id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-013415-110b95cg	Aquino-Martinez, Ruben	Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem?	2020-10-09		.txt	text/plain	10333	522	27	Although the host immune response rapidly protects against bacterial invasion, oxidative stress generated during inflammation can indirectly deteriorate periodontal tissues through the damage to vital cell macromolecules, including DNA. In contrast to transient DNA damage, persistent genomic lesions promote constitutive DNA damage signaling and cellular senescence, which is correlated with increased secretion of inflammatory signals [26, 30] In agreement with this observation, several studies have reported that premature senescence can also be induced by exposing human cells to subtoxic H 2 O 2 concentrations [31, 32] . As a consequence of chronological aging, the burden of senescent cells increases in different tissues in humans, mice, and other species, where they contribute to the development of chronic pathologies including arthritis, osteoporosis, Alzheimer's disease, atherosclerosis, cancer, and diabetes [58, 59] Similar to other agerelated pathologies, the etiology of diabetes may be the result of the impact of different aging mechanism, including stem cell exhaustion, chronic low-grade inflammation, macromolecular damage, and cellular senescence.	./cache/cord-013415-110b95cg.txt	./txt/cord-013415-110b95cg.txt