The plasma cell at the advancing front of the lesion in chronic periodontitis

This study analyses the ultrastructure of the plasma cell population of periodontitis-affected soft tissue close to the advancing front of interdental lesions. Biopsies from 20 patients and 3 control volunteers were examined: 5 with treated adult periodontitis (AP), 5 with untreated AP, 5 with treated juvenile or post-juvenile periodontitis (JP) and 5 with untreated JP. Plasma cell (PC) counts increased significantly (p less than 0.05) with lesion severity. They were absent from epithelium and sparse in the clinically healthy control specimens. Degenerate PC tended to be more numerous within JP tissue but differences were not significant (p greater than 0.05) when compared to AP. Intact plasma cells were never seen within JP superficial connective tissue. Russell bodies were small and few in number. The presence of degenerated plasma cells indicated normal formation and release of immunoglobulins within the tissues of AP and JP. Increased counts of degenerate PC and tissue destruction in JP suggested a correlation, possibly attributable to anti-collagen antibody secretion.     

Comparison of scanning and transmission electron microscopy of the epithelial pocket wall in juvenile and adult periodontitis

Using scanning (SEM) and transmission (TEM) electron microscopy, this study compared fine structural features of the pocket walls in both juvenile and adult periodontitis (JP and AP, respectively) in 40 cases. Gingiva was also obtained from a control group consisting of periodontally noninvolved teeth. Clinical parameters were assessed in both JP and AP patients as well as in controls. Clinical findings showed low plaque accumulation, marked periodontal tissue destruction and less gingival inflammation in JP. Bone destruction and attachment loss were more marked in JP than in AP. AP had a higher plaque index and more evident gingival inflammation. SEM observations of JP as compared to AP showed gross distortions in pocket walls, an increased beaded appearance of microridges, and separation between pocket epithelial cells. TEM showed partially desquamated and separated superficial epithelial cells, but only in JP were fine granular precipitates observed in the intercellular spaces. The observations demonstrated structural features indicative of more prominent degenerative changes in JP than in AP. Also, these features were coincidental with a higher plaque index in AP than in JP, where clinical features (including a low plaque index) were not proportional to the epithelial destructive changes present.     

Bacterial penetration of the pocket tissues in juvenile/postjuvenile periodontitis after the presurgical oral hygiene phase

Previous ultrastructural investigations of untreated sites of both adult and juvenile periodontitis have shown bacteria within the periodontal soft tissues. In the present study biopsies of the soft tissue walls of deep pockets from seven patients with juvenile (JP) or postjuvenile periodontitis (PJP) were removed at the end of the presurgical oral hygiene phase of treatment and examined in the transmission electron microscope. Bacteria were sparse, regardless of the level of tissue breakdown, both on the surface and within the superficial layers of the epithelium, deep to the basement membrane and throughout the underlying connective tissue. Of the 140 blocks from 20 biopsies, only two revealed intratissue accumulations of microorganisms. The organisms observed were gram-positive or gram-negative and appeared to be exclusively coccoid or rod-shaped. It is suggested that the reduced tissue content of bacteria reflects the establishment of adequate oral hygiene. Evidently either the tissue content of bacteria is less than has been reported previously or the host response is able to cope with residual bacteria that have penetrated the soft tissue.     

牙龈上皮中的中性白细胞和单核细胞

本研究对健康龈（Ｈ）、边缘性龈炎（Ｇ）、青少年牙周炎（ＪＰ）和成人牙周炎（ＡＰ）牙龈上皮内的中性白细胞（ＰＭＮ）和单核细胞及龈下菌进行了定量观察，并分析了它们之间的关系。结果表明，ＪＰ组袋上皮和表面上皮内的ＰＭＮ显著低于Ｇ组和ＡＰ组。ＡＰ组的ＰＭＮ数均明显高于其它三个组。直线相关分析表明，沟（袋）上皮ＰＭＮ数与龈下能动菌％呈正相关（ｒ＝０．５３６．Ｐ＜０．０１）。单核／吞噬细胞用ＮＡＥ方法显示主要位于结合上皮和袋上皮深处，三个炎症组的数目均高于健康组，而这些部位未见郎格罕氏细胞，可能此处的单核细胞替代了郎格罕氏细胞的功能。     

