Inflammation is a series of events that occur in vascular connective tissue (pulp), with the aim to neutralize or eliminate the damaging factors and to initiate tissue repair. In short, it is the host response to injury.
Early changes include: fibrosis and thickening of basement membrane of small blood vessels of pulp.
Repair is observed as: calcific foci associated with an amorphous, partially mineralized connective tissue matrix with degenerated cells.
CLASSIFICATION OF PULPAL DISEASES:
CLASSIFICATION OF INFLAMMATORY PULPAL DISEASES (PULPITIS):
|(1) BASED ON SEVERITY & DURATION
||(2) BASED ON EXTENT
||(3) BASED ON COMMUNICATION
||(4) BASED ON HEALING POTENTIAL
||(5) BASED ON SYMPTOMS
Chronic Inflammation –
Whatever be the type of bacteria or its pathogenicity, the 1st response to caries/ microleakage by the pulp is a low-grade, chronic inflammation (often symptomless, with rise in T-lymphocyte number)
Acute Inflammation –
- Presence of microbial toxins à local (pulpal) synthesis of histamine, bradykinin, or prostaglandins à damage to pulpal cells à formation of foci of acute inflammation within the chronically inflamed tissue.
- When acute inflammatory foci develop, the pulpal nerves become sensitized to normal stimuli à the patient reports sensitivity of short duration to cold/ hot food or drink, to cold air, or to osmotic change while eating.
Open-form Chronic pulpitis –
- In the presence of a more advanced necrosis of the pulp tissue drainage may occur from the pulp chamber through the overlying carious dentine. The pulpitis is then regarded as ulcerative or open-form, and may not be painful.
- Drainage allows the development of chronic pulpitis, with the inflammatory response being confined to the superficial area.
- This may persist for a considerable period of time, even years, because of the development of a balance between the injurious agents and tissue resistance.
- At this point the elimination of drainage by the placement of a temporary or permanent restoration by a dentist can lead to severe pain, total pulp necrosis and progression to a periapical lesion.
Pulp Polyp (Chronic Hyperplastic Pulpitis) –
- Commonly seen in – In young people with untreated, gross carious lesions exposing the body of the pulp, Proliferation of hyperplastic granulation tissue into the carious cavity à pulp polyp.
- The pulp polyp has a relatively thin pedicle connecting it to the remainder of the pulp, and is covered with a well-developed epithelial layer, presumably seeded from desquamated oral epithelial cells via saliva.
Diffuse Calcification –
Chronic pulpal inflammation may also induce the secretion of ectopic dentinal matrix by fibroblasts or undifferentiated mesenchymal cells, causing either diffuse or well-organised calcification, often leading to narrowing or obstruction of the root canal.
Idiopathic Resorption –
The resorption or Pathogenesis – Osteoclasts proliferate and cause resorption of dentin from the internal surface of the pulp chamber.
|Commences internally within the pulp tissue, probably at the interface between the pulp and the dentin
SYNONYMS: Pink tooth, pink tooth of mummery.
|Commences externally at the cemento-enamel junction (CEJ).
|In both cases it is difficult to recognize in the early stages. If it is not diagnosed early, can lead to the loss of a tooth
|Associated with –
Trauma, including cavity preparation, or external blow to tooth.
|Associated with –
Trauma, or orthodontic tooth movement.
· It will remain asymptomatic.
· Earliest signs will show radiographically as ill-defined radiolucency in relation to the pulp chamber.
· Ultimately it will show as a pinkish disccolouration through the enamel à this is the pulp tissue occupying a large area of the crown.
· An external lesion may be found at this time at CEJ, often disguised within the gingival crevice.
Generally commences in the region of the cemento-enamel junction.
· In early stages, pulpectomy is the only available treatment but if it is allowed to progress until it reaches the external surface, the tooth will probably be lost.
· In early stages it may be successfully treated by careful debridement of lesion and cauterising with trichloracetic acid followed by placement of a GIC restoration.
· However, this lesion is very prone to recurrence along gingival margin in relation to inflammation in the gingival tissue.
[From: Mount and Hume, 2008.]
ENDODONTIC DIAGNOSIS (PULPAL & PERIAPICAL DIAGNOSIS):
||Symptomatic Apical Periodontitis
||Asymptomatic Apical Periodontitis
|Symptomatic Irreversible Pulpitis
|Asymptomatic Irreversible Pulpitis
[According to the: American Association of Endodontists. 2008]
No one test alone can give an accurate picture of the state of the dental pulp or periapex. It is only by the correlation of all available information that the clinician can arrive at a diagnosis. A careful visual examination, using good illumination and magnification, plus a radiographic examination should be used in conjunction with the tests described below.
|Methods for testing Pulpal status
||Methods for testing Periapical status
|Heat [Pulp Sensibility Test]
(The tooth is tapped gently – vertically & laterally with the handle of a mouth mirror – sharp pain may be elicited which may persist for a brief time).
|Cold [Pulp Sensibility Test]
(Cold testing is especially useful for patients with
porcelain jacket crowns or porcelain-fused-to-metal crowns where there is no natural tooth surface (or much metal) accessible).
