ABSTRACT
PURPOSE: The host response to infection differs between peri-implantitis and periodontitis, but the mechanisms underlying these differences are not understood. In this study, the distribution of dendritic cell subpopulations in healthy peri-implant mucosa (HPIM) was compared to that of healthy gingiva (HG). MATERIALS AND METHODS: HPIM and HG specimens were obtained from nonsmoking, systemically healthy subjects. Immunohistochemistry was used to quantify the number of Langerhans cells (LCs) (CD1a+) and interstitial dendritic cells (IDCs) (factor XIIIa+) in the oral epithelium, sulcular/junctional epithelia, and lamina propria without inflammatory infiltration and with inflammatory infiltration. RESULTS: Fourteen HPIM and 13 HG specimens were obtained from subjects aged 29 to 55 years. The lamina propria of the HPIM had fewer LCs than that of the HG (HPIM: 7.99 ± 10.76, HG: 25.68 ± 16.98; P = .003). There was no significant difference in the number of CD1a+ cells in the oral epithelium or the sulcular/junctional epithelia between the HPIM and the HG (P ≥ .23). A greater number of IDCs was observed in the lamina propria with inflammatory infiltration of the HPIM compared to the HG (HPIM: 57.02 ± 35.70, HG: 33.89 ± 26.98; P = .06). CONCLUSIONS: In the lamina propria of HPIM, fewer LCs and more IDCs were observed. These differences may be associated with reduced stimulation of the innate and acquired immune responses initiated by LCs and the greater matrix remodeling of peri-implant tissue associated with IDCs.
Subject(s)
Dendritic Cells/cytology , Epithelial Attachment/cytology , Gingiva/cytology , Mucous Membrane/cytology , Adult , Antigens, CD1/analysis , Biomarkers/analysis , Cell Count , Dendritic Cells/immunology , Epithelial Attachment/immunology , Epithelium/immunology , Factor XIIIa/analysis , Female , Gingiva/immunology , Humans , Immunohistochemistry , Langerhans Cells/cytology , Langerhans Cells/immunology , Male , Middle Aged , Mucous Membrane/immunology , Periodontitis/immunology , Periodontitis/pathologyABSTRACT
AIM: To characterize the histologic and cellular response to A. actinomycetemcomitans (Aa) infection. MATERIAL & METHODS: Wistar rats infected with Aa were evaluated for antibody response, oral Aa colonization, loss of attachment, PMN recruitment, TNF-α in the junctional epithelium and connective tissue, osteoclasts and adaptive immune response in local lymph nodes at baseline and 4, 5 or 6 weeks after infection. Some groups were given antibacterial treatment at 4 weeks. RESULTS: An antibody response against Aa occurred within 4 weeks of infection, and 78% of inoculated rats had detectable Aa in the oral cavity (p < 0.05). Aa infection significantly increased loss of attachment that was reversed by antibacterial treatment (p < 0.05). TNF-α expression in the junctional epithelium followed the same pattern. Aa stimulated high osteoclast formation and TNF-α expression in the connective tissue (p < 0.05). PMN recruitment significantly increased after Aa infection (p < 0.05). Aa also increased the number of CD8(+) T cells (p < 0.05), but not CD4(+) T cells or regulatory T cells (Tregs) (p > 0.05). CONCLUSION: Aa infection stimulated a local response that increased numbers of PMNs and TNF-α expression in the junctional epithelium and loss of attachment. Both TNF-α expression in JE and loss of attachment was reversed by antibiotic treatment. Aa infection also increased TNF-α in the connective tissue, osteoclast numbers and CD8(+) T cells in lymph nodes. The results link Aa infection with important characteristics of periodontal destruction.
Subject(s)
Aggregatibacter actinomycetemcomitans/immunology , Aggressive Periodontitis/immunology , Aggressive Periodontitis/microbiology , Alveolar Bone Loss/immunology , Alveolar Bone Loss/microbiology , Periodontal Attachment Loss/immunology , Periodontal Attachment Loss/microbiology , Actinobacillus Infections/drug therapy , Aggressive Periodontitis/drug therapy , Alveolar Bone Loss/drug therapy , Ampicillin/therapeutic use , Animals , Anti-Bacterial Agents/therapeutic use , Antibodies, Bacterial/biosynthesis , Antibodies, Bacterial/blood , CD8-Positive T-Lymphocytes/immunology , Chemotaxis, Leukocyte , Disease Models, Animal , Epithelial Attachment/immunology , Kanamycin/therapeutic use , Monocytes/immunology , Neutrophil Activation , Osteoclasts/microbiology , Periodontal Attachment Loss/drug therapy , Rats , Rats, Wistar , Tumor Necrosis Factor-alpha/biosynthesisABSTRACT
An immunoperoxidase technique was used to compare the number of CD1a+ and factor XIIIa+ dendritic cells (DCs), and CD68+ Macrophages (M) in 30 gingival samples from subjects with clinically healthy periodontitium (HP) and 10 samples from subjects with drug-induced gingival enlargement (DIGE). Fewer CD1a+ and factor XIIIa+ DCs were found in areas with inflammatory infiltration (II) of the lamina propria (LP) in the group with immunosuppressed DIGE (IDIGE) compared to the group with HP. In the sulcular and junctional/pocket epithelia, the number of CD1a+ DCs was decreased in the group with IDIGE (p<0.05). There was a tendency toward a reduced number of CD1a+ DCs and CD68+ M in areas without inflammatory infiltrate of the LP in the group with IDIGE. The alterations in the number of antigen-presenting cells (APCs) may be the reason for the decreased periodontal inflammation and breakdown clinically observed in subjects who are immunosuppressed.