Ridge preservation using FDBA and a collagen membrane improved ridge height and width dimensions when compared to extraction alone. These dimensions may be more suitable for implant placement, especially in areas where loss of ridge height would compromise the esthetic result. The quantity of bone observed on histologic analysis was slightly greater in preservation sites, although these sites included both vital and non-vital bone. The most predictable maintenance of ridge width, height, and position was achieved when a ridge preservation procedure was employed.

Evidence from cross-sectional and case-control studies in various populations demonstrates that adult smokers are approximately three times as likely as non-smokers to have periodontitis. The association between smoking and attachment loss is even stronger when the definition of periodontitis is restricted to the most severely affected subjects. Smokers have a diminished response to periodontal therapy and show approximately half as much improvement in probing depths and clinical attachment levels following non-surgical and various surgical modalities of therapy. Implant failures in smokers are twice those of non-smokers, with a higher failure rate in the maxillary arch accounting for the majority of the difference. Tobacco-induced alterations in microbial and host factors contribute to these deleterious effects of smoking on the periodontium. In longitudinal studies, the rate of periodontal disease progression is increased in smokers, but decreases to that of a non-smoker following tobacco cessation. Likewise, recent non-smokers respond to periodontal therapy in a manner similar to patients who have never smoked. Data regarding the impact of smoking on periodontal status included in this review will be helpful to dental health professionals as they counsel their patients regarding tobacco use. The role of dental health professionals in tobacco cessation is discussed, including the use of the five A's: ask--identify tobacco users; advise--advise them to quit; assess--evaluate the patient's readiness to quit; assist--offer assistance in cessation; and arrange--follow up on the patient's cessation efforts. The addition of pharmacotherapy to behavioral therapy, including nicotine replacement therapy and bupropion, can increase cessation rates. The most popular form of nicotine replacement therapy is the patch, and its use has been shown to double cessation rates compared to behavioral therapy alone. Use of bupropion in combination with nicotine replacement therapy may be particularly helpful for heavy smokers or smokers who have experienced multiple failed attempts at cessation. The American Academy of Periodontology Parameters of Care include tobacco cessation as a part of periodontal therapy, and the 2000 Surgeon General's Report on Oral Health in America encourages dental professionals to become more active in tobacco cessation counseling. Doing so will have far-reaching positive effects on our patients' oral and general health.

Treatment with a CPF plus an ADM allograft significantly increased gingival thickness when compared with a CPF alone. Recession defect coverage was significantly improved with the use of ADM.

Results of this trial demonstrate that treatment of periodontitis with subgingivally delivered doxycycline in a biodegradable polymer is equally effective as scaling and root planing and superior in effect to placebo control and oral hygiene in reducing the clinical signs of adult periodontitis over a 9-month period. This represents positive changes resulting from the use of subgingivally applied doxycycline as scaling and root planing was not limited regarding time of the procedure or use of local anesthesia.

The coronally positioned flap plus ADM produced a defect coverage of 95%, whereas the tunnel technique plus ADM produced only 78% coverage. This difference was considered clinically significant but was not statistically significant.

These clinical and histologic findings suggest that PRP enhanced bone regeneration and resulted in increased horizontal bone gain and percentage vital bone.

The CPT plus ADM and PRP produced defect coverage of 90%, whereas the CPT with ADM produced only 70% defect coverage. This difference was not statistically significant, but it may be clinically significant.

Intrahepatic cholangiocarcinoma (iCCA) is a primary liver cancer epidemiologically linked with liver injury, which has poorly understood incipient stages and lacks early diagnostics and effective therapies. While iCCA is conventionally thought to arise from the biliary tract, studies have suggested that both hepatocytes and biliary cells (cholangiocytes) may give rise to iCCA. Consistent with the plasticity of these cell lineages, primary liver carcinomas exhibit a phenotypic range from hepatocellular carcinoma (HCC) to iCCA, with intermediates along this spectrum. Here, we generated mouse models to examine the consequence of targeting mutant and, common alterations in human iCCA, to different adult liver cell types. Selective induction of these mutations in the SOX9 population, predominantly consisting of mature cholangiocytes, resulted in iCCA emerging from premalignant biliary intraepithelial neoplasia (BilIN). In contrast, adult hepatocytes were relatively refractory to these mutations and formed rare HCC. In this context, injury accelerated hepatocyte-derived tumorigenesis and promoted a phenotypic switch to iCCA. BilIN precursor lesions were absent in the hepatocyte-derived iCCA models, pointing toward distinct and direct emergence of a malignant cholangiocytic phenotype from injured, oncogenically primed hepatocytes. loss enhanced the reprogramming of hepatocytes to cholangiocytes, which may represent a mechanism facilitating formation of hepatocyte-derived iCCA. Overall, our work shows iCCA driven by and may originate from both mature cholangiocytes and hepatocytes, and factors such as chronic liver injury and underlying genetic mutations determine the path of progression and resulting cancer phenotype. The histopathogenesis of biliary tract cancer, driven by and mutations, can be differentially impacted by the cell of origin within the mature liver as well by major epidemiologic risk factors. .