(Digital pressure on the tooth itself, and then on the soft tissues adjacent to root apex may elicit pain, or may reveal soft/ hard tissue swelling).
|Electrical (Pulp Sensibility Test)
(Sub-periosteal infiltration or intraligamentary local anesthesia)
[Adapted from: Mount & Hume].
- Heat testing is most useful when a patient’s chief complaint is intense dental pain on contact with any hot liquid or food. When a patient is unable to identify which tooth is sensitive, a heat test is appropriate. Starting with the most posterior tooth in that area of the mouth, each tooth is individually tested. That tooth will exhibit an immediate, intense painful response to the heat.
- With heat testing a delayed response may occur, so waiting 10 seconds between each heat test will allow sufficient time for any onset of symptoms.
- Often a tooth that is sensitive to heat may also be responsible for some spontaneous pain. In these cases the patient may present with cold liquids in hand just to minimize the pain. In these cases, the application of cold to a specific tooth may eliminate the pain and greatly assist in the diagnosis. Typically, a tooth that responds to heat and then is relieved by cold is found to be necrotic.
- Cold is the primary pulp testing method for many clinicians today. To be most reliable, cold testing should be used in conjunction with an electric pulp tester so that the results from one test will verify the findings of the other test.
- If a mature, untraumatized tooth does not respond to both electric pulp test and cold test, then the pulp should be considered necrotic.
- Multirooted teeth with at least one root containing vital pulp tissue may respond to a cold test even if one or more of the roots contain necrotic pulp tissue.
- This technique for cold testing is especially useful for patients presenting with porcelain jacket crowns or porcelain-fused-to-metal crowns where there is no natural tooth surface (or much metal) accessible.
Reversible Pulpitis –
The inflammation may resolve if the etiological factors are removed (by debridement or denial of a substrate by creation of an effective seal) at the stage of chronic inflammation and/or small acute foci. In other words, the pulpal inflammation is reversible. But such pulp tissue may be less able to withstand any future insults. This is because the cycle of inflammation and repair leads to reduced vascularity, cellularity, and increased fibrous nature of the pulp.
Irreversible Pulpitis –
In severe injury, or if there is a major immune-mediated response to the microbial challenge, the pulp tissue changes may become irreversible. There are 2 outcomes:
(1) Pulp may die painlessly over time, or
(2) Total necrosis occurs quite rapidly with considerable discomfort.
If the level of stimulus remains relatively constant, (eg. under a leaking but otherwise stable restoration – microleakage), the ability of the tissue to resist bacterial toxins will decline over time, and the reversible inflammation becomes irreversible.
The boundary between reversible and irreversible pulpitis is impossible to define. Remove the cause and a pulp in a healthy young patient may heal from a state of chronic, suppurative inflammation such as a pulp micro-abscess. On the other hand, in older individuals or in teeth which have been subjected to previous episodes of inflammation, a pulp micro-abscess is more likely to spread because the tissue is less able to elaborate repair. In such circumstances toxic products of cell lysis may kill adjacent cells.
Clinically it is important to develop the ability to discriminate between a pulp which might heal following conservative therapy and one which will not.
In an adult, irreversible inflammation is characterized by:
||· Pain/ sensitivity to cold;
· Pain is provoked (not spontaneous);
· Pain subsides soon after provocation;
· No radiating pain.
|Symptomatic Irreversible Pulpitis
||· Pain due to consumption of hot foods/ drinks;
· Spontaneous (unprovoked) pain;
· Pain lingers are removal of provocation;
· Pain due to heat, pain subsided on cold (this is because the thermal threshold of nociceptors is lowered);
· Patient cannot localize pain to a particular tooth, or whether it is in maxilla or mandible (this is because pulp has no/ scarce pressure receptors);
· Pain at night (supine posture leads to increased blood flow to head & offending tooth).
|Asymptomatic Irreversible Pulpitis
||· The typical pain associated with the symptomatic variety is absent.
Histological examination: of the tooth responsible will generally reveal at least one pulpal micro-abscess, often in the area of a pulp horn (Micro-abscess is an accumulation of polymorphonuclear (PMN) leucocytes and dead, dying pulp cells in the form of pus). The area of pus formation will be surrounded by fibrous connective tissue infiltrated with PMN leucocytes and, slightly further away, chronic inflammatory cells.