls during the periodontal therapy. No similar longitudinal changes were seen in whole saliva but during therapy salivary peroxidase concentrations declined below the control values, in accordance with our previous observations in parotid saliva samples of LJP patients. CONCLUSIONS: In LJP the concentrations of lysozyme, lactoferrin and myeloperoxidase are significantly elevated in peripheral blood PMNs, also reflected in GCF. During periodontal therapy these values decline and approach those observed in healthy controls. No similar changes are seen in stimulated whole saliva.
In search of direct in vivo evidence of matrix metalloproteinases (MMPs) in periodontal tissue destruction, we studied the presence and localization of MMP-9 and neutrophil gelatinase-associated lipocalin (NGAL) in adult periodontitis (AP) and localized juvenile periodontitis (LJP) gingival tissue specimens by immunohistochemistry, and the activities of gelatinases by Western blot, enzymography, and activity measurements, using radioactive gelatin as substrate in gingival crevicular fluid (GCF) and saliva. In gingival tissue obtained from AP and LJP patients, polymorphonuclear leukocyte (PMN) 92-kDa MMP-9 and NGAL were seen in the connective tissue, but both the sulcular and the oral epithelia were consistently negative. Whereas PMNs located in the gingival blood vessels showed strictly cytoplasmic MMP-9 and NGAL immunoreactivities, in the case of PMN extravasation the staining reactions extended extracellularly. Gelatinase activities consisting mainly of 92-kDa gelatinase were increased in AP GCF relative to LJP GCF and periodontally healthy control GCF. Western blot with specific anti-NGAL antibodies revealed the presence of 25-kDa NGAL and its high-molecular-weight forms in AP and LJP GCF and saliva and in culture medium of oral keratinocytes, but not in gingival fibroblast culture medium. We conclude that extravasated degranulating PMNs are the major source of MMP-9 and NGAL in periodontitis gingiva, GCF, and saliva.
BACKGROUND: Patients with Kostmann syndrome (severe congenital neutropenia [SCN]) typically normalize their absolute neutrophil count (ANC) upon granulocyte colony-stimulating factor (G-CSF) therapy. However, although they no longer experience life-threatening bacterial infections, they frequently still have recurrent gingivitis and even severe periodontitis, often starting in early childhood. METHODS: We studied the periodontal disease in the four surviving patients belonging to the family originally described by Kostmann. Their odontological records, x-rays, color photos, bacterial cultures, serum antibodies to oral bacteria, and histopathological examinations were reviewed. The data were also correlated to previous investigations on their antibacterial peptides and molecular biology. RESULTS: Three patients had periodontal disease, despite normal ANC and professional dental care, and had neutrophils deficient in antibacterial peptides. One of these patients also had a heterozygous mutation in the neutrophil elastase gene, had severe periodontal disease and overgrowth of the periodontal pathogen Actinobacillus actinomycetemcomitans in the dental flora, and 15 permanent teeth had been extracted by the age of 27. One bone marrow-transplanted patient had no periodontal disease. CONCLUSIONS: Normalized ANC levels are not sufficient to maintain normal oral health in SCN patients, and because neutrophils are important for first-line defense and innate immunity, the deficiency of the antibacterial peptide LL-37 probably explains their chronic periodontal disease. Professional dental care is still important for SCN patients, despite treatment with G-CSF and normal ANC levels. Whether antibacterial peptides play a role in the pathogenesis of periodontitis in other patients remains to be elucidated.
