ABSTRACT
Periodontitis is an infectious and inflammatory disease associated with significant loss of alveolar crest and soft tissue attached to the teeth. Chitosan and hydroxyapatite are biomaterials used for bone tissue repair because of their biodegradability and biocompatibility in nature. The present study evaluated the effects of chitosan (CH) in combination with hydroxyapatite (HAP) to promote alveolar bone growth. A chitosan implant mixed with hydroxyapatite was implanted into the affected area of 9 patients suffering chronic periodontitis. Patients were evaluated through X-ray images and a millimetric slide over a one year period. The application of CH/HAP produced an average alveolar bone growth of 5.77 mm (±1.87 mm). At the onset of the study, the dental pocket exhibited a depth level (DPDL) of 8.66 mm and decreased to 3.55 mm one year after the implant. Tooth mobility grade was 2.44 mm at the onset and 0.8 mm at the end of the study with a significant difference of p < 0.001. Moreover, the bone density in the affected areas was similar to the density of the bone adjacent to it. This result was confirmed with the software implant viewer from Anne Solutions Company. In conclusion, the CH/HAP implant promoted alveolar bone growth in periodontitis patients.
ABSTRACT
BACKGROUND: The anti-inflammatory effect of the cerebral dopamine neurotrophic factor (CDNF) was shown recently in primary glial cell cultures, yet such effect remains unknown both in vivo and in 6-hydroxydopamine (6-OHDA) models of Parkinson's disease (PD). We addressed this issue by performing an intranigral transfection of the human CDNF (hCDNF) gene in the critical period of inflammation after a single intrastriatal 6-OHDA injection in the rat. METHODS: At day 15 after lesion, the plasmids p3xNBRE-hCDNF or p3xNBRE-EGFP, coding for enhanced green florescent protein (EGFP), were transfected into the rat substantia nigra (SN) using neurotensin (NTS)-polyplex. At day 15 post-transfection, we measured nitrite and lipoperoxide levels in the SN. We used ELISA to quantify the levels of TNF-α, IL-1ß, IL-6, endogenous rat CDNF (rCDNF) and hCDNF. We also used qRT-PCR to measure rCDNF and hCDNF transcripts, and immunofluorescence assays to evaluate iNOS, CDNF and glial cells (microglia, astrocytes and Neuron/Glial type 2 (NG2) cells). Intact SNs were additional controls. RESULTS: In the SN, 6-OHDA triggered nitrosative stress, increased inflammatory cytokines levels, and activated the multipotent progenitor NG2 cells, which convert into astrocytes to produce rCDNF. In comparison with the hemiparkinsonian rats that were transfected with the EGFP gene or without transfection, 6-OHDA treatment and p3xNBRE-hCDNF transfection increased the conversion of NG2 cells into astrocytes resulting in 4-fold increase in the rCDNF protein levels. The overexpressed CDNF reduced nitrosative stress, glial markers and IL-6 levels in the SN, but not TNF-α and IL-1ß levels. CONCLUSION: Our results show the anti-inflammatory effect of CDNF in a 6-OHDA rat of Parkinson's disease. Our results also suggest the possible participation of TNF-α, IL-1ß and IL-6 in rCDNF production by astrocytes, supporting their anti-inflammatory role.
