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Review
. 2022 Feb;20(1):90-105.
doi: 10.1007/s11914-022-00722-1. Epub 2022 Feb 7.

Pathophysiology of Demineralization, Part I: Attrition, Erosion, Abfraction, and Noncarious Cervical Lesions

W Eugene Roberts  1 , Jonathan E Mangum  2 , Paul M Schneider  3
Affiliations
Review

Pathophysiology of Demineralization, Part I: Attrition, Erosion, Abfraction, and Noncarious Cervical Lesions

W Eugene Roberts et al. Curr Osteoporos Rep. 2022 Feb.

Abstract

Purpose 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. 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.

Keywords: Biomechanics; Enamel; Fluoride; Hydroxyapatitie; Percolation; Remineralization.

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Conflict of interest statement

W. Eugene Roberts and Paul Schneider. declare no conflict of interest. Jonathan Magnum reports a grant, personal fees as an employee, and owning shares of Incisive Technologies, and has a patent issued (WO2011/113107A1).

Figures

Fig. 1
Fig. 1
The upper aspect of the flow chart defines the etiology of demineralization as a combination of acid, biomechanics, and percolation of intercrystalline fluid. Demineralization is defined as a unique disease process. There are differential effects on the sterile bone and septic dentition compartments. Loss of mineralized tissue (osteopenia, noncarious cervical lesions, and caries) is collectively the most pandemic disease in the world (prevalence ~100%). See text for details
Fig. 2
Fig. 2
Labial (left) and cross-sectional (right) planes of a maxillary premolar show dental structures: enamel (E), dentin (D), pulp, cementum (C), dentino-enamel junction (DEJ), and cementoenamel junction (CEJ). A noncarious cervical lesion (NCCL) is depicted in both planes. The multifactorial etiology for a NCCL is (1) toothbrush abrasion, (2) dietary acid, and (3) functional flexure. The line of force for non-axial and lateral loads (dotted lines) produce surface flexure in tension and compression that results in mechanical damage at the stress riser (star) along an enamel surface or within the maximum depth of a NCCL. See text for details
See this image and copyright information in PMC

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