This document discusses various pathologies that can affect the dental pulp and their sequels. It begins with definitions of pulp and pulpitis, describing pulpitis as an inflammatory response to noxious stimuli. Pulpitis is classified as reversible or irreversible. Causes and risk factors of pulpitis include mechanical, thermal, chemical, and bacterial factors. Sequels of untreated pulpitis include pulp necrosis, periapical abscesses, and periapical lesions such as granulomas or scars. Other topics covered include pulp degeneration, calcification, polyps, and dry socket. Throughout, the document provides details on clinical features, mechanisms, management approaches, and importance of prevention for these dental pulp conditions and their outcomes
3. What is pulp? What is pulpits? How does pulpitis takes place
(mechanism)?
Definition and classification01
Major causes and risk factors
Clinical features02
What are signs and symptoms?
complications03
How many divisions need to be under consideration to obtain a
good classification for pulpal inflammation?
Management04
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PULP
What is pulp?
Pulp is inner portion of tooth after enamel
and dentin which has been described as both
a highly resistant organ and as an organ with
little resistance or recuperating ability. It is a
delicate connective tissue liberally
interspersed with tiny blood vessels,
lymphatics, myelinated and unmyelinated
nerves, and undifferentiated connective
tissues cells.
6. WHAT IS
PULPITIS?
Pulpitis or inflammation of the pulp in human teeth
occurs most commonly secondary to dental caries
that has penetrated the enamel and dentin, and is
usually associated with pain. Because of the intimate
relationship between dentin and pulp, together they
have been termed the dentinopulp complex, which
emphasizes the fact that an insult to dentin can also
insult pulp.
The inflammatory response by pulp includes the
development of edema and the influx of lymphocytes,
plasma cells, and macrophages. Due to pulp being
completely encased in its rigid dentinal chamber, the
inflammatory response increases the pressure in the
pulp chamber/horn that can cause a collapse of the
venous microcirculation. This can result in areas of
pulpar hypoxia and anoxia that may lead to localized
or generalized pulp necrosis and death.
If the pulp survives, it allows tertiary dentin
formation to seal off the area of insulted (e.g.,
exposed) pulp, and this hopefully results in complete
resolution of the pulpitis.
8. Causes and risk factors
Mechanical (attrition, abrasion, trauma …)
Thermal (uninsulated restorations, polishing…)
Chemical (erosions due to dental materials’ acids and base
properties)
Bacterial (anachoresis, streptococci, staphylococci)
Heat Chemical Mechanical Bacterial Life-style
Life-style (tobacco, high sugar diet, chronic bruxism, poor
oral hygiene habit…)
9. Reversible pulpitis: It is a mild to moderate inflammatory condition of the pulp caused by
noxious stimuli in which the pulp is capable of returning to un-inflammed state following
removal of the stimuli.
Irreversible pulpitis: It is a persistent inflammatory condition of the pulp, which may be
symptomatic or asymptomatic and is caused by a noxious stimulus.
It is by bacterial involvement of the pulp through caries, although many clinical factors, chemical,
thermal or mechanical injury may also be the cause.
Reversible vs
irreversible Clinical differences
The pain of irreversible pulpitis is
more severe and lasts longer. In
reversible pulpitis, the cause of pain
is generally traceable to a stimulus
such as cold water or air whereas in
irreversible pulpitis, the pain may
come without any apparent stimulus.
10. DEFINITION
MECHANISM
CLINICAL FEATURES
• It is a productive pulpal inflammation developed from
granulation tissue, covered by epithelium, resulting long-term
with low-grade pulpal infectious exposure.
• In order to a polyp be developed, a large open cavity (pulpitis
operta), a young resistant pulp and a chronic low-grade
stimulus are necessary.
• Mostly involved teeth are deciduous molars and first
permanent molars of children and youngs due to large root
openings and well blood supply. It appears as a fleshy, reddish
pulpal mass, filling most of the pulpal chamber and sometimes
even more that interferes comfortable closure. It is
asymptomatic, more resistant that pulp tissue but less resistant
than gingiva. Due to pressure during chewing bolus, pain may
be felt and bleeding may happen (because of large venous
mesh
Chronic pulp
hyperplasia
(pulp polyp)
11. What
is PULP
DEGENERATION
Present in elder people as a result
of persistent irritants in teeth
since youngsters.
In early stages, there are no symptoms and no clinical findings. As
degeneration progresses, the tooth may become discolored and the
pulp within does not respond to stimuli.
Calcific degeneration—A part of pulp tissue is replaced by calcific material
that is pulp stones and denticles are formed. The calcific material has a
laminated structure like the skin of an onion and lies unattached within the
body of pulp. In another type of calcification, the calcified material is
attached to the wall of the pulp cavity and is an integral part of it which is
called as diffuse calcification.
