Pulpitis.

Etiology and
pathogenesis of pulpitis.
Classification of pulpitis.
Diagnosis.
Musteata Olesea, assistant professor
2019
Pulpitis is the inflammation of dental pulp, the result
of tissue reaction to different excitants.

Etiology
Classification of etiologic factors:
I group: pathogenic agents with determining role.
II group: pathogenic agents with predisposing role.
I group includes:
a. physical factors: thermal, traumatic (mechanical,
physical, chemical);
b. chemical: acids, base, oxidants;
c. biological factors: virus, bacteria, micelle (Bacteria:
Streptococcus haemolytic, Staphylococcus, bacilli, gram
negative, gram positive streptococcus, lactobacillus).

II group includes general pathologies:

- Dismetabolism
- Systemic diseases
- Avitaminosis
- Endogenic intoxications
Thermal factors are:
- Decrease of temperature;
- Rough action of electrode in diathermia;
- Incorrect appreciation of pulp vitality in electrocautery – the
passing into carious cavity;
- Metallic obturations ( absence of isolation base);
- Variations of temperature in nourishing;
- Thermal agent with violent action: accidental opening of pulp
cavity;
- The traumatism with slowly repeated action: high obturation
(overocclusion), the incorrect adaptation of crowns, orthodontic
devices.
Chemical agents are:
In the past were used materials as Noracryl,
Acryloxide, Evicrol that cased action on fibers
(hyperexcitability) and hemodynamic disorders. Agents
with high concentration causes pulpitis (alcohol, sol.
H2O2 6%).
The recommended medication in pulpitis cleaning are
Iodinol, Furaciline.
Microbial agents are:
The incorrect working cause the extention of infection in dentine
tubules.
The reaction is developed in following way: biochemical – none
symptom is evident, a physiological silence, in 2-15 hours are
produced actively tissular enzymes that inactivate odontoblasts.
Ex.: kinase, act by interference of RNA-ase – a messenger of
proteins synthesis: excites the odontoblasts, cause vascular
dilatation, increase vascular permeability.
Occurs hypoxia, reaction of cellular metabolism and cell’s
modifications.
The cells are increased in volum, their shape are modified and the
organs of cell are increased. The phenomenon of picnosis and
vacuolization occur, lipids are gathered and the cell is destroyed, PH
of pulp is modified because of toxins accumulation.
First PH is neutral, then arises permanent acidosis with value PH=5
that cause depolymerization of cells and favours the increasing of
vascular permeability, hyperemia, hobbles the impulse transmission,
favours processes of cellular lysis.
The intratissular pressure is increased for 3-4 times. For nervous
fibers excitability is increased, then decreased and deterioration by
detaching of myelin sheath, then are divided into fragments because
of excitability. A purulent infiltration is formed, pulpal abscess and
the process comprises whole the pulp.
WHO classification:
K.04 Pulpal diseases
K.04.0 Pulpitis
K.04.00 hyperemia of the pulp
K.04.01 acute
K.04.02 abscess of the pulp
K.04.03 chronic
K.04.04 chronic ulcerative
K.04.05 chronic hyperplastic (pulpal polyp)
K.04.08 other specified pulpitis
K.04.09 unidentified pulpitis
K.04.1 Pulp necrosis. Pulp gangrene.
K.04.2 Pulp stones. Denticles.
K.04.3 Abnormal formation of hard dental tissue in the pulp: secondary irregular formation of
dentine.
 
Classification of pulpal diseases ( from R.E. Walton
and M. Torabinejad book, 2002):
 Reversible pulpitis
 Irreversible pulpitis
 Hyperplastic pulpitis
 Pulp necrosis
 Hard tissue responses include calcifications and
resorbtion
 
Classification of E.M.Gofung (1927):

1. Acute pulpitis:
a. partial,
b. general,
c. purulent.
2. chronic pulpitis:
a. simple,
b. hypertrophic,
c. gangrenous.
Classification of Moscow Medical Institute of Stomatology:

1. acute pulpitis:
a. focal,
b. diffuse.
2. chronic pulpitis:
a. fibrous (simple),
b. gangrenous,
c. hypertrophic.
 3. Exacerbation of chronic pulpitis
4. State after partial or complete pulp extirpation
Classification of pulp lesions according to M. Gafar and C. Andreescu
(Bucharest, 1990):

1. Acute pulpitis:
a. serous:
* with limited morphopathological lesions (acute serous partial or
coronal pulpitis);
* with morphopathological lesions in whole pulp (serous total or corono-
radicular pulpitis);
b. purulent:
* with limited focuses (acute purulent partial or coronal pulpitis);
* with focus in whole pulp ( acute purulent total or corono-radicular
pulpitis).
 
