Within the limitation of this systematic review, the application of grafting materials and barrier membranes resulted in greater PD reduction and RBF, but there is a lack of high-quality comparative studies to support this statement. The results might be used to project treatment outcomes after surgical management of peri-implantitis.

Background Varying degrees of cortical amyloid deposition are reported in the setting of Parkinsonism with cognitive impairment. We performed a systematic review to estimate the prevalence of Alzheimer disease (AD) range cortical amyloid deposition amongst patients with Parkinson disease with dementia (PDD), Parkinson disease with mild cognitive impairment (PD-MCI) and dementia with Lewy bodies (DLB). We included amyloid PET imaging studies using Pittsburgh Compound B (PiB). Methods We searched the databases Ovid MEDLINE, PubMed, Embase, Scopus, and Web of Science for articles pertaining to amyloid imaging in Parkinsonism and impaired cognition. We identified 11 articles using PiB imaging to quantify cortical amyloid. We used the metan module in Stata, version 11.0, to calculate point prevalence estimates of patients with “PiB-positive” studies, ie patients showing AD range cortical Aβ-amyloid deposition. Heterogeneity was assessed. A scatterplot was used to assess publication bias. Results Overall pooled prevalence of “PiB-positive” studies across all three entities along the spectrum of Parkinson disease and impaired cognition (specifically PDD, PD-MCI and DLB) was 0.41 (95% CI 0.24-0.57). Prevalence of “PiB-positive” studies was 0.68 (95% CI 0.55-0.82) in the DLB group, 0.34 (95% CI 0.13-0.56) in the PDD group and 0.05 (95% CI -0.07-0.17) in the PD-MCI group. Conclusion There is substantial variability in the prevalence of “PiB-positive” studies in subjects with Parkinsonism and cognitive impairment. Higher prevalence of PiB positive studies was encountered among subjects with DLB as opposed to subjects with PDD. PD-MCI subjects showed overall lower prevalence of PiB positive studies than reported findings in non-PD related MCI.

IMPORTANCE Risk of nephrogenic systemic fibrosis (NSF) to individual patients with stage 4 or 5 chronic kidney disease (CKD; defined as estimated glomerular filtration rate of <30 mL/min/1.73 m 2 ) who receive a group II gadolinium-based contrast agent (GBCA) is not well understood or summarized in the literature.OBJECTIVE To assess the pooled risk of NSF in patients with stage 4 or 5 CKD receiving a group II GBCA. DATA SOURCES A health sciences informationist searched the Ovid (MEDLINE and MEDLINE Epub Ahead of Print, In-Process & Other Non-Indexed Citation, and Daily and Versions), Embase, Cochrane Central Register of Controlled Trials, Web of Science, and Open Grey databases from inception to January 29, 2019, yielding 2700 citations.STUDY SELECTION Citations were screened for inclusion in a multistep process. Agreement for final cohort inclusion was determined by 2 blinded screeners using Cohen κ. Inclusion criteria consisted of stage 4 or 5 CKD with or without dialysis, administration of an unconfounded American College of Radiology classification group II GBCA (gadobenate dimeglumine, gadobutrol, gadoterate meglumine, or gadoteridol), and incident NSF as an outcome. Conference abstracts, retracted manuscripts, narrative reviews, editorials, case reports, and manuscripts not reporting total group II GBCA administrations were excluded.DATA EXTRACTION AND SYNTHESIS Data extraction was performed for all studies by a single investigator, including publication details, study design and time frame, patient characteristics, group II GBCA(s) administered, total exposures for patients with stage 4 or stage 5 CKD, total cases of unconfounded NSF, reason for GBCA administration, follow-up duration, loss to follow-up, basis for NSF screening, and diagnosis. MAIN OUTCOMES AND MEASURESPooled incidence of NSF and the associated upper bound of a 2-sided 95% CI (risk estimate) for the pooled data and each of the 4 group II GBCAs. RESULTSSixteen unique studies with 4931 patients were included (κ = 0.68) in this systematic review and meta-analysis. The pooled incidence of NSF was 0 of 4931 (0%; upper bound of 95% CI, 0.07%). The upper bound varied owing to different sample sizes for gadobenate dimeglumine (0 of 3167; upper bound of 95% CI, 0.12%), gadoterate meglumine (0 of 1204; upper bound of 95% CI, 0.31%), gadobutrol (0 of 330; upper bound of 95% CI, 1.11%), and gadoteridol (0 of 230; upper bound of 95% CI, 1.59%).CONCLUSIONS AND RELEVANCE This study's findings suggest that the risk of NSF from group II GBCA administration in stage 4 or 5 CKD is likely less than 0.07%. The potential diagnostic harms of withholding group II GBCA for indicated examinations may outweigh the risk of NSF in this population.