PULPAL AND PERIAPICAL DISEASES

Oral Pathology & Diagnosis Susan D. Richards, D.D.S.

ODRP 761 (CRN 10506) Winter Quarter 2018

A. Objectives

At the completion of this lecture on Pulpal and Periapical Diseases, the student will be able to:
1. List methods used to test the pulp and describe how to distinguish a vital tooth from a non-
vital tooth.
2. Be able to describe the different routes an apical infection may take and describe the clinical
effects it may have on the patient.
3. Discuss lesions using proper nomenclature.
4. State how common a given lesion is relative to other the pulpal/periapical lesions.
5. Discuss the following disease characteristics for each lesion studied.
a. Typical history for lesion
b. Clinical features
1) Age predilection
2) Gender predilection
3) Site predilection
4) Signs and symptoms, including those unique to the lesion
c. Radiographic features – especially classic radiographic presentations
d. Histologic features
e. Treatment and prognosis

6. Discuss the following lesions in terms of the above characteristics.

a. Pulpitis
b. Chronic hyperplastic pulpitis
c. Pulpal calcifications
d. Asymptomatic apical periodontitis
e. Symptomatic apical periodontitis
f. Acute apical periodontitis
g. Chronic apical periodontitis = dental granuloma
h. Dental abscess
i. Cellulitis
j. Osteomyelitis
k. Parulis
l. Ludwig's angina
m. Radicular cyst
n. Condensing osteitis

B. The tooth pulp may be assaulted by caries, trauma, ischemia, etc. Pulp responses to these assaults
can be evaluated using the following methods.

1. History of pain – particularly the pain character, triggers and duration

2. Thermal testing – cold and heat
3. Electronic pulp testing
4. Percussion of teeth
5. Palpation of area surrounding teeth
6. Visual examination
7. Radiographic examination

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C. Pulpitis (NDAC Ch. 3, p. 111)

1. These definitions are quoted from the Glossary of the American Academy of Endodontics.

2. Pulpitis is defined as a clinical and histologic term denoting inflammation of the dental pulp;
clinically described as reversible or irreversible and histologically described as acute, chronic
or hyperplastic.

3. Types of Pulpitis

a. Reversible Pulpitis
1) A clinical diagnosis based on subjective and objective findings indicating that the
inflammation should resolve and the pulp return to normal.

b. Symptomatic Irreversible Pulpitis

1) A clinical diagnosis based on subjective and objective findings indicating that the
vital inflamed pulp is incapable of healing.
2) There may be lingering thermal pain, spontaneous pain or referred pain.

c. Asymptomatic Irreversible Pulpitis

1) A clinical diagnosis based on subjective and objective findings indicating that the
vital inflamed pulp is incapable of healing.
2) There are no clinical symptoms.

d. Chronic Hyperplastic Pulpitis

1) A form of chronic pulpal inflammation usually following carious or traumatic
exposure.
2) Characterized by proliferation of dental pulp tissue from the exposed pulp
chamber, filling the cavity with a pedunculated or sessile, pinkish-red, fleshy
mass.
3) Usually covered by epithelium.

D. Chronic Hyperplastic Pulpitis (Pulp Polyp) (NDAC Ch. 3, p. 112)

1. Definition: Overgrowth of inflamed granulation tissue coming from the pulp.

2. Clinical Features
a. Usually occurs in children and young adults.
b. Tissue in pulp is vital.
c. Usually is painless, except when biting on area.
d. Most often occurs in deciduous molars and first permanent molar.
e. Associated with a large carious pulp exposure
f. Tissue grows out of pulp.

3. Histology
a. Granulation tissue
b. Chronic inflammatory infiltrate
c. Surface covered by stratified squamous epithelium

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 4. Treatment
a. Extraction, OR
b. Endodontic treatment

E. Pulpal Calcifications (NDAC Ch. 3, p. 115)

1. Though uncommon, calcifications may be acquired within the pulp tissue.

2. Pulp stones may occur in as many as 20% of the population.

3. Pulp stones may occur due to chronic pulpal irritation or as part of a genetic disorder.
Contributing conditions include:
a. Chronic pulpal irritation – attrition, abrasion, erosion, caries, periodontitis, dental
restorative procedures, orthodontic tooth movement, and tooth injury.
b. Miscellaneous contributing factors – aging, fluoride supplementation, excess vitamin D
c. Genetic disorders – dentin dysplasia type II, Id, Ehlers-Danlos syndromes
d. Metabolic disorders – calcinosis, end-stage renal disease
e. Some cases are idiopathic.

