Pathophysiology of Demineralization, Part II: Enamel White Spots, Cavitated Caries, and Bone Infection

Abstract

Purpose of Review Compare noninfectious (part I) to infectious (part II) demineralization of bones and teeth. Evaluate similarities and differences in the expression of hard tissue degradation for the two most common chronic demineralization diseases: osteoporosis and dental caries. Recent Findings The physiology of demineralization is similar for the sterile skeleton compared to the septic dentition. Superimposing the pathologic variable of infection reveals a unique pathophysiology for dental caries. Summary Mineralized tissues are compromised by microdamage, demineralization, and infection. Osseous tissues remodel (turnover) to maintain structural integrity, but the heavily loaded dentition does not turnover so it is ultimately at risk of collapse. A carious tooth is a potential vector for periapical infection that may be life-threatening. Insipient caries is initiated as a subsurface decalcification in enamel that is not detectable until a depth of ~400μm when it becomes visible as a white spot. Reliable detection and remineralization of invisible caries would advance cost-effective wellness worldwide.

Noncarious cervical lesions: Morphology and progression, prevalence, etiology, pathophysiology, and clinical guidelines for restoration

“…Demineralization is a broad‐spectrum disease that has both an infectious and noninfectious etiology 3,77 . Cariogenic bacteria do not contribute to NCCLs, but other oral microorganisms such as Fusobacteriales may protect a cervical lesion from acidic degradation via bacterial interaction (interference) and pH regulation 78 .…”

“…Despite transient occlusal trauma inherent in tooth movement, orthodontic treatment has no known effect on NCCL incidence or progression. However, the plaque load associated particularly with fixed appliance treatment is a concern since deep cervical lesions inoculated with cariogenic pathogens in plaque may result in a rapid progression of caries that could result in serious bone infections 77 . In a seeming paradox, “orthodontics treatment” was found to be a significant contributing factor for NCCLs in male athletes (footballers) 82 .…”

“…Protecting oral structures from fatigue‐related demineralization is an important clinical priority 3,77 . Teeth, jaws, and TMJ are damaged by both cyclic and sustained loads that result in flexure that exceeds the fatigue resistance of mineralized tissues 88 .…”

“…Environmental acidity, mechanical loading, and percolation of endemic fluoride regulate resistance to demineralization such as osteopenia, NCCLs, and dental caries. 3,77 In general, the etiology of demineralization involves fluid percolation, metabolism, homeostasis, biomechanics, mechanical wear (attrition or abrasion), and biofilm-related infections. 3,77 An NCCL has a multifaceted etiology that draws on the same mechanisms for demineralization, but in a unique pattern that is specific for each tooth.…”

Resin Infiltration of Non-Cavitated Enamel Lesions in Paediatric Dentistry: A Narrative Review

“…The presence of the orthodontic bracket and the archwire might hinder routine oral hygiene care and requires meticulous effort by the patient to maintain the area clean. Retention of dental plaque elevates the cariogenic bacterial count in the saliva, causing depletion in pH value at the dental plaque-enamel interface, thus initiating mineral loss from the enamel structure leading to enamel subsurface porosities [ 57 , 58 ]. The initiation of enamel decalcification can be seen as early as four weeks post orthodontic bracket placement [ 59 ].…”