Periodontal And Periapical
Diseases
Periodontal Disease
Usefulness of Radiographs
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Amount of bone present
Condition of alveolar crest
Bone loss in furcation areas
Width of periodontal ligament
Local factors: calculus, overhanging
restorations
• Crown/root ratio
Limitations of Radiographs
• No indication of morphology of bony
defects
• No indication of successful
management
• No indication of hard/soft tissue
relationship, i.e., depth of pockets
Normal Alveolar Crest
• 1.0-1.5 mm apical to
cemento-enamel
junction
• Parallel to line joining
the CEJ of adjoining
teeth
• Smooth
• Continuation of lamina
dura, has the same
radiopacity
Evidence of Early Periodontitis
• Localized erosion of crest of bone
• Blunting of crest- anterior teeth
• Loss of sharp angle between lamina
dura and crest
• Widening of PDL near crest
Local Factors
• Calculus
• Overhanging restorations
• Poor restoration contours
Calculus
Overhanging Restoration
Buccal VS Lingual Bone Loss
Direction Of Bone Loss
Horizontal Bone Loss:
Crest of bone is parallel to CEJ line
between adjoining teeth. The remaining
bone is still horizontal but may be
positioned apically.
Direction Of Bone Loss
Vertical bone loss
Crest of remaining bone is not parallel to
the CEJ line between adjoining teeth
(displays an oblique angulation to the
CEJ line )
Bone Loss In Bifurcation/trifurcation
Areas
Bitewing Radiographs Most Reliable For
Crestal Bone Evaluation
Generalized Periodontal Disease
Juvenile Periodontitis
(Early-onset Periodontitis, Rapidly Progressing Periodontitis)
• Occurs in healthy individuals between
puberty and age 25
• Amount of bone loss is not consistent
with local factors and oral Hygiene
habits. Rate of bone loss is 3-4 times
faster than in typical periodontitis
Juvenile Periodontitis(cont.)
• Typically affects crestal bone of first
molars and incisors. Eventually affects
greater # of teeth.
• Bone loss is progressive and frequently
bilaterally symmetrical. Many teeth
show vertical bone loss.
• Host neutrophil dysfunction has been
demonstrated by several investigators.
Papillon-Lefevre Syndrome
• Autosomal recessive trait
• Hyperkeratosis of palms and soles
• Occasional keratosis of other skin
surfaces
• Calcification in falx cerebri
• Severe destruction of alveolar bone
involving all deciduous and perm. teeth
• Exfoliation of teeth
Langerhans’ Cell Histiocytosis
(Histiocytosis X)
• Complex of three diseases:
• Eosinophilic granuloma (usually solitary)
• Hand-Schuller-Christian disease
(chronic)
• Letterer-Siwe disease (acute)
• Due to abnormal proliferation of
Langerhans’ cells or their precursors
Eosinophilic Granuloma of Bone
• Most common in children and young
adults
• Usually single radiolucency
• Skull, mandible, vertebra and long
bones commonly involved
• Painful, mobile teeth and gingival
lesions
Hand-Schuller-Christian Disease
• Most cases reported in children under 10
years. Has been reported in older individuals
• Skeletal and soft tissues may be involved
• Classic triad of symptoms:
– “punched out” destructive bone lesions
– unilateral or bilateral exophthalmos
– diabetes insipidus
• Complete triad occurs in 25% of patients
Hand-Schuller-Christian (Cont.)
• Oral manifestations include:
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loose teeth
exfoliated teeth
gingivitis
loss of alveolar bone / advanced
periodontitis
• Sharply outlined multiple radiolucent
lesions in skull, jaws and other bones
Letterer-Siwe Disease
• Acute, disseminated form of disease
• Usually occurs before age 3. Most patients
die
• Involves several bones and organs
• Skin rash
• Intermittent fever, enlargement of liver and
spleen, lymphadenopathy common
• Destructive radiolucencies in jaws
• Loosening and premature loss of teeth
Hand-Schuller-Christian Disease
Hand-Schuller-Christian Disease
Skull lesions of Histiocytosis X
Other Diseases Influencing
Course Of Periodontal Disease
• Diabetes mellitus
• Leukemia
Leukemia
Leukemia
Periapical Inflammatory Lesions
• Bone destruction around
apex of tooth, mostly
secondary to pulp
exposure due to caries or
trauma.
