Impact of connective tissue graft thickness on surgical outcomes: A pilot randomized clinical trial.

BACKGROUND: The aim of this study was to compare thick versus thin connective tissue grafts (CTG) for the treatment of gingival recession, over a 3-month period. METHODS: Forty-two CTG procedures were performed on single tooth Miller Class I or II recession defects at either premolar or anterior sites in 30 individuals. Procedures were randomized (1:1 ratio) to CTG thickness of 1 or 2 mm (parallel group design). Primary outcomes were the change in the width of the zone of keratinized tissue and the amount of root coverage achieved 3 months postoperatively at the recipient site. Secondary outcomes included change in the thickness of keratinized tissue at 3 months and patient-reported outcomes, such as pain, bleeding, and swelling at both the recipient and donor sites at 1 week, 2 weeks, 1 month, and 3 months. RESULTS: No significant differences were found between the two groups for any of the primary or secondary outcomes. Mean root coverage achieved was 2.1 ± 0.2 mm in the 1-mm thick group and 2.5 ± 0.2 mm in the 2-mm thick group (P = 0.33). Keratinized tissue width was increased by 2.2 ± 0.2 mm in the 1-mm thick group and by 2.7 ± 0.3 mm in the 2-mm thick group (P = 0.18). Keratinized tissue thickness was increased by 1.0 ± 0.1 mm and by 1.2 ± 0.1 mm in the 1- and 2-mm thick groups, respectively (P = 0.09). CONCLUSION: Within the current study limitations, our results suggest that similar root coverage and increase in the width and thickness of keratinized tissue can be achieved at 3 months whether a 1- or 2-mm thick CTG is used.

The fidelity of HPV16 E1/E2-mediated DNA replication.

Human papillomaviruses (HPV) are causative agents in a variety of human diseases; for example over 99% of cervical carcinomas contain HPV DNA sequences. Often in cervical carcinoma the HPV genome is integrated into the host genome resulting in unregulated expression of the viral transforming proteins E6 and E7. Therefore viral integration is a step toward HPV-induced carcinogenesis. Integration of the HPV genome could occur following double-strand DNA breaks that could arise during viral DNA replication. We investigated the fidelity of HPV 16 E1- and E2-mediated DNA replication of non-damaged and UVC-damaged templates in a variety of cell lines with different genetic backgrounds; C33a (derived from an HPV-negative cervical carcinoma), XP30RO (deficient in the by-pass polymerase eta (poleta)), XP30eta (expressing a restored wild-type poleta), XP12RO (nucleotide excision repair defective), and MRC5 (derived from a 14-week-old human fetus). The results demonstrate that the fidelity of E1- and E2-mediated DNA replication is reflective of the genetic background in which the assays are carried out. For example, restoring poleta to the XP30 cell line results in a 3-fold drop in the number of mutants obtained following replication of a UVC-damaged template. A relatively high percentage of the mutant-replicated molecules arise as a result of genetic rearrangement. This is the first time such studies have been carried out with an HPV replication system, and the results are discussed in the context of the HPV life cycle and what is known about HPV genomes in human cancers.