title: Numerical modelling of tooth enamel subsurface lesion formation induced by dental plaque.
abstract: Using a one-dimensional mathematical model that couples tooth demineralisation and remineralisation with metabolic processes occurring in the dental plaque, two mechanisms for subsurface lesion formation were evaluated. It was found that a subsurface lesion can develop only as the result of alternating periods of demineralisation (acid attack during sugar consumption) and remineralisation (resting period) in tooth enamel with uniform mineral composition. It was also shown that a minimum plaque thickness that can induce an enamel lesion exists. The subsurface lesion formation can also be explained by assuming the existence of a fluoride-containing layer at the tooth surface that decreases enamel solubility. A nearly constant thickness of the surface layer was obtained with both proposed mechanisms. Sensitivity analysis showed that surface layer formation is strongly dependent on the length of remineralisation and demineralisation cycles. The restoration period is very important and the numerical simulations support the observation that often consumption of sugars is a key factor in caries formation. The calculated profiles of mineral content in enamel are similar to those observed experimentally. Most probably, both studied mechanisms interact in vivo in the process of caries development, but the simplest explanation for subsurface lesion formation remains the alternation between demineralisation and remineralisation cycles without any pre-imposed gradients.
authors.affiliation: Department of Biotechnology, Delft University of Technology, Delft, The Netherlands.
authors.forename: O
authors.initials: O
authors.lastname: Ilie
authors.forename: A G
authors.initials: AG
authors.lastname: van Turnhout
authors.forename: M C M
authors.initials: MC
authors.lastname: van Loosdrecht
authors.forename: C
authors.initials: C
authors.lastname: Picioreanu
mesh_terms: D000136:Acid-Base Equilibrium / Q000502:physiology; D000465:Algorithms; D002327:Cariostatic Agents / Q000494:pharmacology; D003731:Dental Caries / Q000209:etiology / Q000378:metabolism / Q000382:microbiology; D003743:Dental Enamel / Q000378:metabolism / Q000473:pathology*; D003747:Dental Enamel Solubility / Q000187:drug effects; D003773:Dental Plaque / Q000150:complications* / Q000378:metabolism / Q000382:microbiology; D019422:Dietary Sucrose / Q000009:adverse effects; D017886:Durapatite / Q000378:metabolism; D005285:Fermentation; D005459:Fluorides / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism; D006801:Humans; D006863:Hydrogen-Ion Concentration; D006882:Hydroxyapatites / Q000378:metabolism; D017665:Hydroxyl Radical / Q000378:metabolism; D019344:Lactic Acid / Q000378:metabolism; D008903:Minerals / Q000378:metabolism; D008954:Models, Biological; D016877:Oxidants / Q000378:metabolism; D012463:Saliva / Q000378:metabolism; D013291:Streptococcus / Q000378:metabolism; D017001:Tooth Demineralization / Q000209:etiology* / Q000378:metabolism; D014089:Tooth Remineralization
chemical_list: D002327:Cariostatic Agents; D019422:Dietary Sucrose; D006882:Hydroxyapatites; D008903:Minerals; D016877:Oxidants; D017665:Hydroxyl Radical; D019344:Lactic Acid; C028869:fluor-hydroxylapatite; D017886:Durapatite; D005947:Glucose; D005459:Fluorides