Background: Little is known about the mechanisms of bacterial interaction with implant materials in the oral cavity. A correlation between plaque accumulation and progressive bone loss around implants has been reported. Bacterial adhesion shows a direct positive correlation with surface roughness. Other surface characteristics also seem to be extremely important with regard to plaque formation. Different adhesion affinities of bacteria have been reported for different materials. The aim of this study was to characterize the percentage of surface covered by bacteria on commercially pure titanium and zirconium oxide disks.Methods: Ten patients participated in this study. A removable acrylic device was adapted to the molar‐premolar region, and commercially pure titanium (control) and zirconium oxide (test) disks were glued to the buccal aspect of each device. The surface roughness of titanium and test specimens was similar. After 24 hours, all disks were removed and processed for scanning electron microscopy, for the evaluation of the portion of surface covered by bacteria.Results: In control specimens, the area covered by bacteria was 19.3% ± 2.9; in test specimens, the area was 12.1% ± 1.96. The disk surface covered by bacteria on test specimens was significantly lower than that of control specimens (P = 0.0001).Conclusion: Our results demonstrate that zirconium oxide may be a suitable material for manufacturing implant abutments with a low colonization potential. J Periodontol 2004;75:292‐296.

Background: Multiple sclerosis is a demyelinating disease mostly of autoimmune origin that affects and damages the central nervous system, leading to a disabling condition. The aim of the present study was to investigate whether administration of mesenchymal stem cells from human periodontal ligament (hPDLSCs) could ameliorate multiple sclerosis progression by exerting neuroprotective effects in an experimental model of autoimmune encephalomyelitis (EAE). Methods: EAE was induced by immunization with myelin oligodendroglial glycoprotein peptide (MOG)_35–55 in C57BL/6 mice. After immunization, mice were observed every 48 hours for signs of EAE and weight loss. At the onset of disease, approximately 14 days after immunization, EAE mice were subjected to a single intravenous injection of hPDLSCs (10⁶ cells/150 μl) into the tail vein. At the point of animal sacrifice on day 56 after EAE induction, spinal cord and brain tissues were collected in order to perform histological evaluation, immunohistochemistry and western blotting analysis. Results: Achieved results reveal that treatment with hPDLSCs may exert neuroprotective effects against EAE, diminishing both clinical signs and histological score typical of the disease (lymphocytic infiltration and demyelination) probably through the production of neurotrophic factors (results focused on brain-derived neurotrophic factor and nerve growth factor expression). Furthermore, administration of hPDLSCs modulates expression of inflammatory key markers (tumor necrosis factor-α, interleukin (IL)-1β, IL-10, glial fibrillary acidic protein, Nrf2 and Foxp3), the release of CD4 and CD8α T cells, and the triggering of apoptotic death pathway (data shown for cleaved caspase 3, p53 and p21). Conclusions: In light of the achieved results, transplantation of hPDLSCs may represent a putative novel and helpful tool for multiple sclerosis treatment. These cells could have considerable implication for future therapies for multiple sclerosis and this study may represent the starting point for further investigations.

Background: The aim of the present study in humans was to conduct a comparative immunohistochemical evaluation of vascular endothelial growth factor (VEGF) and nitric oxide synthase (NOS) expression, inflammatory infiltrate, proliferative activity expression, and microvessel density (MVD) in peri‐implant soft tissues of titanium and zirconium oxide healing caps.Methods: Five patients, three men and two women (aged 30 to 66 years; mean: 49 years), participated in this study. All patients received dental implants that were 3.8 mm in diameter and 11 mm in length. All implants were left to heal in a non‐submerged (single‐stage) mode. Healing caps (3.8 mm in diameter and 3.0 mm in height) were inserted in all implants. Half of the implants were supplied with standard, prefabricated caps of commercially pure titanium, whereas the other half were provided with test zirconium oxide caps. After a 6‐month healing period, a gingival biopsy was performed with a circular scalpel (5.5 mm in diameter) around the healing caps of both groups, without unscrewing or removing the healing caps. The dimensions of the gingival biopsies were 1.7 mm (5.5 − 3.8 mm) in thickness and 3 mm in height.Results: Statistically significant differences were found in the microvessel density between titanium and zirconium oxide healing caps and group II (P ≤0.0001). Statistically significant differences were likewise found in the low and high intensities of NOS1, NOS3, and VEGF (P ≤0.0001). In conclusion, the high intensity of NOS1, NOS3, and VEGF were mostly expressed in the titanium group, whereas the low intensity of NOS1, NOS3, and VEGF were mostly expressed in the zirconium oxide group.Conclusions: In our specimens, the inflammatory infiltrate was mostly present in the titanium specimens. Their extension was much larger than that of the zirconium oxide specimens. Higher values of MVD were observed in the titanium specimens (29.1 versus 15.8). In addition, a higher expression of VEGF intensity was observed in the peri‐implant tissues of titanium healing caps, whereas predominantly lower expressions of VEGF intensity were noted around the zirconium oxide healing caps. The Ki‐67 expression was higher in the titanium specimens. All these data revealed that the tissues around titanium healing caps underwent a higher rate of inflammation‐associated processes, most probably correlated to the higher inflammation processes observed in these tissues. A higher intensity expression of NOS1 and NOS3 was recorded in the tissues around titanium, whereas, on the contrary, a lower intensity of expression was found in the tissues around zirconium oxide specimens. These latter data indicate that the higher expression of these two mediators could be correlated to the higher amount of bacteria present around the titanium samples.