2. Chronic pulpitis:
a. closed (no outside communication):
* chronic properly-closed pulpitis;
* chronic internal granulomatous pulpitis (internal
granuloma Palazzi)
b. opened:
* ulcerous;
* granulomatous (polypous).
Classification according to V.Moghilnitski, A.I.Evdokimov (1925):

I. group: vascular disturbance: hemorrhagic, hyperemia;

II. group:
 exudative inflammation (superficial pulpitis, partial serous
pulpitis, purulent generalized pulpitis);
 proliferative inflammation (fibrous pulpitis, granulomatous
pulpitis);
III. group: regressive processes:
 atrophy, necrosis, gangrene, concrements.
IV. group: progressive processes (denticles).
Classification of Shkoler (1967):

I. group acute incipient pulpitis;

II. group acute purulent pulpitis with lateness;
III. group addressing;
IV. group chronic fibrous pulpitis;
V. group chronic ulcerous pulpitis;
VI. group chronic granulomatous pulpitis;
VII. group radicular pulpitis (gangrene);
VIII. group aggravated pulpitis.
Diagnosis of pulpitis
1. patient complaints:
* pain: sharp, severe, localized (focal), caused from thermal excitants
(first from cold then from hot/warm)
* pain duration is 15-20 minutes called pain attack then comes light
period 2-4 hours (in acute focal pulpitis) and with disease progression
reach over 2 hours and light periods are reduced to 10-20 minutes (in
acute diffuse pulpitis); pain episodes are intermittent then become more
frequent, pain occur spontaneously especially in the evening or at night
and may pass spontaneously, and for pain relief are recommended
analgetics;
* pain is spontaneous;
* pain in the night prevails over the day, because during the night the
parasympathetic nervous system activity dominate under sympathetic;
during the night heart rate is slow and circulation is slow that leads to
accumulation of toxins products in the pulp; this produces irritation of
nerve receptors that is called pain;
* pain can be violent, progressive, unbearable ( in acute diffuse pulpitis
the pain is as “crazy tooth”);
* pain irradiation along the branches of trigeminus nerve, irradiation
zones: to adjacent teeth, temporal region, orbital region,
submandibular, occipital region, sterno-cleido-mastoideus muscle
(figure 1);
* pain irradiation does not pass the median line.
 
