Tumor necrosis factor (TNF)-alpha is a pro-inflammatory cytokine and crucial mediator in many aspects of immunity. Although several studies have shown that recurrent aphthous ulcers (RAU) can be prevented by treatment that prevents the synthesis of endogenous TNF-alpha little is known about the location and distribution of TNF-alpha-expressing cells at disease sites. The aim of the present work is, therefore, to investigate TNF-alpha and its cellular distribution in RAU lesions compared with those in induced oral traumatic ulcers (TUs). Twelve biopsies of RAU lesions of oral mucosa were obtained from 12 patients with RAU. They were compared to a control group consisting of ten samples of induced TUs. All samples were analyzed for TNF-alpha expression by using monoclonal mouse anti-human TNF-alpha antibody in avidin-biotin-peroxidase complex (ABC) staining. Results were quantified by a semi-automatic VIDAS image analysis system. TNF-alpha immunoreactivity was contained mainly in monocyte/macrophages and lymphocytes within the mononuclear inflammatory infiltrates. TNF-alpha was often seen in mast cells and vascular endothelial cells in connective tissue lateral to the inflammatory infiltrates. Interestingly, 32%-60% of the mononuclear cells were found to be TNF-alpha immunoreactive in RAU lesions. TNF-alpha containing cells were more numerous in aphthae (188+/-46 cells/0.2 mm2) compared with controls (52+/-14 cells/0.2 mm2, P<0.001). These findings suggest that RAU lesions are characterized by high expression of TNF-alpha. Because such expression occurred in the mononuclear inflammatory cells, mast cells and vascular endothelial cells, TNF-alpha, which is a major inflammatory mediator, may contribute to the activation and recruitment of leukocytes that are found in RAU lesions.

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Abstract— Tissue lesions from eight patients with recurrent oral ulcers (ROU) were subjected to detailed immunohistopathologic studies. In five patients, a specimen of an unaffected area from the opposite site was obtained. The main inflammatory cells in situ were CD3 positive T lymphocytes, with CD4 cells forming approximately half (range 30‐60%) and CD8 cells 20% (range 10‐30%) of all cells. CD19 positive B lymphocytes formed 5‐12% of all cells. Furthermore, 45% (range 15‐65%) of all lymphoid cells had signs of previous antigenous contact and had helper/inducer CDw29 type. Suppressor/inducer CD45R cells formed only about 20% (range 7‐50%) of all cells. Although this observation suggests involvement of antigen as a causative and/or triggering stimulus, elements of a non‐specific inflammatory response were observed as well. Endogenous peroxidase‐positive neutrophils were present at the ulcer site, and were occasionally observed intravascularly and in th extracellular matrix in areas characterized by inflammatory mononuclear cell infiltrates. Although the proportion of endogenous peroxidase‐positive, recently recruited monocytes was low, CD11b and nonspecific esterase‐positive mature tissue macrophages formed about 14% (range 5‐35%) of all inflammatory cells in situ, particularly at the periphery of the lymphoid cell infiltrates. Mast cells were also observed in all samples studied, forming 2‐5% of inflammatory cells in the richly vascularized connective tissue beneath the basement membrane. In the specimens from clinically unaffected areas, inflammatory cells were rare. Our observations stress the multifaceted nature and participation of multiple effector systems in the local tissue pathogenesis of ROU.

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Objective. The presence and spatial distribution of peptide-containing nerves in labial salivary glands from 10 Sjogren's syndrome patients were compared with those in salivary glands from 7 healthy controls.Methods. Results. Acini, intralobular ducts, small arteries, and postcapillary veins were richly innervated by VIP-IR fibers, whereas CPON-, CGRP-, and substance P-IR fibers were restricted to blood vessels. Peptide-containing nerves were found surrounding, but not in the middle of, the highly inflamed mononuclear cell areas.Conclusion. This topologic distribution suggests involvement of VIP-IR fibers in vascular, motor, and secretory components of the reflex salivary secretion, whereas the distribution and the vasoactive actions of CPON, CGRP, and substance P suggest a role in the regulation of the salivary gland circulation, and thus of transcapillary flow. Excessive release may contribute to a neurogenic inflammation. Local depletion and absence of trophic neuropeptide stimuli may contribute to acinar atrophy.Aside from Sjogren's syndrome, an autoimmune disease of unknown etiology characterized by keratoconjunctivitis sicca, xerostomia, and focal adenitis, psychogenic and iatrogenic factors are also common causes of "dry mouth." These factors relate, respectively, to inhibitory influences of higher central nervous system control on salivary nuclei and to peripheral anticholinergic effects, and thus illustrate the role of the autonomic nervous system in the control of reflex salivary flow. The sialopenia of Sjogren's syndrome, however, has been generally attributed to autoimmune destruction of the glandular parenchyma, the flow of saliva being roughly proportional to the mass of the secretory end-piece elements. More recently, it has become evident that in addition to the integrated vascular, motor, and secretory control of reflex salivary flow, the autonomic nervous system delivers trophic stimuli to parenchymal tissue ( 1 4 ) .

– Monoclonal anti‐CD4, anti‐CD8, and anti‐GD18 antibodies were applied in avidinbiotin‐peroxidase complex staining using a pre‐embedding immunoelectron microscopy technique. Although most of the local T cells in situ were of CD4+ subtype, local CD8+ cells generally had a lower nucleus/cytoplasm ratio and contained more cell organelles than CD4+ cells. This suggests a local activation of CD8+ subpopulation, rather than activation of the numerically predominant CD4+ cells. Topographical analysis disclosed that all lymphocytes, regardless of location, were CD18+ and that most of the CD8 + cells were located subbasally and intraepithelially, whereas CD4+ cells often occurred in small clusters deeper down in the subepithelial lymphocyte‐rich band. Furthermore, CD8+ cells were often in close contact with macrophages, whereas CD4+ cells were in some instances in direct contact with plasma cells. This indicates that CD4+ cells may be involved in T cell‐dependent B cell‐mediated immunoglobulin synthesis, whereas CD8+ cytotoxic lymphocytes and tissue macrophages may be involved in the local pathogenetic process leading to basement membrane alterations.

The records were analyzed of 106 patients with sports-related dental traumas treated in 1983 at the public oral surgery unit in Helsinki, Finland; 51 were examined six years after injury. The mean age was 11.8 years (range 7-24 years). The woman/man ratio was 1:3. In 39% of cases, the injuries had arisen from ice hockey or skating; 30% happened during school hours; 80% were uncomplicated crown fractures, concussions or subluxations. During the six-year follow-up, of 80 teeth in 51 patients, root resorption was found in 6 teeth (7.5%), periapical lesions were noted in 2 teeth (2.5%), and obliteration of the pulp was seen in 4 teeth (5%). Three teeth (3.7%) had suffered loss of vitality. The pulp had been extirpated in 13 of the traumatized teeth (16%). In all, 13.7% of the patients were found to have complications six years later. The results showed that long follow-up periods are needed after dental injury.