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We consider a non-standard design for a fixed dental implant, incorporating a soft layer which simulates the presence of the periodontal ligament (PDL). Instead of being aimed at causing an a priori defined stress/strain field within the surrounding bone, upon loading, such a design simply tries to better reproduce the natural tooth-PDL configuration. To do this, the mechanical properties of the internal layer match those of the PDL, determined experimentally to be strongly nonlinear. Three-dimensional finite element analyses show that the presence of such a layer produces (i) a prosthesis mobility very similar to that of a healthy tooth, for several loading conditions, and (ii) a stress/strain distribution substantially different from that arising, upon loading, around a conventional implant. The lack of knowledge of the real mechanical fields existing, under loading, in the bone around a healthy tooth makes it very difficult to state that the stress distribution produced by the modified implant is "better" than that produced by the standard one. Nevertheless, the comparison of the results obtained here, with those of previous refined analyses of the tooth-PDL-bone system, indicates that the modified implant tends to produce a stress distribution in the bone, upon loading, closer to "natural" than that given by the standard one, within the limits imposed by the presence of threads coupling the implant with the bone. [ABSTRACT FROM AUTHOR]

Objective: To investigate the clinical features of burning mouth syndrome (BMS) in a large cohort of patients and to correlate them with the results of tongue biopsy., Methods: We screened 98 patients complaining of oral burning pain for at least 6 months. Forty-two patients were excluded after screening for contact sensitivity to dental materials, food allergies, tongue injuries, malignancies, connective tissue and metabolic disorders, oral infectious diseases, vitamin deficiencies, and other systemic diseases known to cause neuropathy. Fifty-six patients underwent neurologic examination and assessment of pain intensity, depression, anxiety, quality of sleep, and quality of life. Tongue biopsy with the quantification of epithelial nerve fibers (ENF) was performed in 51 patients., Results: Compared with 9 healthy participants (4.13+/-1.85 SD), epithelial innervation density was significantly reduced in 38 patients (1.35+/-1.46 SD; P<0.0001) and normal in 13 patients (6.1+/-2.19 SD). The clinical features differed in the two groups: patients with reduced ENF density complained of pain in the whole tongue, lips, hard palate, and alveolar ridges, reported dysgeusia and xerostomia in 29% of cases (P<0.001), and 24% of them were depressed. Patients with normal innervation complained of pain on the tip of the tongue, reported dysgeusia and xerostomia in 7.7% of cases, and 54% of them were depressed (P<0.017)., Discussion: The diagnostic criteria for BMS are not defined yet and the relationship with depression and anxiety is debated. We proposed a biopsy-supported approach for the diagnosis. Our study shows that BMS can present with two distinct clinical pictures and that tongue biopsy can contribute to the assessment of the diagnosis. Mood disorders occur frequently and should be considered when approaching patients and treatment options. These observations could help physicians in identifying patients with BMS and addressing them with the appropriate diagnostic work-up and treatment.

Using immunohistochemistry the presence of different dendritic cell (DC) subsets was analysed in 16 biopsies from patients with oral lichen planus (OLP). A significant increase of CD1a+/Langerin+ Langerhans cells, DC-SIGN+ DC and CD123+/BDCA2+ plasmacytoid DCs (PDCs) was found in the epithelium and in the stroma of OLP biopsies compared to normal oral mucosa. A proportion of DCs were mature DC-LAMP+ and expressed S100 or CD11c, typically found in the interdigitating DCs of nodal T-cell areas. Double staining revealed that mature DCs co-expressed CCR7, thus indicating the development of a nodal migratory phenotype upon maturation. Significant recruitment of PDCs producing IFN-alpha was demonstrated by the expression of MxA within the lichenoid inflammatory infiltrate and close cell-to-cell contacts between PDCs and mature DCs were observed, with a significant correlation between the numbers of these two populations. Moreover, PDCs were also found to contain Granzyme-B, an associated-cytotoxic granule protein, inducing target cell apoptosis. Taken together, these results suggest that PDCs may promote maturation of DCs and amplify the cytotoxicity of lymphoid cells. Finally, the recruitment of different subtypes of DC, such as Langerhans cells, stromal DC-SIGN+ DCs and PDCs, associated with a significant proportion of mature DCs, acquiring a CCR7+ 'migratory' phenotype, indicate that they may play a pivotal role in the development of the lichenoid inflammatory infiltrate that occurs typically in OLP.

We evaluated the expression of T cell-restricted intracellular antigen (Tia-1), granzyme B, and perforin by lymphocytes and the degree of epithelial apoptosis in oral and cutaneous lichen planus (LP) in 51 untreated cases, including 27 oral LP (OLP) and 24 cutaneous LP (CLP) cases. The number of total dermal-positive lymphocytes in OLP and CLP was similar, indicating similar activity of the inflammatory process. Intraepithelial Tia-1-positive, perforin-positive, and granzyme B-positive lymphoid cells were more numerous in OLP than in CLP (P < .05). The epithelial cell apoptotic index (AI) was increased significantly in OLP (P < .05), particularly in erosive-atrophic variants. A linear correlation between AI and the mean +/- SEM number of intraepithelial and dermal perforin+ cells (6.85 +/- 2.44 and 27.48 +/- 10.19, respectively), per 10 high-power fields for OLP and for CLP (1.17 +/- 0.88 and 10.42 +/- 5.74, respectively), was found (intraepithelial, r = 0.50; dermal, r = 0.51; P < .01). These data suggest a pivotal role for perforin in triggering epithelial cell apoptosis. The differences of infiltrating cytotoxic cells and related AI observed in OLP and CLP are in keeping with the clinical behaviors that distinguish these LP variants.

Lichen planus (LP) is a chronic inflammatory disorder involving cutaneous and mucosal surfaces, characterized by a T-cell-mediated immune response against epithelial cells, with persistent accumulation of T lymphocytes and epithelial cell damage. The mechanisms involved in this chronic inflammatory disease are largely unknown. A pivotal role in the pathogenesis of long-lasting inflammatory processes is played by the activation of nuclear factor kappa B (NF-kappaB), a primary transcription factor which upon translocation to the nucleus, binds to promoter regions of different genes encoding immune and pro-inflammatory mediators. Using immunohistochemistry, the present study analysed the expression of NF-kappaB in 25 cases of cutaneous LP (CLP) and 28 cases of oral LP (OLP) and correlated this with the recruitment of cytotoxic T-cells (expressing Tia-1 or perforin) in the inflammatory infiltrate. Nuclear NF-kappaB was expressed on basal and suprabasal keratinocytes in all cases of LP, while normal epithelium was consistently negative; OLP contained significantly higher numbers of NF-kappaB-positive keratinocytes than CLP (means: 89.32 versus 22.6; p<0.05). Furthermore, nuclear NF-kappaB expression by epithelial cells correlated with the amount of cytotoxic cell infiltration (p<0.02). These data suggest that increased NF-kappaB activity may represent the basis of maintenance of the inflammatory response. The differences observed between NF-kappaB expression on epithelial cells in OLP and CLP and their correlation with the degree of cytotoxic inflammatory infiltrate might explain the different clinical courses of the two variants of the disease, since OLP is typically more recalcitrant than CLP. As proposed for other chronic inflammatory disorders associated with increased NF-kappaB activity, the involvement of NF-kappaB in the pathogenesis of LP could be considered for selective therapeutic inhibitory targeting., (Copyright 2003 John Wiley & Sons, Ltd.)