• Bacterial invasion of pulp
produces toxic
metabolites which escape
to the periapical bone
through apical foramen
and cause inflammation.
Periapical Inflammatory Lesions
• Periapical granuloma:
Localized mass of
chronic granulation
tissue containing
PMN’s, lymphocytes,
plasma cells.
Periapical Granuloma
• Radiographically,
widening of PDL
or variable size
of periapical
radiolucency
may be present
Periapical Granuloma
Periapical Granuloma
Periapical Abscess
• Periapical abscess:
When pus forms in
the area. It may
develop directly as an
acute process or
develop in a preexisting granuloma.
Radiographically,
appears identical to
granuloma.
Periapical Granuloma Or Abscess
• Can one differentiate between the two
on the basis of radiographs alone?
Periapical Inflammatory Lesions
• Radicular cyst (periapical cyst): Cell rests of
Mallasez (remnants of epithelial root sheath
of Hertwig) proliferate due to inflammatory
stimulus of a granuloma or an abscess and
provide the epithelial lining.
• A cyst is an epithelium lined cavity which is
filled with fluid or semi-solid material.
• Radicular cyst is the ONLY cyst related to
non-vital pulp.
Periapical Inflammatory Lesions
• Can you definitively differentiate between
a periapical granuloma, abscess or
radicular cyst on the basis of radiograph
alone?
Periapical Inflammatory Lesions
• Sclerosing osteitis (chronic sclerosing
osteomyelitis). Occasionally, the reaction to
periapical inflammation is predominantly
osteoblastic, i.e., more sclerotic bone is
formed (radiopaque mass).
• Usually occurs in children or young adults
when the resistance is high.
• Most common location is mandibular 1st
molar.
Sclerosing Osteitis
(Idiopathic) Osteosclerosis
Osteosclerosis
• How do you differentiate between
osteosclerosis and condensing osteitis?
• In osteosclerosis, the pulp is vital. There are
no clinical signs or symptoms. No treatment is
necessary.
• Sclerosing osteitis is secondary to pulp
exposure. Patient is symptomatic. Endodontic
treatment or extraction is indicated.
Calcific Degeneration
(Calcific Metamorphosis)
Secondary to Trauma to the Tooth
Calcific Degeneration
Calcific Degeneration
Radiographic Evidence Of
Non-vital Teeth
• Widening of apical PDL or periapical
radiolucency ( associated with indication
of pulp exposure)
• Discontinuity of lamina dura
• Displacement of lamina dura
• Sclerosing osteitis
• Calcific degeneration (metamorphosis)
• Radiographic indication of pulp
exposure
Periapical Cemental Dysplasia
• Also called Cementoma. Localized alteration
in periapical area. Osseous structure is
replaced by fibrous tissue, cementum-like
material, abnormal bone or combination of
these.
• Pulp is vital. Patient is asymptomatic. There
are no clinical signs.
• No treatment is required.
• Mean age is 39 years.
Periapical Cemental Dysplasia
• 85% patients are females.
• 3 times more common in African-americans.
• Most commonly seen in mandibular anterior
areas.
• May be multiple.
• May be bilateral.
• Well-defined radiolucency, opacity or mixed.
Periapical Cemental Dysplasia
• Stage I ( Osteolytic stage )
• Stage II ( Osteo or cementoblastic
stage)
• Stage III ( mature stage )
Stage II
Stage III
Multiple
Apical Scar (Fibrous Scar )
• Variation in healing process. Normally
surgical site fills with blood clot which
organizes and eventually mineralizes
and remodels like surrounding bone.
• Occasionally, normal mineralization and
remodeling fails to occur.
• Patient is asymptomatic and no
treatment is required.
Apical Scar (Fibrous Scar )
Apical Scar (Fibrous Scar )
Apical Scar (Fibrous Scar )
Periapical Lesions (Bhaskar)
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Periapical granuloma
48%
Radicular cyst
43%
Periapical abscess
1.1%
Residual cyst
3.5%
Apical scar
3.0%
Periapical cemental dysplasia 1.7%
Rare lesions
1.0%
Rare Periapical Lesions (Bhaskar)
• Central giant cell granuloma
• Traumatic (simple) bone cyst
• Hyperparathyroidism
Periapical Lesions
(LaLonde and Leubke)
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Periapical granuloma
Radicular cyst
Periapical abscess
Other periapical lesions
45.2%
43.8%
3.0%
8.0%