Pulpal and Periapical Disease

Clinically Normal Pulp

⮚ These teeth respond to cold with mild pain that resolves in 1 to
2 seconds
⮚ Heat is not associated with pulpal discomfort.
⮚ Pain to percussion will not be evident.
⮚ Normal on radiographic examination .
 01 02 03

Mechanical damage: iatrogenic damage

from dental procedures, attrition and
Thermal injury Chemical irritation
abrasion

Bacterial effects: Bacteria can damage the pulp

04 through toxins or directly after extension from
caries or transportation via the vasculature.

PULPITIS
Four main types of noxious stimuli are common
causes of pulpal inflammation (pulpitis):
PULPAL
PATHOPHYSIOLOGY
CLASSIFICATION OF PULPAL DISEASES

Reversible pulpitis:
pulpal inflammation in which the tissue is capable
of returning to a normal state of health if the
noxious stimuli are removed.

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Irreversible pulpitis:
implies that a higher level of inflammation has
developed in which the dental pulp has been
damaged beyond the point of recovery
 Clinically Normal Pulp
• Discomfort resolves within a few seconds after
elimination of the stimulus (cold or sweet foods, but
sometimes heat).
• Pain does not occur spontaneously and does not
continue when stimulus has been removed
• Mobility and sensitivity to percussion are absent
 Clinical Features Of Revisable
Pulpitis
• Discomfort resolves within a few seconds after elimination of the stimulus
(cold or sweet foods, but sometimes heat).
• Pain does not occur spontaneously and does not continue when stimulus
has been removed
• Mobility and sensitivity to percussion are absent
Clinical Features Of Irreversible Pulpitis

Sharp, severe pain on thermal

01 stimulation, and the pain continues
for a longer period of time after the
stimulus is removed

Cold is especially uncomfortable, although

heat or sweet and acidic foods also can
02 elicit pain. In addition, the pain may be
spontaneous or continuous and may be
exacerbated when the patient lies down
Early stages of irreversible pulpitis:

The pain often can be localized easily

to the individual offending tooth;
with increasing discomfort, however,
the patient may be unable to identify
the offending tooth within a quadrant
 Later stages of irreversible pulpitis,
The pain increases in intensity and is
experienced as a throbbing pressure that can
keep patients awake at night. At this point,
heat increases the pain; however, cold may
produce relief
 Treatment and Prognosis
• Reversible pulpitis is treated by removal of the local
irritant. On occasion, analgesic medications sometimes
are desirable. The prognosis of reversible pulpitis is
good if action is taken early enough.
• Irreversible and chronic hyperplastic pulpitis are
treated by extraction of the tooth or by root canal
therapy.
 Chronic Hyperplastic Pulpitis
❖ chronic hyperplastic pulpitis (pulp polyp)
❖ This condition occurs in children and young adults(high tissue response ,healing
and repair) who have large exposures of the pulp in which the entire dentinal roof
often is missing
❖ The pulp response to stimuli in proliferative manner instead of destruction
❖ The most frequently involved teeth are the deciduous or succedaneous molars,
which have large pulp chambers in these age groups.
❖ Mechanical irritation and bacterial invasion result in a level of chronic
inflammation that produces hyperplastic granulation tissue that extrudes from the
chamber.
❖ The apex may be open and reduces the chance of pulpal necrosis secondary to
venous compression.
❖ The tooth is asymptomatic except for a possible feeling of pressure when it is
placed into masticatory function and bleeding
Infographic Style
PULPAL CALCIFICATIONS
⮚ Calcifications within the dental pulp are not rare.
The three types of pulpal calcifications are:

