Roberts, W. EugeneMangum, Jonathan E.Schneider, Paul M.2024-05-012024-05-012022Roberts WE, Mangum JE, Schneider PM. Pathophysiology of Demineralization, Part I: Attrition, Erosion, Abfraction, and Noncarious Cervical Lesions. Curr Osteoporos Rep. 2022;20(1):90-105. doi:10.1007/s11914-022-00722-1https://hdl.handle.net/1805/40396Purpose of the review: Compare pathophysiology for infectious and noninfectious demineralization disease relative to mineral maintenance, physiologic fluoride levels, and mechanical degradation. Recent findings: Environmental acidity, biomechanics, and intercrystalline percolation of endemic fluoride regulate resistance to demineralization relative to osteopenia, noncarious cervical lesions, and dental caries. Summary: Demineralization is the most prevalent chronic disease in the world: osteoporosis (OP) >10%, dental caries ~100%. OP is severely debilitating while caries is potentially fatal. Mineralized tissues have a common physiology: cell-mediated apposition, protein matrix, fluid logistics (blood, saliva), intercrystalline ion percolation, cyclic demineralization/remineralization, and acid-based degradation (microbes, clastic cells). Etiology of demineralization involves fluid percolation, metabolism, homeostasis, biomechanics, mechanical wear (attrition or abrasion), and biofilm-related infections. Bone mineral density measurement assesses skeletal mass. Attrition, abrasion, erosion, and abfraction are diagnosed visually, but invisible subsurface caries <400μm cannot be detected. Controlling demineralization at all levels is an important horizon for cost-effective wellness worldwide.en-USAttribution 4.0 InternationalFluorideBiomechanicsPercolationRemineralizationHydroxyapatitieEnamelPathophysiology of Demineralization, Part I: Attrition, Erosion, Abfraction, and Noncarious Cervical LesionsArticle