Pathogenesis

Mild and moderate injury to the odontoblast cell

processes may produce tubular sclerosis and reparative

dentine, but prolonged or severe irritation can cause the

death of the odontoblasts and initiation of an

inflammatory response. The dynamics of pulp

inflammation is not different to that of inflammation in

the periapical and other tissues. Depending on the

severity and duration of the irritants, the pulp response

ranges from reversible to irreversible pulpitis, then to

partial necrosis which leads to total necrosis. This may

occur without pain.

The dental pulp may also

respond to irritation with a range of degenerative

changes including fibrosis and calcification.

Inflammation

The initial inflammatory cell infiltrate consists

principally of lymphocytes, plasma cells and

macrophages. A wide range of non-specific mediators

of inflammation such as histamine, bradykinin,

serotonin, interleukins (IL) and arachidonic acid

metabolites are released in response to bacterial

invasion and tissue injury.

In addition, many

neuropeptides, e.g., substance P (SP) and calcitonin

gene-related peptide (CGRP), are also involved and

may interact with the mediators produced during

inflammation.

The IL-1 and IL-2 producing cells are located 

within the connective tissue stroma of pulps.

Mast

cells, which are the main source of histamine, are found

in inflamed pulp. A fourfold increase can be found in

pulp histamine levels within 30 minutes of thermal

injury, suggesting that histamine may play a role in the

initial stages of pulp inflammation.

Platelets

aggregated in the vessels release serotonin, which along

with the other inflammatory mediators induce a state of

hyperalgesia in the pulp nociceptors. Plasma or tissue

kallikreins contact kinogens leading to the production

of bradykinin and other kinins to produce many signs

and symptoms of inflammation. Phospholipase A

causes release of arachidonic acid from cell membranes,

resulting in the formation of various prostaglandins,

thromboxanes, and leukotrienes.

Immune defense system

In addition to non-specific inflammatory reactions,

immunologic responses may also initiate and perpetuate

pulp disease. It has been reported that in patients with

hereditary combined immunodeficiency, deep caries

only produces a mild inflammation and relatively little

destruction of the pulp despite the presence of a large

number of bacteria.

In mild to moderate

inflammation, the cell-mediated immunity

predominates.

In severe inflammation, the appearance

of B cells and plasma cells indicates local antibody

production, hence the predominance of humoral

immunity.

Specific IgG has been found in pulp with

deep caries.

Bacterial substances may trigger the

complement system via the antigen and antibody

complex, which become chemotactic for poly-morphonuclear leukocytes. 

There is a distinct ratio

difference between T-helper and T-suppressor

lymphocytes in reversible and irreversible pulpitis. The

predominant T-suppressor cells are able to suppress the

inflammatory process and reverse the condition in the

pulp.
Odontoblasts
As mentioned above, the earliest sign of pulp
inflammation is disruption of the odontoblastic layer.
Even before the appearance of inflammatory changes in
the pulp, there is an overall reduction in the number
and size of odontoblast cell bodies. The nuclei of the
cells may be aspirated into the dentinal tubules due to
the outward flow of tubular fluid, or the cells may be
irreversibly damaged which results in the release of
tissue injury factors affecting neigbouring odontoblasts
and underlying connective tissue. Cells may undergo
vacuolization, ballooning degeneration of mitochondria,
and reduction in the number and size of the endoplasmic
reticulum. However, it is still unknown whether

odontoblasts die of apoptosis or necrosis.