Cell division, synthetic capacity and apoptosis in periodontal lesions analysed by in situ hybridisation and immunohistochemistry

In this study, we investigated the synthetic and proliferative activity of infiltrating mononuclear cells in sections of granulation tissue from periodontitis lesions in both adult periodontitis (AP) and early onset periodontitis (EOP) patients. We also investigated the role of apoptosis in the remodelling of the inflamed tissue. We utilised a Ki-67 antigen specific antibody and a histone messenger RNA (mRNA) probe to detect cells undergoing cell division in the sections. Oligonucleotide probes for 28S ribosomal RNA and for the detection of poly A mRNA were utilised to detect cells with synthetic capacity. Apoptosis was determined using terminal transferase labelling of fragmented DNA with Biotin labelled dUTP. Biopsies of granulation tissue were obtained from 9 AP patients, from 10 EOP patients and for comparative purposes, biopsies of gingival tissue from 4 patients with AP. There were no differences regarding the relative proportions of cells with synthetic capacity or in the numbers of dividing cells in the periodontitis tissue sections. However, we observed an increase in the number of dividing cells in the AP granulation tissues compared to the AP gingival sections and that these cells were predominantly fibroblast like in appearance. Apoptotic cells consisted mainly of connective tissue cells; mainly fibroblasts with few if any leukocytes being apoptotic other than polymorphonuclear leukocytes. Only a few cyto-phagocytic macrophages were ever observed in the gingival and granulation tissues. We conclude that the turnover of infiltrating leukocytes in inflamed periodontal tissue is low, that they probably arrive at this site by recruitment from distant lymph nodes, and that neither cell division nor programmed cell death significantly alter the numbers of inflammatory cells. On the other hand, fibroblast apoptosis and cell division occur within the periodontium as these are typical processes in the normal turnover and remodelling of these tissues.     

Bacterial invasion of the periodontium; an important factor in the pathogenesis of periodontitis?

Abstract Tissue samples from 2 humans suffering from severe periodontitis were investigated by transmission electron microscopy. Confirming earlier observations in gnotobiotic rats, bacteria were found in various regions of gingival tissues. We observed bacteria invading the pocket epithelium, the underlying connective tissue, and microorganisms were also present deep in the connective tissue. The bacterial invasion of the periodontium was accompanied by different stages of tissue degradation. Various morphologically distinct types of Gram-negative and Gram-positive bacteria were evident. These microorganisms were found in the apical part of the periodontium. More coronally, a heavy infiltrate consisting predominantly of plasma cells was present. It is suggested that bacteria cannot invade regions of connective tissue protected by a massive cellular infiltrate. It seems that they rather circumvent this strong defense by penetrating more apically through the pocket epithelium while producing as camouflage leucochemophobic compounds which paralyze the chemotactically regulated mobile defense. It seems to us that bacterial invasion is a consistent feature of advanced periodontitis, leading to focal necrosis or microabscesses, and may well explain the cylic nature of this disease.     

Ultrastructure of the periodontal lesion in a case of Papillon-Lefèvre syndronne (PLS)

Abstract In this study, 11 permanent teeth and their associated soft tissues from an 11-year-old boy with PLS were examined. Plaque, cementum and periodontal tissues were examitied by scanning (SEM) and transmission electron microscopy (TEM), Except for depressed lymphocyte transformation, there were no abnormal haematological data. Local findings included abnormally thin cementum, extensive destruction of the periodontal ligament were still attached to the root, and severe inflammation of the soft tissues. Few bacteria were found in any of the soft tissue layers. The apical border plaque was restricted to gram- cocci and rods. The features observed in this case of PLS may indicate primary defects of cementum or ligament attachment, or disruption of fibroblast and cementoblast function due to the rapid advance of the disease process. Lack of bacterial invasion in the pocket soft tissue casts doubt on its involvement in the present case of severe periodontitis. The restricted range of morphotypes observed suggests a limited range of associated organisms. Further research is required to clarify the rôle of the host response and to identify the organisms involved.     