4. Pulp calcifications occur in three patterns.

a. Denticles – formed of tubular dentin
b. Pulp stones – form within coronal pulp, may be concentric, not formed of dentin
c. Diffuse linear calcifications
1) These fine fibrillar calcifications running parallel to blood vessels are not
radiographically visible.

F. Spread of Pulpal Pathology to the Periapical Region

1. Introduction
a. There is a close relationship between pulpal and periapical pathosis.
b. Periapical pathology logically follows pulp pathology.
c. Periapical disease meets a more effective resistance than pulpal disease.

Blood Stream Periapical Acute Periapical Inflammation

1. Bacteremia Abscess
Chronic
2. Cavernous
sinus thrombosis
Chronicity Periapical
Penetration 1. Chronic abscess
1. Mucosal sinus Granuloma
2. Chronic osteomyelitis
2. Skin sinus
Spread to Soft Tissues Spread through Jaw
1. Abscess 1. Osteomyelitis Peripaical (Radicular)
2. Cellulitis 2. Periostitis Cyst

G. Apical Periodontitis

1. Defined as inflammation of the periodontium at the apex of a tooth, i.e., the apical periodontal
ligament space, arising from inflammation of the pulp.

2. American Academy of Endodontic recognizes two forms of apical periodontitis.

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 a. Asymptomatic Apical Periodontitis
1) Inflammation and destruction of the apical periodontium that is of pulpal origin
2) Appears as an apical radiolucent area.
3) Does not produce clinical symptoms.

b. Symptomatic Apical Periodontitis

1) Inflammation usually of the apical periodontium
2) Produces clinical symptoms including a painful response to biting and/or
percussion or palpation.
3) Might or might not be associated with an apical radiolucent area.

3. The AAE forms of apical periodontitis are clinical designations, significantly dependent on
symptomology and thus do not correlate with specific morphologic changes in the tissues.

4. Pathologists recognize the following morphologic patterns of apical periodontitis.

a. Acute Apical Periodontitis – characterized by predominantly acute inflammation
b. Chronic Apical Periodontitis – characterized by predominantly chronic inflammation
c. Subacute Apical Periodontitis – characterized nearly equally by acute and chronic
inflammation

H. Acute Apical Periodontitis (NDAC Ch. 3, p. 117, 123)

1. Clinical Features
a. Pain – localized; frequently spontaneous; can be excruciating; often throbbing
b. Extremely painful to touch
c. Tooth is in supra occlusion
d. No overt swelling
e. Tooth vitality testing usually indicates necrotic pulp, but pain from periapical area may
give false positive vitality test results.

2. Radiographic features – no change or slight thickening of periodontal membrane

3. Histology
a. Implies inflammation to periodontal ligament (no gross death of tissue)
b. Localized inflammatory infiltrate (acute and chronic cells)
c. Central zone of necrotic tissue around apex of outer zone surrounded by granulation
tissue

4. Treatment
a. Establish drainage and possible antibiotic therapy, then
b. Endodontic therapy, OR
c. Extraction

I. Chronic Apical Periodontitis (Dental Granuloma) (NDAC Ch. 3, p. 117)

1. Clinical Features
a. “Stand-off” between local resistance and noxious stimuli
b. Common
c. Painless

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 d. Vitality testing indicates pulp is necrotic.
e. Slowly progressing
f. May transform into a cyst.

2. Radiographic features – radiolucency, usually small, up to 1 cm

3. Histology
a. Proliferation of granulation tissue, formed of fibroblasts and endothelial-lined vascular
channels
b. Lymphocytes, plasma cells and phagocytes (foam cells and cholesterol clefts)

4. Treatment
a. Endodontic therapy, OR
b. Extraction

J. Dental Abscess (Periapical Abscess) (NDAC Ch. 3, p. 123)

1. Defined as a dental infection characterized by a necrotic pulp and an accumulation of acute

inflammatory exudate beyond the apex of the tooth; clinically characterized by pain and
swelling.