BACKGROUND: A subcategory of chronic neutropenia is chronic benign neutropenia, which is characterized by a prolonged non-cyclic neutropenia as the sole abnormality, with no underlying disease to which the neutropenia can be attributed. Chronic neutropenia is defined as a low absolute neutrophil count for >6 months. In this presentation, periodontitis seems to be the sole manifestation of a juvenile patient with chronic benign neutropenia. A 7-year-old white male presented with periodontitis of the primary dentition and early tooth loss. His medical and dental history was otherwise unremarkable. Suspecting some systemic illness as the underlying cause, the patient was referred for a medical consultation and a series of blood tests. METHODS: Blood analyses included a complete blood count (CBC), sequential multiple analyzer 24 (SMA 24), glycated hemoglobin levels, and screening for anti-white blood cell antibodies. Blood levels of calcium, vitamin D, dihydroxyvitamin-D, phosphorus, and alkaline phosphatase were also measured. Liver function tests were performed. RESULTS: Following analysis of recent and previous blood test results, a diagnosis of chronic benign neutropenia was assigned. The patient's periodontal condition was treated with scaling and root planing, oral hygiene instruction, and antimicrobial mouthrinses. Three-month recall visits were recommended as a follow-up protocol. CONCLUSIONS: This case represents the importance of diagnosing periodontal disease as a possible indicator of underlying systemic disease. When a patient presents with an unusual, generalized form of periodontal disease, screening for systemic disorders is required, as the oral condition may be the first or only manifestation of a systemic abnormality. This case also illustrates the reason for the change in classification of such a condition to periodontitis as a manifestation of systemic disease. This condition was previously classified as prepubertal periodontitis, a disease diagnosis that focused on the patient's age at the onset of the disease rather than the etiology.
Actinobacillus actinomycetemcomitans and Capnocytophaga are subgingival bacteria that have correlation with juvenile periodontitis. Studies were carried out in a group of 20 patients with juvenile periodontitis before, after treatment by scaling, root planing, oral hygiene instruction and 20 patients with healthy gingiva as a control group. Gingival index, plaque index, pocket depth were measured. Subgingival bacteria were counted on selective media and compared by phase contrast microscopy. Before treatment all measurements in the patients and the control group were significantly different (P less than 0.05). In the patients before and after treatment all clinical measurements were significantly different (P less than 0.05) but the amount of A.actinomycetemcomitans and Capnocytophaga were not significantly different (P greater than 0.05). These results indicate that treatment of juvenile periodontitis by scaling, root planing and oral hygiene instruction improve the clinical measurements but are not effective in reducing proportions of subgingival bacteria.
HLA system plays an important role in the regulation of the immune response. Association between HLA genes and disease has been shown for several disorders, in particular auto-immune diseases. HLA system may also be associated with periodontal diseases. It has been suggested that HLA-A2 is related to resistance in juvenile periodontitis and A9 to susceptibility in juvenile periodontitis (JP) and rapidly progressive periodontitis (RPP). DR2, DR4 and DQw1 may also be susceptibility factors in JP and RPP. If implicated in periodontal diseases, HLA system may be associated with low or non-responsiveness to plaque bacterial antigens which could result in disease progression.
Pathophysiological features were studied on 7 patients with rapidly progressive periodontitis but without any evidence of systemic disease, to analyse the clinical pathogenesis. The patients consisted of 5 females, 2 males, between the ages of 32 and 42 years. All patients had severe and rapid alveolar bone destruction on the basis of radiographic measurement. Abnormal serum levels of IgG and IgM were detected in some patients. Higher IgG level was found in 4 patients and higher IgM level was found in 2 patients. The proportion of lymphocyte subsets was calculated in mononuclear cells from peripheral blood of patients. Higher OKT4/OKT8 ratio was found in all patients. The percentage of OKT4 positive cells in 2 patients was higher than that in normal subjects while the percentage of OKT8 positive cells in 4 patients was lower than that in the healthy controls. Microorganisms from periodontal pockets were examined in 5 patients. Bacteriodes was isolated in all 5 patients and Haemophilus actinomycetemcomitans in 2 patients.