In recent years, several studies have suggested a strong association of microorganisms with several human cancers. Two periodontopathogenic species in particular have been mentioned frequently: Fusobacterium nucleatum (F. nucleatum) and Porphyromonas gingivalis. Chronic periodontal disease has been reported to be a risk factor for oral squamous cell carcinoma (OSCC), colorectal cancer (CRC) and pancreatic cancer. F. nucleatum is a Gram-negative anaerobic bacterium that lives in the oral cavity, urogenital, intestinal and upper digestive tract. It plays a significant role as a co-aggregation factor, with almost all bacterial species that participate in oral plaque formation acting as a bridge between early and late colonizers. F. nucleatum, gives an important inflammatory contribution to tumorigenesis progression and is associated with epithelial-derived malignancies, such as OSCC and CRC. F. nucleatum produces an adhesion protein, FadA, which binds to VE-cadherin on endothelial cells and to E-cadherins on epithelial cells. The last binding activates oncogenic pathways, such as Wnt/βcatenin, in oral and colorectal carcinogenesis. F. nucleatum also affects immune response because its Fap2 protein interacts with an immune receptor named TIGIT present on some T cells and natural killer cells inhibiting immune cells activities. Morover, F. nucleatum release outer membrane vesicles (OMVs), which induce the production of proinflammatory cytokines and initiating inflammation. F. nucleatum migrates from the oral cavity and reaches the colon hematogenously but it is not known if in the bloodstream it reaches the CRC as free, erythrocyte-bound bacteria or in OMV. F. nucleatum abundance in CRC tissue has been inversely correlated with overall survival (OS). The prevention and treatment of periodontal disease through the improvement of oral hygiene should be included in cancer prevention protocols. FadA virulence factors may also serve as novel targets for therapeutic intervention of oral and colorectal cancer.

Background: It has been hypothesized that a certain width of the peri‐implant mucosa is required to enable a proper epithelialconnective tissue attachment and, if this soft tissue dimension is not adequate, bone resorption will occur to ensure the establishment of attachment with an appropriate biological width. The reason for the accelerated bone loss around submerged 2‐piece implants in the first year after the restoration is not known, but one possibility is that the gap between components plays a role in this process. Recent studies have shown that for all 2‐part implants, the bone crest level changes appeared dependent on the location of the microgap.Methods: The aim of the present study was a retrospective histologic evaluation in monkeys of the bone response to implants inserted 1 to 2 mm above the alveolar crest (group 1, 15 implants), at the level of the alveolar crest (group 2, 12 implants), or 1 to 1.5 mm below the alveolar crest (group 3, 13 implants). These implants had been early loaded, immediately loaded, and inserted immediately postextraction.Results: In group 1, a 0.13 ± 0.12 mm bone increase in a coronal direction was seen. In group 2, a 2.1 ± 0.29 mm vertical bone loss was present. In group 3, a mean 3.6 ± 0.46 mm vertical bone loss extending in an apical direction was observed. Statistically significant differences were observed between all 3 groups.Conclusions: Our results confirm data published previously that if the microgap was moved coronally away from the alveolar crest, less bone loss would occur and if the microgap was moved apical to the alveolar crest, greater amounts of bone resorption were present. This remodeling is not dependent on early and immediate loading of the implants or on immediate postextraction insertion. J Periodontol 2003;74:346‐352.