2. Clinical Features and Symptoms

a. Usually painful with rapid onset
1) Painful to percussion
2) Often pain somewhat less in intensity than acute apical periodontitis (because
more tissue destroyed)
3) Not as localized (adjacent teeth painful)
b. Patient usually has swelling
c. May get sinus tract formation
d. Vitality testing indicates pulp is necrotic.
e. Can be potentially dangerous

3. Radiographic features – may vary from widened PDL to large alveolar radiolucency.

4. Histology
a. Same as acute apical periodontitis, but much more extensive
b. Involves adjacent bone and soft tissue
c. Pus formation and necrosis of tissue are characteristic.

5. Treatment
a. Antibiotic therapy, OR
b. Establish drainage
c. After swelling is controlled, then treat the tooth by RCT or extraction.

6. Complications of an Untreated or Inadequately Treated Dental Abscess

a. Parulis - “gum boil”
b. Cellulitis – spreading infection with swelling involving facial planes
c. Osteomyelitis – infection spreading through medullary spaces of bone
d. Ludwig's angina
1) Cellulitis involving the three spaces of the neck – submandibular, submental and
sublingual spaces – such that there is

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 2) Severe board-like swelling may compress airway.
e. Cavernous sinus thrombosis – infection from maxillary anterior premolar and molar
teeth with extension into maxillary sinus, orbit, and cranial vault; very serious.

7. Spread of Periapical Infection – exudate takes path of least resistance

a. Buccal plate - most common (bone thinner)
b. Outside on face (outside buccinators muscle)
c. Palate
d. Lingual sulcus of mouth
e. Neck (below mylohyoid muscle)
f. Periodontal ligament
g. Pulp canal
h. Maxillary sinus
i. Mandibular canal

K. Radicular Cyst (Periapical Cyst, Lateral Radicular Cyst) (NDAC Ch. 3, p. 119)

1. Clinical features
a. Most common cyst of jaws
b. May be asymptomatic (majority) or become symptomatic.
c. Slow continuous enlargement
d. Vitality testing indicates pulp is necrotic.

2. Radiographic features
a. Well-circumscribed radiolucency
b. Associated with apices of teeth
c. May cause resorption of teeth or bone.
d. May become very large.
e. May appear identical to a periapical granuloma.
f. Associated with loss of lamina dura of adjacent tooth

3. Histology
a. Same as dental granuloma except for epithelial lining
b. Body of tissue lined by epithelium and filled with fluid or semifluid material
c. Stratified squamous epithelium lines cyst, usually without keratin.
d. Dense connective tissue capsule
e. Chronic (primarily) and acute inflammatory cells
f. Also may have cholesterin clefts, multinucleated giant cells, and/or hemosiderin

4. Treatment
a. To treat the tooth
1) Endodontic therapy, OR
2) Extraction
b. To treat the cysts – surgical removal (excisional biopsy)
c. Follow up 6 months to 1 year later
d. May get fibrous scar after treatment

5. Squamous cell carcinomas may arise in radicular cysts.

L. Condensing Osteitis (Chronic Focal Sclerosing Osteomyelitis) (NDAC Ch. 3, p. 134)

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1. Bone sclerosis associated with apices of a tooth which has pulpitis.

2. Occurs because of high tissue resistance to low grade infection.

3. Clinical Features
a. Usually young (children and young adults)
b. Usually mandibular first molar
c. Tooth usually has large caries.
d. No clinical symptoms
e. Vitality testing in early lesions indicates reversible/irreversible pulpitis. Over time, the
pulp may become necrotic.

4. Radiographic features
a. Circumscribed area of radiopaque sclerotic bone (no radiolucent border)
b. Entire root outline is visible.
c. May disappear after extraction of tooth (85% will regress partially or totally).

5. Histology – dense bony trabeculation

6. Treatment – many cases may need endodontic treatment, some need no treatment.

7. The residual area of condensing osteitis that remains after extraction of the associated tooth
is termed bone scar.

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