Local immunoglobulin synthesis in juvenile and adult periodontitis

Local immunoglobulin synthesis by the gingival plasma cells in 5 patients with juvenile periodontitis (JP) was compared to that in 5 patients with adult periodontitis (AP). The peroxidase-antiperoxidase method was used with specific antisera to alpha, gamma, and mu heavy chains and kappa and lambda light chains. The following relative distribution of plasma cells in JP/AP was found: IgA 22.7/19.5, IgG 75.6/78.5 IgM 1.7/2.0, kappa 55.5/53.5 and lambda 44.5/46.5, calculated as a % of their sum, indicating that the relative distribution of the different immunoglobulin chains was similar in both patient groups. The ratio light:heavy chains was 1.78 in JP and 1.72 in AP. The ratio kappa:lambda was 1.28 in JP and 1.17 in AP, similar to the known free kappa:free lambda chain ratio in normal serum (1.2). This indicates that the excessive staining for light chains is caused by a physiological overproduction of light chains rather than a pathological imbalance in the synthesis of immunoglobulins.     

Relative proportions of mononuclear cell types in periodontal lesions analyzed by immunohistochemistry

In this study, we investigated the relative proportions of infiltrating mononuclear inflammatory cells in sections of granulation tissue from periodontitis lesions in both adult periodontitis (AP) and early onset periodontitis (EOP) patients. We utilised a set of cluster of differentiation (CD) antigen-specific monoclonal antibodies to detect different cell types within the tissues. These included anti-CD 20 (B cells), anti-CD 3 (pan T cells) and anti-CD 45RO (memory T cells), anti-CD 4 (helper T cells) anti-CD 8 (suppressor T cells) and anti-CD 68 (monocyte/macrophage). Biopsies of granulation tissue were obtained from 9 patients with adult periodontitis (AP), from 10 patients with early onset periodontitis (EOP) and for comparative purposes, biopsies of gingival tissue from 4 patients with AP. A significantly greater number of T cells (p < 0.05) were observed in EOP and gingival sections than in AP sections. In addition, a greater number of B cells were observed in the granulation tissues than in the gingiva (p < 0.05). The relative numbers of B cells (CD 20). T cells (CD 3) and macrophages (CD 68) were expressed as a percentage of their combined total for each of the patient groups and indicated that the proportion of B lymphocytes was greater in AP sections than in EOP or gingival sections (p < 0.02). The proportion of T cells was lower in the AP periodontitis sections than in the EOP periodontitis sections (p < 0.05). There were no significant differences in the proportion of macrophages between the 3 categories of tissue specimens. The relative ratios of B cells (CD 20) to T cells (CD 3) and B cells (CD 20) to memory T cells (CD 45RO) and macrophages (CD 68) to T cells (CD 3) and memory T cells (CD 45RO) were analyzed and indicated that there was a significant increase in the B to T cell ratio in AP sections compared to EOP and gingival sections (p < 0.02). There was also a significant increase in the macrophage to T cell ratio in AP sections as indicated by CD 68 to CD 3 ratios (p < 0.05). There were no differences regarding the relative proportions of memory T cells or in the ratios of CD 4+ to CD 8+ T cells in the different disease categories. In conclusion, these differences in the relative proportions of B cells, T cells and macrophages may reflect a difference in the immunopathology of AP and EOP.     

T cells and T-cell subsets in periodontal diseases

Acetone-fixed cryostat gingival tissue sections from marginal gingivitis (MG), juvenile periodontitis (JP), adult periodontitis (AP) patients and clinically healthy subjects (H) were immunohistochemically stained with monoclonal antibodies to aid in identification and quantification of T cells and T-cell subsets in the inflammatory infiltrates. T cells were present in all specimens studied. The number of T cells in the connective tissue (CT) zone of AP was much greater than in any other groups. The amounts of T cells in oral epithelium and sulcular (pocket) epithelium zones of diseased groups were larger than in the healthy group. There was a significant positive correlation between the number of T cells and the percentage of infiltrated connective tissue. While there were no significant differences between the mean ratios of T-helper/T-suppressor cells from diseased and healthy tissues, large individual variance existed in the three diseased groups. The existence of a high or low T4/T8 ratio in inflamed gingiva might be related to an abnormal immunoregulation.     

