Is Periodontal and Peri- Implant Disease Associated with Fixed Partial Denture Use? A 25-year Prospective Case Series.

INTRODUCTION: The association of the periodontium with the fixed prosthesis is the basis of prosthetic rehabilitation. This prospective case series aimed to evaluate periodontal health through the relation between periodontal/peri-implant disease progression and the use of fixed partial dentures (FPDs). METHODS: Probing depth (PD), clinical attachment level (CAL), gingival index (GI), and plaque index (PI) on either teeth or implants were evaluated at up to 25-year follow-up and compared with the baseline. Statistical analysis was performed using the Kaplan-Meier test (p⟨0.05). RESULTS: The prospective evaluation showed that the patients maintained adequate periodontal health. Failure (severe periodontal stages) occurred in 12.5% of patients. The survival rate for 107 teeth/implants was 80.48%. The comparisons for clinical parameters revealed no statistically significant difference (p⟩ 0.05). At T1, the measurements for anterior and posterior regions, respectively, were PD =2.7mm and 3.1mm; CAL= 3.3mm and 3.6mm; GI=0.5 (both regions); and PI=0.79 and 0.62. Periodontal/peri-implant disease progression did not relate to the use of prostheses. CONCLUSIONS: Patients with more frequent follow-up appointments and lower GI and PI showed periodontal health for longer periods. Patients with different oral hygiene levels present different periodontal disease progression. Periodic hygiene control and motivation are vital factors for extensive oral rehabilitation success.

Lacaziosis-like disease in Tursiops truncatus from Brazil: a histopathological and immunohistochemical approach

ABSTRACT: Cetacean lacaziosis-like disease or lobomycosis-like disease (LLD) is a chronic skin condition caused by a non-cultivable yeast of the order Onygenales, which also includes Lacazia loboi, as well as Paracoccidioides brasiliensis and P. lutzii, respectively responsible for lacaziosis and paracoccidioidomycosis in humans. Complete identification and phylogenetic classification of the LLD etiological agent still needs to be elucidated, but preliminary phylogenetic analyses have shown a closer relationship of the LLD agent to Paracoccidioides spp. than to L. loboi. Cases of LLD in South American cetaceans based on photographic identification have been reported; however, to date, only 3 histologically confirmed cases of LLD have been described. We evaluated multiple tissue samples from 4 Tursiops truncatus stranded in the states of Santa Catarina (n = 3) and Rio Grande do Sul (n = 1), southern Brazil. Macroscopically, all animals presented lesions consistent with LLD. Hematoxylin-eosin, periodic acid-Schiff, Grocott's methenamine silver, and Mayer's mucicarmin stains were used for histological evaluation. Microscopically, numerous refractile yeasts (4-9 µm in diameter) were observed in skin samples (4/4), and for the first time in dolphins, also in a skeletal muscle abscess (1/4). Immunohistochemistry using anti-P. brasiliensis glycoprotein gp43 as a primary antibody, which is known to cross-react with L. loboi and the LLD agent, was performed and results were positive in all 4 cases. We describe 3 new cases of LLD in cetaceans based on histopathology and immunohistochemistry. This is the first report of LLD in the muscle of cetaceans.

A novel DFNB1 deletion allele supports the existence of a distant cis-regulatory region that controls GJB2 and GJB6 expression.

Eleven affected members of a large German-American family segregating recessively inherited, congenital, non-syndromic sensorineural hearing loss (SNHL) were found to be homozygous for the common 35delG mutation of GJB2, the gene encoding the gap junction protein Connexin 26. Surprisingly, four additional family members with bilateral profound SNHL carried only a single 35delG mutation. Previously, we demonstrated reduced expression of both GJB2 and GJB6 mRNA from the allele carried in trans with that bearing the 35delG mutation in these four persons. Using array comparative genome hybridization (array CGH), we have now identified on this allele a deletion of 131.4 kb whose proximal breakpoint lies more than 100 kb upstream of the transcriptional start sites of GJB2 and GJB6. This deletion, del(chr13:19,837,344-19,968,698), segregates as a completely penetrant DFNB1 allele in this family. It is not present in 528 persons with SNHL and monoallelic mutation of GJB2 or GJB6, and we have not identified any other candidate pathogenic copy number variation by arrayCGH in a subset of 10 such persons. Characterization of distant GJB2/GJB6 cis-regulatory regions evidenced by this allele may be required to find the 'missing' DFNB1 mutations that are believed to exist.