-
International Journal of Environmental... Mar 2022Premature loss of primary teeth can occur as a consequence of dental trauma, neonatal tooth extraction, early childhood caries, or periodontal problems, or it can be a... (Review)
Review
BACKGROUND
Premature loss of primary teeth can occur as a consequence of dental trauma, neonatal tooth extraction, early childhood caries, or periodontal problems, or it can be a manifestation of systemic disease. This review aims to present systemic disorders that can lead to premature loss of deciduous teeth in children and to provide a comprehensive resource for clinical practice for both physicians and dentists.
METHODS
This study is a narrative review of original studies and case reports published in English and Polish between 1957 and 2021 that was conducted by searching electronic scientific resources: PubMed, Google Scholar, Web of Science, and Science Direct. The schema of the qualification process is represented by a Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). In total, 196 articles were identified; after provisional assessment of the titles and abstracts by two reviewers, 46 were found to be relevant to the topic, including 1 review, 16 original papers, and 27 case reports regarding systemic disease resulting in premature tooth loss.
RESULTS
In this study, 16 systemic diseases were linked to premature primary tooth loss in children: Papillon-Lefèvre syndrome, mucocutaneous dyskeratosis, Coffin-Lowry syndrome, congenital adrenal hyperplasia, Langerhans cell histiocytosis, cherubism, hypophosphatasia, acatalasia, Chediak-Higashi syndrome, cyclic neutropenia, erythromelalgia, Down syndrome, Hajdu-Cheney syndrome, short bowel syndrome, leukocyte adhesion deficiency type 1 (LAD-1), and Wiedemann-Steiner syndrome (WSS).
Topics: Child; Child, Preschool; Humans; Infant, Newborn; Leukocyte-Adhesion Deficiency Syndrome; Neutropenia; Papillon-Lefevre Disease; Tooth Loss; Tooth, Deciduous
PubMed: 35329073
DOI: 10.3390/ijerph19063386 -
Oxidative Medicine and Cellular... 2019Reactive species produced in the cell during normal cellular metabolism can chemically react with cellular biomolecules such as nucleic acids, proteins, and lipids,... (Review)
Review
Reactive species produced in the cell during normal cellular metabolism can chemically react with cellular biomolecules such as nucleic acids, proteins, and lipids, thereby causing their oxidative modifications leading to alterations in their compositions and potential damage to their cellular activities. Fortunately, cells have evolved several antioxidant defense mechanisms (as metabolites, vitamins, and enzymes) to neutralize or mitigate the harmful effect of reactive species and/or their byproducts. Any perturbation in the balance in the level of antioxidants and the reactive species results in a physiological condition called "oxidative stress." A catalase is one of the crucial antioxidant enzymes that mitigates oxidative stress to a considerable extent by destroying cellular hydrogen peroxide to produce water and oxygen. Deficiency or malfunction of catalase is postulated to be related to the pathogenesis of many age-associated degenerative diseases like diabetes mellitus, hypertension, anemia, vitiligo, Alzheimer's disease, Parkinson's disease, bipolar disorder, cancer, and schizophrenia. Therefore, efforts are being undertaken in many laboratories to explore its use as a potential drug for the treatment of such diseases. This paper describes the direct and indirect involvement of deficiency and/or modification of catalase in the pathogenesis of some important diseases such as diabetes mellitus, Alzheimer's disease, Parkinson's disease, vitiligo, and acatalasemia. Details on the efforts exploring the potential treatment of these diseases using a catalase as a protein therapeutic agent have also been described.
Topics: Aging; Alzheimer Disease; Catalase; Diabetes Mellitus; Humans; Oxidative Stress; Parkinson Disease; Reactive Oxygen Species
PubMed: 31827713
DOI: 10.1155/2019/9613090 -
Aging Mar 2020Peroxisomes are small, membrane-enclosed eukaryotic organelles that house various enzymes with metabolic functions. One important feature in both Hutchinson-Gilford...
Peroxisomes are small, membrane-enclosed eukaryotic organelles that house various enzymes with metabolic functions. One important feature in both Hutchinson-Gilford Progeria Syndrome (HGPS) and normal aging is the elevated levels of Reactive Oxygen Species (ROS), which are generated from metabolic pathways with the capacity to cause oxidative damage to macromolecules within the cells. Although peroxisomal bioreactions can generate free radicals as their byproducts, many metabolic enzymes within the peroxisomes play critical roles as ROS scavengers, in particular, catalase. Here, we observed impaired peroxisomes-targeting protein trafficking, which suggested that the poorly assembled peroxisomes might cause high oxidative stress, contributing to the premature senescent phenotype in HGPS. We then investigated the ROS clearance efficiency by peroxisomal enzymes and found a significantly decreased expression of catalase in HGPS. Furthermore, we evaluated the effects of two promising HGPS-treatment drugs Methylene Blue and RAD001 (Everolimus, a rapamycin analog) on catalase in HGPS fibroblasts. We found that both drugs effectively reduced cellular ROS levels. MB, as a well-known antioxidant, did not affect catalase expression or activity. Interestingly, RAD001 treatment significantly upregulated catalase activity in HGPS cells. Our study presents the first characterization of peroxisomal function in HGPS and provides new insights into the cellular aspects of HGPS and the ongoing clinical trial.
Topics: Acatalasia; Cell Line; Cellular Senescence; Enzyme Inhibitors; Everolimus; Fibroblasts; Humans; Lamin Type A; Methylene Blue; Mutation; Peroxisomes; Phenotype; Progeria; Reactive Oxygen Species
PubMed: 32186522
DOI: 10.18632/aging.102941 -
Endocrine Journal Jan 2024We encountered five cases that exhibited false-high Hemoglobin A1c (HbA1c) levels when samples were examined using the enzyme-based NORUDIA N HbA1c kit. HbA1c levels...
We encountered five cases that exhibited false-high Hemoglobin A1c (HbA1c) levels when samples were examined using the enzyme-based NORUDIA N HbA1c kit. HbA1c levels were higher than those obtained using other methods, such as HPLC, immune-based methods, and other enzyme-based kits. This kit produced inaccurate results for HbA1c when residual peroxides were present in samples. The addition of peroxidase solution restored false-high HbA1c levels in the five cases, indicating that reduced catalase activity was responsible for these values because catalase eliminates peroxide. Catalase activity and gene mutations were examined in the five cases and an immunohistological analysis was performed to assess the expression of catalase. Cases #1 and 2 were diagnosed as acatalasemia and cases #3, 4, and 5 as hypocatalasemia based on compound heterozygous SNP and heterozygous splicing mutations in the catalase gene. Therefore, impaired catalase activity was responsible for false-high HbA1c levels measured by the NORUDIA N HbA1c kit.
Topics: Glycated Hemoglobin; Catalase; Antioxidants; Peroxidase
PubMed: 38030260
DOI: 10.1507/endocrj.EJ23-0212