Bacterial invasion of periodontal tissues in advanced periodontitis in humans

Bacterial invasion of the pocket epithelium and underlying connective tissue was found in seven cases of advanced human periodontitis. Four cases showed invasion of the epithelium as well as the connective tissue while in the other three cases bacterial invasion was limited to the pocket epithelium. The microorganisms observed included cocci, rods, filaments, fusiforms and spirochetes and these were morphologically similar to those observed in the apical zone of the subgingival plaque. Most bacteria showed typical Gram-negative cell walls. Bacteria were seen in enlarged epithelial intercellular spaces and among debris of disintegrated epithelial cells. In the connective tissue the bacteria were seen among remnants of collagen fibers and degenerated fibroblasts. Identification of the invading microorganisms may assist in understanding the pathogenesis of chronic periodontitis.     

Chemotactic response of neutrophil polymorphonuclear leukocytes in juvenile periodontitis measured by the Leading Front method

Abstract – Previous studies have implied that chemotaxis defects, of neutrophil polymorphonuclear leukocytes (PMNs) can be found in approximately 75% of patients with juvenile periodontitis (JP). In the present study, the Leading Front (LF) method was used to study whether the chemotactic response of PMNs from JP-patients differed from that of adult periodontitis (AP) patients and periodontally healthy control individuals (C). Sixteen JP-patients, 21 AP-patients, and 13 C-individuals were studied. PMNs from each individual, and from a daily reference person were tested against three chemoattractants (N-f-Met-Leu-Phe (FMLP), casein (CA), bacterial chemotactic factor (BCF)) and a neutral buffer (Gey's solution (GEY)). Regardless of the test solution a greater difference among individuals could be observed in the JP-group than in the other groups. Apart from this, there were no differences among the groups as regards CA, BCF, and GEY. However, with FMLP, the PMNs of the JP-group had a significantly greater migration distance as compared to the other groups. This finding can probably be ascribed to the fact that the LF method detects other aspects of the PMN response than do the methods used for earlier studies of JP. The finding, in this study, of an enhanced PMN response in JP as regards FMLP may be a reflection of the presence of a non-uniform PMN population whose composition in JP differs from that of the other groups.     

Immunohistological analysis of gingival lymphocytes in adult periodontitis

Inflammatory periodontal diseases are mediated by interactions between the dental plaque and the components of the host immune system. This study was designed to analyse the phenotypic properties of gingival lymphocytes in adult periodontitis. Biopsies were obtained from 12 patients and aged between 35 and 55 years. The tissues were processed for both histopathological and immunohistological examinations. Gingival tissue lymphocytes were identified using monoclonal and polyclonal antibodies with the immunoperoxidase technique. All specimens revealed a significant degree of CD3(+) cell infiltration beneath the pocket epithelium, which is located adjacent to the bacterial plaque, compared to that on the oral epithelial side. CD4(+) and CD8(+) cells were evenly distributed within these infiltrates. Numerous HLA-DR(+) cells were also noted. The majority of plasma cells in the central lamina propria bore IgG isotypes. These findings suggest that T-cell mediated regulatory mechanisms play an important role in the pathogenesis of adult periodontitis.     