Atrophic degeneration—It is observed in older people. The pulp tissue is less
sensitive than normal.
Fibrous degeneration—It is characterized by replacement of the cellular
element by fibrous connective tissue. On removal from the root canal, the
pulp has the characteristic appearance of a leathery fiber.
12. PULP CALCIFICATION
Various forms of pulp calcifications
are found within the pulp which may
be located in the pulp chamber or in
the root canals. It can occur in any sex
and in any teeth in the dental arch.
They can be seen in forms of pulp
stones, pulp denticles and pulp
diffuse calcification.
CLINICAL FANIFESTATION
There is no clear-cut etiology. There is
no relation between pulpal
inflammation and irritation, as that
arising from caries or trauma, since pulp
calcification can be found in unerupted
teeth. Extremely high percentage of
pulp stones yield pure growth of
streptococci on culture but often the
affected teeth are normal.
ETIOLOGY
13. SEQUELS OF PULPITIS If none of the irritating products of pulp necrosis
reach the periapical tissue, then no periapical
pathos is induced.
Carious tooth
(reversible state)
Pulpitis
(irreversible state)
Pulp necrosis
(no treatment applied)
Periodontal diseases
(infections spread
through root canal
into periodontal
tissues)
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14. An abscess is a localized
collection of pus, surrounded
by an area of inflamed tissue
in which hyperemia and
infiltration of leucocytes is
marked.
Periapical abscess is a
localized collection of pus in
the alveolar bone, at the root
apex of a tooth, following
death of the pulp.
PERIAPICAL
ABCESS
15. It develops in the periapical region of the
tooth as sequelae to necrosis of pulp. Pain
is severe and of throbbing type.
Periapical abscess may confine to osseous
structures and during the early period of
abscess formation, may cause excruciating
pain without observable swelling. The
patient may appear pale, irritable and
weak from pain, loss of sleep as well as
from absorption of septic products. He may
have slight fever (99 to 100°F).
Patients experience sensitivity or pressure
in the affected area. Ice relives the pain and
heat intensifies it aspiration yield
yellowish pus. The tooth becomes more
painful, appears elongated and mobile.
16. Establish drainage immediately, if possible — may be done
by opening the pulp chamber and passing file through the
canal into the periapical region.
Antibiotics like Penicillin 500 mg, qid, for 5 days and
analgesics should be given. In 24 to 48 hours, it can be
determined if the tooth can be treated endodontically or
extraction is necessary.
MANAGEMENT
17. DRY SOCKET
Dry socket (alveolar osteitis) is a painful dental
condition that sometimes happens after you
have a permanent adult tooth extracted. Dry
socket is when the blood clot at the site of the
tooth extraction fails to develop, or it dislodges
or dissolves before the wound has healed.
Exposure of the underlying bone and nerves
results in intense pain, not only in the socket but
also along the nerves radiating to the side of
your face. The socket becomes inflamed and
may fill with food debris, adding to the pain. If
you develop dry socket, the pain usually begins
one to three days after your tooth is removed.
Dry socket is the most common complication
following tooth extractions, such as the removal
of third molars (wisdom teeth).
18. Clinical features & causes
Signs and symptoms
Severe pain within a few days after a tooth extraction
Partial or total loss of the blood clot at the tooth
extraction site, which you may notice as an empty-
looking (dry) socket
Visible bone in the socket
Pain that radiates from the socket to your ear, eye,
temple or neck on the same side of your face as the
extraction
Bad breath or a foul odor coming from your mouth
Unpleasant taste in your mouth
Causes and risk factors
Bacterial contamination of the socket
Trauma at the surgical site from a difficult extraction,
as with an impacted wisdom tooth
Smoking and tobacco use.
Oral contraceptives.
Improper at-home care.
Having dry socket in the past.
Tooth or gum infection.
19. It is composed of dense fibrous tissue
and is situated at the periapex of
pulpless tooth, in which usually
Confined in the periapical area, which
leads to accumulation of chronic
inflammatory cells. Young fibroblasts,
endothelial cells and capillaries
proliferate, which lead to granuloma
formation. After endodontic treatment,
the granuloma resolves, but in some
cases, granulation tissue gets slowly
organized with the production of more
and more collagen fibers, which in
turn leads to scar formation.
PERIAPICAL
SCAR
20. Clinical features
of apical scar
It occurs usually after
endodontic treatment and in
patients treated by periapical
curettage or root resection. It is
more common in anterior region
of maxilla. Tooth is nonvital and
the patient is asymptomatic.
Periapical scar (fibrous scar)