The present study includes the clinical, microbiological and immunological examinations of 2 patients with post-juvenile periodontitis. Bacteroides intermedius was the predominant isolate from periodontal pockets with post-localized juvenile periodontitis. Bacteroides gingivalis, Bacteroides forsythus and Actinobacillus actinomycetemcomitans were detected in samples from periodontal pockets with post-generalized juvenile periodontitis. IgG antibody levels to B. gingivalis were significantly higher in the patients than these of periodontally healthy group. Spirochetes, including Treponema denticola, were found at very high frequencies in all samples from the patients.
Myeloperoxidase is an enzyme released by polymorphonuclear leukocytes which has been used, experimentally, as an indicator of periodontal disease activity when measured in gingival crevicular fluid. There are three myeloperoxidase isoforms: MPO I, MPO II and MPO III. We examined the activities of myeloperoxidase isoforms released by neutrophils in response to serum-opsonized Actinobacillus actinomycetemcomitans, Haemophilus aphrophilus, Eikenella corrodens, Capnocytophaga sputigena and Streptococcus sanguis. Isoform activities were determined using intermediate-pressure liquid chromatography and microenzyme assay. A. actinomycetemcomitans stimulated higher levels of myeloperoxidase release than any other oral bacteria unless pre-opsonized with serum (or protein-A-purified immunoglobulin) from an individual with localized juvenile periodontitis. Most oral bacteria stimulated the release of all myeloperoxidase isoforms with a profile enriched in MPO I and diminished in MPO III. Exceptionally, serum-opsonized A. actinomycetemcomitans stimulated myeloperoxidase isoform release in proportion to the neutrophil granule constituency with or without localized juvenile periodontitis serum pre-opsonization. Because myeloperoxidase isoform profiles reflect how neutrophils were stimulated, isoform analysis may refine future diagnostic tests based upon myeloperoxidase.
The purpose of the present study was to investigate the effect of mechanical oral hygiene procedures on bleeding on probing in relation to age and periodontal status. The study was carried out on 49 individuals divided into 7 experimental groups according to age and having been either treated for destructive periodontal disease or having an intact healthy periodontium. In order to eliminate any pre-existant gingival inflammation, all subjects received a carefully controlled oral hygiene program. At the start of the experiment, all subjects were instructed to abstain from oral hygiene procedures for 24 h. Thereafter, clinical baseline measurements were carried out, including bleeding on probing (BOP) using a standardized probing pressure. Next, all subjects cleaned their teeth according to their normal oral home care protocol using a multitufted toothbrush, toothpicks and interdental brushes. BOP scores were again assessed 30 min after completed tooth cleaning procedures. The results revealed a significant increase in BOP after the mechanical oral hygiene procedures in every individual in all experimental groups (p less than 0.05). Further analysis showed that the increase in BOP was independent of the periodontal status of the subjects. However the BOP scores after mechanical oral hygiene procedures were higher in the young age groups. It was concluded that the diagnostic predictability of BOP in the treatment of periodontal diseases might be affected by temporarily elevated BOP scores shortly after mechanical oral hygiene procedures.
The Papillon-Lefèvre syndrome (PLS) is a rare, autosomal recessive trait that is characterized by palmar plantar keratosis (PPK) and severe, early onset periodontitis, affecting both deciduous and permanent dentitions. The clinical presentation of PLS is variable; the disease occurs so infrequently as to limit clinical cases for study. The exception is a few families with extensive consanguinity in which numerous cases occur. Of particular interest to mapping the genetic origin of the syndrome is the co-expression of the major traits of hyperkeratosis and periodontitis, and their severity. In this paper, we report 2 families with multiple affected individuals from geographically remote areas. A large extended family, from the Cochin region of India, currently residing in Israel, in which there is documented consanguinity and a family from the southwest region of Germany. In each family, 1 individual presents with hyperkeratotic lesions with the complete absence of periodontal lesions. Further, the difference in severity of the hyperkeratotic lesions between families is marked, and one sibling in the German family expressed rapid, early onset periodontitis in the absence of PPK. The genetic nature and penetrance of the genetic defect are discussed.