Healing following surgical and non-surgical treatment of juvenile periodontitis

The patient sample used in the present study comprised 16 young individuals who were referred for treatment of advanced periodontal disease. Based upon the age of the patients and the location of the diseased sites, the patients were divided into 2 groups; a juvenile periodontitis group (JP) and a post-juvenile periodontitis group (post-JP). The patients in the JP group had periodontal lesions only at first molars and incisors. All 16 subjects were in excellent general health and none had been treated with antibiotics during a period of at least 12 months prior to the 1st examination. At a baseline examination and 6, 24 and 60 months after active therapy, the diseased sites were examined regarding plaque, gingivitis, probing pocket depths, probing attachment level, recession of the gingival margin and marginal alveolar bone level. Following a case presentation and instruction in proper oral hygiene measures, the 16 subjects were subjected to periodontal treatment, utilizing a split mouth design. By random selection, the diseased sites in one side of the jaws were treated by scaling and root planing in conjunction with a "modified Widman flap" procedure, while in the contralateral jaw quadrants treatment was restricted to scaling and root planing. During the 1st 6 months following active therapy, the patients were subjected to professional tooth cleaning once every 4 weeks. Subsequently, the interval between the recall appointment was 3 months. 2 years after treatment, this maintenance care program was terminated. A final examination was performed 5 years after therapy. None of the patients involved in the trial received antibiotic treatment during the 5 years of observation. The findings of the present study revealed that the response of the periodontal tissues to therapy, both in the JP and the post-JP group of patients, was almost identical to that found for similar types of treatment in patients with adult periodontitis. The re-examinations performed after 6, 24 and 60 months following active therapy of JP and post-JP lesions revealed that excision of the granulation tissue in conjunction with flap elevation did not enhance the degree of probing pocket depth reduction, probing attachment gain and bone fill that occurred following meticulous root surface instrumentation.     

Cathepsin B- and L-like activities at local gingival sites of chronic periodontitis patients

The cysteine proteinases cathepsins B and L have the potential to degrade connective tissue in chronic periodontitis and this may progress episodically at individual tooth sites. The activities of cathepsin B- and L-like proteinases in homogenised gingival tissue from control and periodontitis patients were measured biochemically using the selective peptide substrate Z-Phe-Arg-AFC and the selective cathepsin L inhibitor Z-Phe-Phe-CHN2. Each tooth site was divided, where appropriate, into gingival tissue and granulomata. These were assayed separately and the measurements related to the DNA and protein contents of the tissues. Enzyme activity in healthy control tissue was significantly lower than in diseased tissue. Enzyme activity in gingival tissue and total tissue from periodontitis patients decreased with increasing pocket depth, clinical attachment level, gingival index and bleeding index whilst cathepsin B activity in granulomata increased with increasing pocket depth and clinical attachment level but not with increasing gingival index or gingival bleeding index. Mean enzyme activity in gingival tissue was 1.6-2.8 times greater than in granulomata. Mean patient enzyme activity in diseased patients did not correlate positively with their mean pocket depth, clinical attachment level, gingival index or gingival bleeding index. These results are best explained by the probable cellular origins of the enzymes and the likely influence of their serum and tissue inhibitors during the disease process.     

Syndecan‐1 immunohistochemical expression in gingival tissues of chronic periodontitis patients correlated with various putative factors

Kotsovilis S, Tseleni‐Balafouta S, Charonis A, Fourmousis I, Nikolidakis D, Vrotsos JA. Syndecan‐1 immunohistochemical expression in gingival tissues of chronic periodontitis patients correlated with various putative factors. J Periodont Res 2010; 45: 520–531. © 2010 John Wiley & Sons A/S Background and Objective: Limited information is available on the expression and distribution of syndecan‐1 within human gingival tissues/cells and on putative factors that might affect its expression. Therefore, the objective of the present study was to determine immunohistochemically the expression and distribution of syndecan‐1 in the gingival tissues of patients with chronic periodontitis and to examine the correlation of syndecan‐1 expression with various putative factors (environmental, patient/systemic and local factors). Material and Methods: Gingival specimens were surgically excised from the area of the junctional/pocket epithelium (study group 1, including 30 chronic periodontitis patients) or the gingival oral epithelium (study group 2, comprising another 30 chronic periodontitis patients), adjacent to teeth with poor prognosis. Standard two‐step immunohistochemistry and semi‐quantitative evaluation of immunohistochemical staining were used to determine syndecan‐1 expression. Statistical analyses on the impact of various putative factors were performed. Results: In the junctional/pocket epithelium or the oral epithelium, syndecan‐1 expression was weak to moderate in the suprabasal and basal epithelial cells and absent to weak in the internal basal lamina, external basal lamina and gingival connective tissue matrix. Syndecan‐1 expression in the junctional/pocket epithelium was statistically significantly stronger than in the oral epithelium in inflammatory cells within the underlying gingival connective tissue (primarily plasma cells and lymphocytes) and in scattered fibroblast‐like cells. Conclusions: Syndecan‐1 expression in the junctional/pocket epithelium or the oral epithelium can exhibit a significant positive correlation with the severity/degree of histologically evaluated local gingival inflammation, but in general is not significantly correlated with age, smoking, full‐mouth and local clinical (probing pocket depth and clinical attachment level) and radiographical parameters (radiographical bone loss) of periodontal status.     

