Histopathology of Caries

caries affecting different dental tissues in different ways

-enamel: decalcification via acid

-dentin: decalcification and proteolysis (crown/root)

-cementum: resorption

-pulp: inflammation

“pores” between hydroxy-apatite crystallites

-crystallites 200×40×40nm

-pores 2-10nm

-laminar pores in high caries risk group

-cylindrical pores in low caries risk group

caries progression- type 1/2/3/4 lesions

-enamel lesions (pit and fissure)

fissures

should a fissure be treated with fluoride?

-no- use a sealant

progression of plaque formation on enamel surface

bacteria in dental biofilms- production of acid from carbohydrates

-enamel caries- white spot lesion

-early enamel lesion- loss of mineral

structure of enamel caries lesion

-lesion extending into dentin

-white spot lesions- active and arrested

biologic hydroxy-apatite

demineralization generally starts in

-the crystallite cores

-remineralization

caries spreading into dentin

-initially a broad preferential spread along DEJ

differentiated, active odontoblast

spread along dentinal tubules

hydroxyapatite in collagen matrix

-intrafibrillar in “hole” zones

-extrafibrillar between fibrils

initial preferential spread along DEJ

mantle dentin

-in mantle dentin (approximately 100um), two populations of collagen fibers exist:

-typical dentin collagen fibers parallel with DEJ

-thicker fibers perpendicular to DEJ

dentin caries

-decalcification plus:

-degradation of ECM by bacterial proteases

-invasion of degraded intertubular dentin by bacteria

-bacterial invasion of tubules

-total absence of peritubular dentin

-demineralized dentin matrix with some reprecipitation of mineral along tubule wall

-advanced bacterial invasion

arrested dentin caries

-reprecipitation of mineral and some recalcification of decalcified dentin as the result of:

-growth of residual crystallites in intertubular dentin

-maturation of whitlockite into hydroxy-apatite inside tubular lamina

factors leading to neglect

-impaired cognitive skills

-impaired physical skills- resulting from arthritis, following a stroke

-caregiver does not contribute to oral health

-medicare does not cover dental

-lack of mobility limits visits to dentists

nursing homes

-required to do dental screening and help residents with oral hygiene

-does not always happen!

-people with well-maintained oral health throughout their lifetime: once in a nursing home, their oral health may decline in 6-8 months

root caries

-in contrast to caries in the crown, bacterial invasion is a common feature in initial root cares

-resorption lacune in cementum

-some exposed dentin

-colonies of microorganisms in lacunae

-invasion of orifices of dentinal tubules by filamentous bacteria

effects on cementum and dental pulp

-progression of infection along s-shaped tubules that are associated with the lesion

-tissue response in the corresponding pulp region

improve oral care

-single-use SDF

-provides easy, painless, and effective way to halt decay, strengthen compromised teeth, and prevent need for invasive treatments like RCT

-hardens decayed dentin, offers immediate relief from tooth pain, single-use format ensures precise, hygienic application (in-home, bedside tx with minimal discomfort)

angiogenic signaling by cariogenic bacteria

innate response of dentin-pulp complex to caries

-outward flow of dentinal fluid and immunoglobulins

-odontoblasts expressing IL-8

-neuropeptides and neurogenic inflammation

-innate immune cells (not Ag-specific): lymphocytes- NK cells, T cells; dendritic cells, monocytes, macrophages

-innate cytokines

-chemokines

macrophages and dendritic cell actions in initiation stage and advanced stage of pulpal inflammation

cellular events involved in reparative and in reactive dentinogenesis

-progression of infection along s-shaped tubules that are associated with the lesion

-reactive tissue response in the corresponding pulp region

acute symptoms x pulpal exposure