Caries Flashcards
what is the critical pH where demineralization can occur
5.5
what is the definition of caries
ecological shift in dental biofilm environment, driven by frequent access to carbohydrates, leads to change from balanced population of microorganism of low cariogencfty tomicroorganisms that are of high cariogenicity
this leads to an increased production of organic acids > this promotes dental hard tissue net mineral loss >results in a carious lesion
what are the plaque bacterias
s. mutans
lactobillus and biffidobacteria species
what are the various organic acids produced
lactic
acetic
propionic
why is time a factor in the etiology of caries
even though the drop in pH can happen rapidly, sufficient time is required for the plaque biofilm to produce a net mineral loss equating to hard tissue damage to the tooth surface
what can the time of progression of caries be altered by
oral hygiene techniques
saliva buffering
dietary modification
use of fluoride
what is rampant caries
caries process is accelerated and many lesions form rapidly
often involving surfaces of teeth ordinarily relatively caries free
who is often affected by rampant caries
primary dentition
teenagers/young adults with high sucrose diets
adult patients with xerostomia
what are possible reasons for xerostomia
radiation fo the salivary glands - used for orofacial malignant growth
sjrogens
drugs
what is the cross sectional shape of smooth surface caries
inverted cone
what is the clinical manifestation of the active white spot lesion
initially smooth/frosty/white/opaque and non cavitated
as the lesion develops over time it becomes somewhat chalky, eventually becoming roughened or microcavitated
how do we detect a microcavitated WSL
running a blunt probe across the lesion surface
what is the dentine pulp complex reaction during the white spot lesion
no symptoms
DPC reaction mediated by cytokines and bacteria breakdown products within the dentine matrix and tubules
what happens when the carious process reaches dentine
defence reactions in the dentine/pulp complex are stimulated at this stage with evidence of translucent dentine at the lesion boundary and tertiary dentine deposition at the dentine-pulp interface beneath advancing lesions
what does the lesion look like once it has reach the middle third of dentine
often clinically cavitated on both occlusal and smooth surfaces with plaque now able to accumulate on the exposed dentine surface - the spread of the lesion will undermine the overlying enamel with an associated grey shadowing/opacity which becomes brittle and prone to fracture under occlusal loading
what are the different zones to carious dentine
carious infected dentine
carious affected dentine
what is carious infected dentine
Outermost, superficial, irreparable, necrotic zone of destruction
how is the carious infected dentine clinically distinguished
Clinically distinguished as a dark, brown, soft, wet, ‘mushy’ layer
why should the carious infected dentine be clinically removed
as it is necrotic and cannot be repaired and also provides a poor quality bonding substrate for adhesive materials to achieve an adequate seal
what is caries affected dentine
Inner layer of carious dentine that can be repaired by the dentine-pulp complex, often distinguished as paler brown, harder, ‘sticky and scratchy’
what can the deepest layer of infected dentine be described as
hypermineralized translucent dentine (due to its glassy appearance in cross section) - it is one of the several reparative reactions of the dentine-pulp complex to the carious process
what happens as the advancing front of the carious lesion approaches the dentine/pulp boundary
bacteria and toxins will penetrate the pulpal tissues causing an acute inflammatory response
what is the first response of the pulp
initial acute pulpitic response (sharp pain) then it evolves into a chronic response that is a dull pain
what happens if the pulp is breached by a lesion
a carious exposure may be created when excavating deep caries. The exposed pulp will bleed. Prognosis depends on age of patient - younger patients have a more vascularised pulp
why must the dentine and pulp be considered together
they are intimately connected (odontoblasts)
what are the 3 defense reactions of the dentine/pulp complex
translucent dentine
tertiary dentine
pulp inflammation
what is translucent dentine also known as
sclerotic dentine
what is translucent/sclerotic dentine
tubular infill with mineral crystals
what is the purpose of sclerotic dentine
attempt to wall off the advancing lesion
what is the appearance (glassy) of sclerotic dentine due to
Appearance due to the party of refractive indices of intertubular and intratubular mineral so allowing light to pass through the sectioned boundary
why is sclerotic dentine softer than the deeper sound counterpart
due to the weaker crystallite orientation compared to HA
what is tertiary dentine
Dentine that is laid down at the dentine-pulp border in response to noxious stimulis
what is the structure of tertiary dentine
Has an irregular/atubular structure
what is reactionary dentine
deposited as a result of a mild irritant where original odontoblasts survive and are metabolically upregulated
what is reparative dentine
deposited in response to a strong irritant which compromises the vitality of the original odontoblasts
what are the 2 types of plural inflammation
acute
chronic
in a slowly progressing lesion what will happen in regards to pulp inflammation
toxins reaching the pulp may provoke chronic inflammation
what happens once organisms actually reach the pulp (Carious exposure)
acute inflammation may supervene
what happens in chronic inflammation of the pulp
cellular components predominate and there may be increased collagen production leading to fibrosis but without immediately endangering the vitality of the tooth
what happens in acute inflammation
the vascular changes predominate
what is the most common cause of pulpal inflammation
infection
what will dentine caries result in
ulpal inflammation and chronic inflammatory cells will infiltrate the pulp near the odontoblast layer - this reaction may even be seen in response to intial enamel caries - this chronic inflammatory reaction is mainly due to the bacterial toxins moving through the dentinal tubule
what can acute pulpal inflammation result in
pulpal necrosis
