Significance in tooth integrity and longevity The health and longevity of a
tooth is closely tied to the vitality of the
odontoblast, namely, the odontoblast process. The reason for this lies in the function of the odontoblast process in maintaining the patency of the
dentinal tubules, as aging results in its obliteration, causing the
occlusion of
dentinal tubules. This results in diminished mechanical properties of the
tooth such as the ability to withstand functional load and resisting
fracture upon external forces. As mentioned earlier,
odontoblasts are implicated to be associated with
sensory nerve fibers, contributing to
tooth sensitivity. This unique spatial relationship between the odontoblast process and
nerve fibers are thus, stipulated to be contributors to sensory events like
dentin hypersensitivity. This hypothesis explains the reason behind the pain and
hypersensitivity experienced during cavity preparation and
caries. First proposed by Brannstorm, the odontoblast process surrounded by dentinal fluid is said to be compressed upon exposure of
dentinal tubules to osmotic, thermal, mechanical and chemical stimuli through the movement of the dentinal fluid. This results in the transduction of signals which are carried from the odontoblast process to the
pulpal nerve sensory endings which induce pain /
dentinal hypersensitivity. Therefore, odontoblasts are suggested to play a crucial part in the tooth's innate immunity by detecting such bacterial products to initiate an
immune response to prevent potential
spread of infection. It is studied that the odontoblast process senses
pathogen-associated molecular patterns (PAMPs) through specialised
pattern recognition receptor(PRRs). Before the
cariogenic challenge itself, the
dentine matrix already had bioactive materials and
growth factors (such as TGF-1, TGF-3, BMP-7, DMP-1, SDF-1) integrated into it due to its secretion by
odontoblasts. The generation of heat and the desiccation of the
tissue can induce a
tissue reaction similar to that occurring with
caries, leading to intratubular and intertubular
mineralisation which causes
sclerotic dentin formation, followed by the formation of tertiary dentin. In deep cavities, failure to adhere to the minimal remaining dentinal thickness (RDT) of between 0.5 and 0.25mm resulted in higher rates of odontoblast death. The dental
bleaching procedure, where
H2O2 and its
by-products are released, can diffuse to the
pulp via layers of
enamel and
dentine, leading to
inflammation and sometimes,
pulp necrosis. ==References==