成人牙周炎患者全唾液IgA、IgG水平分析

目的：分析成人牙周炎患者全唾液IgA、IgG水平及其与临床牙周检测指标、指数之间的相关关系。方法：收集成人牙周炎患者25例,年龄、性别配对正常对照25例,采集非刺激性全唾液,对成人牙周炎组治疗前及牙周基础治疗后四周进行临床牙周检查与记录,并用自动分析仪测定唾液中IgA、IgG浓度。结果：成人牙周炎组牙周基础治疗后牙周袋探诊深度、牙龈指数、探诊出血显著下降;成人牙周炎组初诊唾液IgG浓度显著高于对照组,并与牙周袋探诊深度、牙龈指数间存在显著正相关关系,治疗后IgG浓度明显下降;初诊唾液IgG、IgA与基础治疗后四周牙周袋探诊深度变化绝对值间有显著正相关关系。结论：唾液IgG水平可以反映成人牙周炎炎症程度与牙周袋深度。唾液IgG、IgA水平可能成为牙周炎患者短期基础治疗预后判断的指标。     

Chemoluminescence generation and MTT dye reduction by polymorphonuclear leukocytes from periodontal disease patients

Alterations of polymorphonuclear leukocytes (PMNs) functions have been reported in patients with severe forms of some periodontal disease. In this study we evaluated the chemoluminescence generation and MTT dye reduction by human PMN in patients with juvenile periodontitis (JP), rapidly progressive periodontitis (RPP) and adult periodontitis (AP) during protein kinase C (PKC) activation or during the phagocytosis of opsonized zymosan. The results demonstrated that only PMNs of JP patients showed a decreased chemoluminescence generation and MTT dye reduction during the phagocytosis of opsonized zymosan (p < 0.05). The time to reach the maximal peak during the PKC activation on the chemoluminescence reaction was evaluated and JP PMNs patients demonstrated a depressed value (7.0 ± 0.4 min) compared with healthy volunteers (13.8 ± 0.5 min). The etiology and importance of such cellular alterations in the immunopathogenesis of the periodontal disease are discussed.     

Real-time polymerase chain reaction quantification of human cytomegalovirus and Epstein-Barr virus in periodontal pockets and the adjacent gingiva of periodontitis lesions

BACKGROUND: Genomic sequences of human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV), two herpesviruses, can frequently be detected in periodontal pockets of progressive periodontitis lesions, but the prevalence and load of the two viruses in gingival tissue are unknown. This study determined levels of HCMV and EBV DNA in the periodontal pocket and in the adjacent gingiva of periodontitis lesions using a real-time polymerase chain reaction (PCR) assay. MATERIAL AND METHODS: A total of 20 systemically healthy periodontitis patients participated in the study. Nine patients below 35 years of age were tentatively diagnosed as having aggressive (early onset) periodontitis, and 11 patients 36-56 years of age as having chronic (adult) periodontitis. Clinical parameters were evaluated using established methods. Using periodontal curettes, specimens were harvested from 6-10 mm periodontal pockets and from the adjacent inflamed periodontal pocket wall. A 5'-nuclease (TaqMan) real-time PCR assay was used to identify and quantify genomic copies of periodontal HCMV and EBV. RESULTS: HCMV DNA was detected in 78% of subgingival and 33% of gingival tissue samples from aggressive periodontitis lesions, but only in 46% of subgingival and 9% of gingival tissue samples from chronic periodontitis lesions. In aggressive periodontitis, HCMV subgingival and gingival tissue counts were positively correlated with periodontal pocket depth and probing attachment loss at sample sites (p6 mm, but none of 14 patients having mean pocket depth at sample teeth相似文献   

Increased rate of salivary epidermal growth factor secretion in patients with juvenile periodontitis

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.