2. Clinical examination: intraoral examination:
* inspection: normal tooth color with deep cavity and
destroyed dentine, after removing the food debris and drying
a thin layer of pigmented dentine can be seen;
* probing causes intense pain reaction (in acute focal pulpitis
at one point, and in diffuse pulpitis on whole the bottom);
* vertical percussion is painless in acute focal pulpitis and
slightly painful in acute diffuse pulpitis;
Figure 1. Regions of pain irradiation in pulpitis.
a. maxillary teeth; b. mandibular teeth.
3. Paraclinical examination:
* thermal probe is intensive, long time pain;
* pulp testing (electro-odontometry) is the health pulp respond to low
intensity current, in norm is 2-6 mA; in acute focal pulpitis is 20-25 mA,
acute diffuse pulpitis is 30-60 mA, chronic forms of pulpitis is 60 mA, pulp
necrosis is up to 100 mA.
mkA=µA=uA=0,000001A=0,001 mA
*Radiography (x-ray diagnosis) is additional method to detect hidden
cavities, denticles, changes of periodontium. Periodontium changes on
radiographs in chronic pulpitis are 28% of cases with periodontal
ligament extension and root apex resorption.
Histopathology
The inflammatory process in the pulp is basically the same as elsewhere in the body,
but the process may be modified by various factors, including the nature and
severity of the insult, the efficiency of the host defence mechanisms, and its special
anatomical location. Figure 2. The pulp is almost totally surrounded by dentine
which limits the ability of the pulp to tolerate oedema . Thus, the pressure rise in the
pulp associated with an inflammatory exudate may cause local collapse of the
venous part of the microcirculation. This leads to local tissue hypoxia and anoxia,
which in turn may lead to localized necrosis. Chemical mediators released from the
necrotic tissue lead to further inflammation and oedema, and total necrosis of the
pulp may follow the continued spread of local inflammation. Reactionary dentine
may continue to form after the onset of pulpitis, providing the odontoblasts and pulp
have been irreversibly damaged, and may in time protect the pulp from further
injury by increasing the thickness of calcified tissue between the pulp and irritant in
the dentine.
Figure 2. Factors influencing the outcome of
inflammation in the dental pulp.
Pulpitis caused by caries always starts as a localized area of
inflammation directly related to the carious dentine, the
inflammation eventually extending throughout the pulp if the
caries is not treated. Carious lesions differ with respect to
bacteriology, rates of progression, and pulpodentinal reactions,
and so the rate of progression of the inflammation in the pulp will
vary from individual and from tooth to tooth. In multirooted
teeth the inflammation may progress to the apex of one root
even before the whole of the pulp chamber is involved.
The severity of the irritation to the pulp from dental caries increases as
the caries advances pulpwards. The relatively low level of irritation
initially leads to a mild inflammatory response in which there is diffuse
infiltration beneath the odontoblasts by a few mononuclear
inflammatory cells, principally lymphocytes and macrophages,
responding to antigenic products from bacteria and carious dentine.
Acute exudative changes are not prominent at this stage, but as the
bacteria in the carious dentine reach the pulp, the vessels in the area
become dilated and congested. Figure 3.
As the inflammatory exudate develops (figure 4) the local
microcirculation may be compromised, leading to local death of
tissue as previously described. This predisposes to suppuration
due to the progressive accumulation of neutrophil leucocytes
which release their lysosomal enzymes when they die.
Suppuration may be local, forming a pulp abscess (figure 5,6), or
may spread diffusely through the pulp depending on the interplay
of the variables outlined in figure 2. Immune reactions in the
inflamed tissue may also contribute to the tissue damage.
Figure 3.Vasodilatation and acute exudative changes in the dental pulp
associated with bacterial invasion of reactionary dentine (purple-streaked
tubules).
Figure 4. Expansion of the area of inflammation in
developing pulpitis.
A pulp abscess may become static ( or even reduce in size) if the pulp
defences are sufficient to contain the level of bacterial challenge, in
which case the area of suppuration is surrounded by a zone of
proliferating granulation tissue (the so-called pyogenic membrane) as a
damaged pulp undergoes organization and repair. In some cases the pus
becomes walled off by fibrous tissue (Figure 6), with temporary
cessation of the spread of suppuration until such time as the level of
bacterial challenge overcomes the host defences.
In other cases the abscess may continue to expand due to
continued tissue damage and massive emigration of neutrophils
into the area of suppuration. As bacteria enter the inflamed
tissue from the carious dentine most are destroyed by the
neutrophil leucocytes and other host defence mechanisms;
larger numbers of bacteria are not generally seen in the pulp
until the late stages of total irreversible pulpitis. If there is
cavitation of the overlying carious dentine the pus may drain into
the mouth.
Figure 5. Suppurative inflammation in the dental
pulp progressing to abscess formation (top left of
field).
Although the rate of progression of pulpal inflammation is very variable, the
end result of an untreated pulpitis is total pulp necrosis except in the case of
pulp polyp formation. However, in clinical practice, providing that the pulp is
not cariously exposed and that the caries is successfully treated, healing of
the pulp is the most likely outcome. In a grossly carious tooth where there is
a risk of pulpal exposure then stepwise excavation of caries, over treatment
intervals of 3 to 6 months, may reduce the bulk of the bacterial challenge
sufficiently to allow the reactive defence mechanisms of the pulp to
overcome the insult and for healing to take place.
Pulpitis resulting from irritants other than caries shows essentially similar
histological changes, except that in some instances the initial response is an
acute exudative inflammation rather than a mononuclear inflammatory cell
infiltration as the irritation to the pulp may be much more severe than in
that provided by caries.
Figure 6. Localized pulpitis with localized
pulp abscess.