01 Denticles

02 Pulp stones

03 Diffuse linear calcifications

All pulpal calcifications start out as free bodies

within the pulp tissue, but many may become
attached or embedded in the dentinal walls of the
pulp.
• Denticles: are believed to form as a result of an epithelia mesenchymal
interaction within the developing pulp. Epithelial strands originating from the
root sheath, or cervical extensions into the pulp chamber adjacent to furcations,
induce odontoblastic differentiation of the surrounding mesenchyme of the
dental papilla, forming the core of the denticle. Odontoblasts deposit tubular
dentin as they move away from the central epithelium and produce thimble
shaped structures surrounding the epithelium. (True pulp stone)
• pulp stones :are believed to develop around a central nidus of pulp tissue (e.g.,
collagen fibril, ground substance, necrotic cell remnants). Initial calcification
begins around the central nidus and extends outward in a concentric or radial
pattern of regular calcified material. (False pulp stone)
• Diffuse linear calcifications: they exhibit areas of fine, fibrillar, irregular
calcification that often parallel the vasculature. (False pulp stone)
 Clinical and Radiographic Features
✔Denticles and pulp stones can reach sufficient size to
be detected on intraoral radiographs as radiopaque
enlargements within the pulp chamber or canal .
✔ Diffuse calcifications are not detectable
radiographically.
Prominent pulpal calcifications have been noted in association
with certain disease processes, such as the following:

• Dentin dysplasia type Id Tumoral calcinosis

• Calcinosis universalis
• Dentin dysplasia type II

• Ehlers-Danlos syndrome
• Pulpal dysplasia

• End-stage renal disease

 Treatment and Prognosis
• No treatment is required. Most pulpal calcifications are not
associated with any significant clinical alterations.
• rare difficulties during endodontic procedures, pulpal
calcifications are typically of little significance
 Acute periapical periodontitis
✔Is the initial phase of periapical inflammatory disease
✔Creates a constant dull, throbbing pain, the associated tooth responds
negatively to vitality testing or reveals a delayed positive result.
✔Typically patient have marked tenderness to percussion and pain
when pressure is applied to the tooth
✔ Radiographically, the periodontal ligament space and lamina dura
may appear normal or there may be just a slight thickening of the
periodontal ligament space and some loss of the lamina dura around
the apex of the tooth root
✔If the acute inflammatory process evolves into a chronic pattern, then
the associated symptoms diminish
 PERIAPICAL GRANULOMA (CHRONIC APICAL
PERIODONTITIS)
Most periapical granulomas are
asymptomatic, but pain and
sensitivity can develop if acute
exacerbation occurs.
Typically, the involved tooth
does not demonstrate mobility
or significant sensitivity to
percussion.
The soft tissue overlying
the apex may or may not
be tender.
The tooth does not respond to thermal
or electric pulp tests unless the pulpal
necrosis is limited to a single canal in a
multirooted tooth.
Most lesions are discovered on
routine radiographic examination,
the associated radiolucencies are
variable.
granulomas can transform into cysts or
abscesses (and vice versa) without
significant radiographic change, it is
not surprising that the radiographic
features are not diagnostic
 Treatment

RCT or Extraction
 PERIAPICAL CYST (RADICULAR CYST)
✔Epithelium at the apex of a nonvital tooth presumably can be stimulated
by inflammation to form a true epithelium lined cyst, or periapical cyst.
The source of the epithelium is usually a rest of Malassez
✔Periapical cysts represent a fibrous connective tissue wall lined by
epithelium with a lumen containing fluid and cellular debris
✔ On occasion, a similar cyst, best termed a lateral radicular cyst, may
appear along the lateral aspect of the root.
✔Periapical inflammatory tissue that is not curetted at the time of tooth
removal may give rise to an inflammatory cyst called a residual
periapical cyst.
 Treatment
• The treatment for radicular cysts includes
conventional nonsurgical root canal therapy
when lesion is localized or surgical treatment like
enucleation, marsupialization or decompression
when lesion is large.
 PERIAPICAL ABSCESS
The accumulation of acute inflammatory
cells at the apex of a nonvital tooth is
termed a periapical abscess
Periapical abscess designated as
symptomatic or asymptomatic on
the basis of their clinical
presentations.
The initial stages produce
tenderness of the affected tooth
may arise as the initial periapical pathosis
or from an acute exacerbation of a chronic
periapical inflammatory lesion
Periapical abscesses become
Contents
symptomatic as the purulent material
Title
accumulates within the alveolus.
With progression, the pain becomes more
intense, often with extreme sensitivity to
percussion, extrusion of the tooth, and swelling
of the tissues.
 PERIAPICAL ABSCESS

