Background: The aim of the present study was to investigate the total proteoglycan (PG) and chondroitin-4-sulfate (C4S) levels in gingival tissue samples obtained from patients with aggressive periodontitis (AgP) and chronic periodontitis (CP) before therapy (baseline) and 1 month after completion of non-surgical periodontal therapy.
Methods: Gingival tissue samples were obtained from 10 AgP and 10 CP patients before initiation of treatment (baseline) and 1 month after non-surgical periodontal treatment. The control group comprised 10 systemically and periodontally healthy subjects. Total PG and C4S levels were determined by biochemical techniques. PG levels were analyzed using a modified Bitter and Muir method. C4S assay was carried out using chondroitin sulphate lyase AC and chondroitin-6 sulphate sulphohydrolase enzymes. The results were tested statistically using parametric tests.
Results: The clinical periodontal parameters demonstrated significant decreases in the periodontitis groups (P<0.05) after treatment, and there was no significant difference between AgP and CP groups at baseline and after treatment (P>0.05). At baseline, total PG and C4S levels in both of the periodontitis groups were significantly lower than that of the control group (P<0.05). One month after the non-surgical periodontal treatment, total PG levels in the periodontitis groups were comparable to the control group (P>0.05), whereas C4S levels in the AgP group were significantly lower than the other study groups (P<0.05). In the CP group, total PG and C4S levels increased significantly (P = 0.001 and P = 0.006, respectively) after non-surgical periodontal treatment, but they did not increase in the AgP group (P>0.05).
Conclusion: The significant increases observed in total proteoglycan and chondroitin-4-sulfate levels after non-surgical periodontal treatment in the CP group but not in the AgP group may suggest that healing patterns differ between the two periodontitis types in terms of PG and C4S composition of extracellular matrix.
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http://dx.doi.org/10.1902/jop.2004.75.3.393 | DOI Listing |
Sci Adv
December 2024
Department of Biology, Saint Louis University, St. Louis, MO, 63103, USA.
Photosystem II (PSII) splits water in oxygenic photosynthesis on Earth. The structure and function of the CSM-type PSII-LHCII (light-harvesting complex II) megacomplexes from the wild-type and PsbR-deletion mutant plants are studied through electron microscopy (EM), structural mass spectrometry, and ultrafast fluorescence spectroscopy [time-resolved fluorescence (TRF)]. The cryo-EM structure of a type I CSM megacomplex demonstrates that the three domains of PsbR bind to the stromal side of D1, D2, and CP43; associate with the single transmembrane helix of the redox active Cyt ; and stabilize the luminal extrinsic PsbP, respectively.
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September 2024
Tanenbaum Centre for Pharmacogenetics, Molecular Brain Science, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, Ontario, Canada; Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada; Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada. Electronic address:
Background: The complement component C4 gene has been identified as a strong marker for schizophrenia (SCZ) risk. The C4 gene has a complex genetic structure consisting of variable structural elements (C4A, C4B, C4L, and C4S) and compound structural forms (C4AL, C4BL, C4AS and C4BS). In addition, the variations in C4 structural forms may have a direct or indirect effect on the brain expression level of C4A and C4B proteins.
View Article and Find Full Text PDFMol Cell Proteomics
August 2024
Department of Immunology and Microbiology, The Scripps Research Institute, La Jolla, California, USA. Electronic address:
Substance use disorder is a major concern, with few therapeutic options. Heparan sulfate (HS) and chondroitin sulfate (CS) interact with a plethora of growth factors and their receptors and have profound effects on cellular signaling. Thus, targeting these dynamic interactions might represent a potential novel therapeutic modality.
View Article and Find Full Text PDFHLA
January 2024
Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, California, USA.
Dev Neurosci
December 2023
Stanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Complex brain disorders like schizophrenia may have multifactorial origins related to mis-timed heritable and environmental factors interacting during neurodevelopment. Infections, inflammation, and autoimmune diseases are over-represented in schizophrenia leading to immune system-centered hypotheses. Complement component C4 is genetically and neurobiologically associated with schizophrenia, and its dual activity peripherally and in the brain makes it an exceptional target for biomarker development.
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