The dental pulp has an unusual combination of
features that makes its circulation rather unique.
Firstly, the compliance of the pulp is low because it
resides in a rigid, unyielding calcified wall. A near
simultaneous increase in pulp tissue pressure has been
recorded as a result of vasodilatation.
Because capillary dilation and the transudation of fluids that
comprise the early stages of acute inflammation
increase the volume of tissue, such swelling in the
dental pulp is likely to cause a pressure increase that
stimulates pulp nerves to register pain. Secondly, the
dental pulp is a firm and resilient connective tissue,
composed principally of a gelatin-like material, such as
proteoglycans and other glycoproteins, reinforced
throughout by irregularly arranged and interlaced
collagen fibres. The resilient ground substance limits
intrapulpal pressures to the site of irritation, and is not
transmitted throughout the pulp space.
Significant
pressure differences have been observed at sites only
1 to 2mm apart.
Pressure from the increased tissue
fluid collapses the thin-walled veins and venules only in
the area of the affected pulp tissue, causing a localized
vascular stasis and ischaemia, resulting in local cellular
death. The gelated extracellular matrix may also act as
a barrier against the spread of micro-organisms and
toxic products. However, the inflammatory process and
resultant intrapulpal pressure changes may progress
apically by increments circumferentially from compart-ment to compartment.
When the structural integrity of
the pulp tissue is lost with overwhelming inflammation,
the increased tissue pressure can spread with a resultant
compression of the blood vessels at the apex and result
in total necrosis.
Thirdly, although the dental pulp is a
rich vascular tissue, terminal arteries supplying it fall
within the microcirculatory diameter range.
Unlike in
most tissues, the pulp circulation lacks a true collateral
blood supply. This restricted blood source may
presumably limit the blood supply to the dental pulp,
making it less capable of overcoming a severe irritant
than other better-supplied tissues. Fourthly, because the
tooth bridges between the bacteriologically sterile
environment of the jawbone and the heavily
contaminated environment of the mouth through an
oral epithelial membrane, diseases in the pulp will
invariably extend through the apical foramen into the
surrounding bone causing further problems.
As a consequence of these features, the degree of pulp
inflammation does not necessarily need to be severe to
cause pulp death, and if left untreated, progression to
the surrounding alveolar bone is likely to occur. Hence,
careful regulation of the pulp microcirculation seems to
be critically important in order to maintain the
well-being of the pulp. The fact that most pulps survive
life-long exposure to various inimical attacks implies
the presence of a well-regulated microcirculation in the
pulp.