Radiographically,
The offending Headache, abscesses may
tooth does not malaise, fever, demonstrate a thickening
respond to cold of the apical periodontal
or electric pulp and chills may ligament, an ill-defined
testing. be present. radiolucency
✔With progression, the abscess spreads along the path of least resistance. The
purulence may extend through the medullary spaces away from the apical area,
resulting in osteomyelitis, or it may perforate the cortex and spread diffusely
through the overlying soft tissue (as cellulitis).
✔Once an abscess is in soft tissue, it can cause cellulitis or may channelize through
the overlying soft tissue. The cortical plate may be perforated in a location that
permits entrance into the oral cavity. The purulent material can accumulate in the
connective tissue overlying the bone and can create a sessile swelling or perforate
through the surface epithelium and drain through an intraoral sinus.
✔At the intraoral opening of a sinus tract, a mass of subacutely inflamed granulation
tissue often is found known as a parulis (gum boil).
• Occasionally, the nonvital tooth associated with the
parulis may be difficult to determine, and insertion of a
guttapercha point into the tract can aid in detection of the
offending tooth during radiographic examination.
• Dental abscesses also may channelize through the
overlying skin and drain via a cutaneous sinus.
• Most dental-related abscesses perforate buccally because
the bone is thinner on the buccal surface. However,
infections associated with maxillary lateral incisors, the
palatal roots of maxillary molars, and mandibular second
and third molars typically drain through the lingual cortical
plate.
• If a chronic path of drainage is achieved, a periapical
abscess typically becomes asymptomatic because of a lack
of accumulation of purulent material within the alveolus.
If the drainage site becomes blocked, then signs and
symptoms of the abscess frequently become evident in a
short time .
 Treatment and Prognosis
✔Treatment of the patient with a periapical abscess consists of drainage and elimination of the focus
of infection.
✔When the abscess causes clinical expansion of the bone or soft tissue adjacent to the apex of the
affected tooth, incisional drainage of the swelling should be considered because this technique
appears to be associated with more rapid resolution of the inflammatory process when compared
with drainage through the root canal
✔Unless contraindicated, treatment with NSAIDs usually is appropriate preoperatively, immediately
postoperatively, and for subsequent pain control.
✔Typically, use of antibiotic medications for a well-localized and easily drained periapical abscess in a
healthy patient is unnecessary. Antibiotic coverage should be reserved for the medically
compromised and patients with significant cellulitis.
✔Once the infection has been resolved by extraction or appropriate endodontic therapy, the affected
bone typically heals.
• IfCELLULITIS
an abscess is not able to establish drainage through the surface of
the skin or into the oral cavity, it may spread diffusely through fascial
planes of the soft tissue This acute and edematous spread of an acute
inflammatory process is termed cellulitis.
• . Although numerous patterns of cellulitis can be seen from the
spread of dental infections, two especially dangerous forms warrant
further discussion: (1) Ludwig angina and (2) cavernous sinus
thrombosis

CELLULITIS
 Ludwig angina
• Acute , firm, non suppurating, necrotizing cellulitis involving bilateral sub
lingual ,submandibular and submental spaces.
• In approximately 70% of cases, Ludwig angina develops from spread of an
acute infection from the lower molar teeth.
• Other situations associated with this clinical presentation are peritonsillar or
parapharyngeal abscesses, tongue piercing, oral lacerations, fractures of the
mandible, or submandibular sialadenitis.
• Once the infection enters the submandibular space, it may extend to the
lateral pharyngeal space and then to the retropharyngeal space.
 Clinical Features
Involvement of the lateral pharyngeal
space can cause respiratory obstruction
Submandibular space spread secondary to laryngeal edema.
causes enlargement and Tachypnea, dyspnea, tachycardia,
tenderness of the neck above the stridor, restlessness, and the patient’s
level of the hyoid bone (bull need to maintain an erect position
neck). suggest airway obstruction.

