Insight Into the Laboratory Diagnosis of Periimplantitis Using Reactive Oxygen Metabolite Levels - A Biochemical Study.

Aim The study aims to substantiate the quantitative role of the predominant periodontopathogen (Porphyromonas gingivalis) associated with peri-implantitis and evaluate the reactive oxygen metabolite levels in peri-implantitis patients. Methodology A total of 40 participants were taken from the department of periodontology, Thai Moogambigai Dental College and Hospital, Chennai, and divided into groups I (control) and II (test). Group I included 20 participants with healthy peri-implant tissue, and group II included 20 participants with infected peri-implant tissues. The predominant periodontopathogen was detected by using a quantitative real-time polymerase chain reaction. Samples (gingival crevicular fluid (GCF), saliva, and plasma) were collected, and a biochemical assay was conducted for reactive oxygen metabolites (ROM) analysis in healthy implants (control group) and peri-implantitis conditions (test group). ROM levels of the patients were statistically analyzed. Results The qualitative and quantitative profiles of Porphyromonas gingivalis (P. gingivalis) associated with Peri-implantitis were analyzed, and the levels of ROM in periimplantitis patients were assessed. The study results substantiate the quantitative picture of Porphyromonas gingivalis in the detection of periimplantitis. The saliva and GCF samples showed significant differences in ROM levels between the test and control groups. Conclusion This is one of the few studies to detect the predominant bacterial pathogen associated with peri-implantitis and assess the ROM levels in periimplantitis patients. The study gives a correlation between the periopathogens and ROM levels, thereby facilitating the attainment of the best possible treatment options.

Urinary mitochondrial DNA is a biomarker of mitochondrial disruption and renal dysfunction in acute kidney injury.

Recent studies show the importance of mitochondrial dysfunction in the initiation and progression of acute kidney injury (AKI). However, no biomarkers exist linking renal injury to mitochondrial function and integrity. To this end, we evaluated urinary mitochondrial DNA (UmtDNA) as a biomarker of renal injury and function in humans with AKI following cardiac surgery. mtDNA was isolated from the urine of patients following cardiac surgery and quantified by quantitative PCR. Patients were stratified into no AKI, stable AKI, and progressive AKI groups based on Acute Kidney Injury Network (AKIN) staging. UmtDNA was elevated in progressive AKI patients and was associated with progression of patients with AKI at collection to higher AKIN stages. To evaluate the relationship of UmtDNA to measures of renal mitochondrial integrity in AKI, mice were subjected to sham surgery or varying degrees of ischemia followed by 24 h of reperfusion. UmtDNA increased in mice after 10-15 min of ischemia and positively correlated with ischemia time. Furthermore, UmtDNA was predictive of AKI in the mouse model. Finally, UmtDNA levels were negatively correlated with renal cortical mtDNA and mitochondrial gene expression. These translational studies demonstrate that UmtDNA is associated with recovery from AKI following cardiac surgery by serving as an indicator of mitochondrial integrity. Thus UmtDNA may serve as valuable biomarker for the development of mitochondrial-targeted therapies in AKI.