01 02 03 04 05

Involvement of the sublingual

space results in elevation,
posterior enlargement, and
protrusion of the tongue
(woody tongue), which can
compromise the airway.
Pain in the neck and floor of mouth
may be seen in addition to restricted
neck movement, dysphagia,
dysphonia, dysarthria, drooling, and
sore throat.
Fever, chills, leukocytosis, and
an elevated sedimentation rate
may be seen. Classically, obvious
collections of pus are not
present
 Treatment of Ludwig angina centers
around two major priorities:
maintenance of the airway and
resolution of the infection.

Treatment and Prognosis Ludwig Angina

✔Cavernous sinus thrombosis appears as an edematous periorbital
enlargement with involvement of the eyelids and conjunctiva.
✔ In cases involving the canine space, swelling is also typically present
along the lateral border of the nose and may extend up to the medial
aspect of the eye and periorbital area .
✔Protrusion and fixation of the eyeball often are evident, in addition
to induration and swelling of the adjacent forehead and nose. Pupil
dilation,

Cavernous Sinus Thrombosis

 OSTEOMYELITIS
Is an acute or chronic inflammatory process in the medullary
spaces or cortical surfaces of bone that extends away from 01
the initial site of involvement.

The vast majority of osteomyelitis cases are

Acute suppurative osteomyelitis: exists
when an acute inflammatory process
spreads through the medullary spaces of
the bone and insufficient time has passed
for the body to react to the presence of
the inflammatory infiltrate.
04
02 caused by bacterial infections and result in an
expanding lytic destruction of the involved
bone, with suppuration and sequestra
03 formation.
Chronic suppurative osteomyelitis: exists when the
defensive response leads to the production of
granulation tissue, which subsequently forms dense
scar tissue in an attempt to wall off the infected area
Clinical Features Acute Suppurative Osteomyelitis

✔Pain, paresthesia of lip

✔Fever, leukocytosis, lymphadenopathy, significant
sensitivity, and soft tissue swelling of the affected area may
be present.
✔Purulent exudate and fetid odor.
✔Mobility of teeth in the affected site.
❑ A fragment of necrotic bone that has separated
from the adjacent vital bone is termed a
sequestrum. Sequestra often exhibit spontaneous
exfoliation.
❑ On occasion, fragments of necrotic bone may
become surrounded by new vital bone, and the
dead bone in this situation is known as an
involucrum.
Chronic Suppurative Osteomyelitis Clinical
Features

✔Less severity.
✔Swelling, mild to moderate pain.
✔ sinus formation, purulent discharge, sequestrum
formation, tooth loss, or pathologic fracture may
occur
 Radiographic Features
o Location: posterior mandible, rare o Internal structure:
.
in maxilla.
1. Acute osteomyelitis: mixed
(RO/RL),trabeculations
patterns has a loss of
o Edge: acute ill defined ,chronic well sharpness ,sequestration
may be present .
defined.
2. Chronic osteomyelitis: mixed
(RO/RL),sequestrations more
common
 Other structure

✔ Acute osteomyelitis:

1. may lead to bone formation or resorption.

2. cortical bone resorption.
3. periosteum may be lifted by inflammation
onion skin appearance of bone referred to
proliferative periostitis

✔ Chronic osteomyelitis:
1. formation of new periosteal bone (proliferative periostitis
2. teeth may undergo external resorption
3. draining fistula
Treatment of
Chronic • Surgical intervention is mandatory, the extent of the surgical intervention
Suppurative depends on the spread of the process; removal of all infected material down
to good bleeding bone is mandatory in all cases. For small lesions, curettage,
Osteomyelitis removal of necrotic bone, and saucerization are sufficient. In patients with

B
more extensive osteomyelitis, decortication or saucerization often is
combined with transplantation of cancellous bone chips.
A
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• Chronic osteomyelitis is difficult to manage • The antibiotic medications are similar to

medically because pockets of dead bone those used in the acute form but must
and organisms are protected from
antibiotic drugs by the surrounding wall of be given intravenously in high doses.
fibrous connective tissue.
 Treatment of Acute Suppurative Osteomyelitis

resolve the source of

infection

establish drainage

removal of obviously
infected bone
obtain bacteriologic samples
for culture and antibiotic
sensitivity testing
THANK YOU
DR.Khairy ABU-Zant