1. Periodontal And Periapical Diseases

2. Periodontal Disease

3. Usefulness of Radiographs
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

4. 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

5. 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

9. 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

12. Local Factors Calculus Overhanging restorations
Poor restoration contours

13. Calculus

14. Overhanging Restoration

15. Buccal VS Lingual Bone Loss

18. 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.

20. 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 )

23. Bone Loss In Bifurcation/trifurcation Areas

26. Bitewing Radiographs Most Reliable For Crestal Bone Evaluation

29. Generalized Periodontal Disease

30. 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

31. 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.

34. 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

40. 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

41. 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

42. 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

43. Hand-Schuller-Christian (Cont.)
Oral manifestations include:
loose teeth
exfoliated teeth
gingivitis
loss of alveolar bone / advanced periodontitis
Sharply outlined multiple radiolucent lesions in skull, jaws and other bones

44. 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

45. Hand-Schuller-Christian Disease

46. Hand-Schuller-Christian Disease

47. Skull lesions of Histiocytosis X

48. Other Diseases Influencing Course Of Periodontal Disease
Diabetes mellitus
Leukemia

49. Leukemia

50. Leukemia

51. 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.

52. Periapical Inflammatory Lesions
Periapical granuloma: Localized mass of chronic granulation tissue containing PMN’s, lymphocytes, plasma cells.

53. Periapical Granuloma
Radiographically, widening of PDL or variable size of periapical radiolucency may be present

54. Periapical Granuloma

55. Periapical Granuloma

56. Periapical Abscess
Periapical abscess: When pus forms in the area. It may develop directly as an acute process or develop in a pre-existing granuloma. Radiographically, appears identical to granuloma.

57. Periapical Granuloma Or Abscess
Can one differentiate between the two on the basis of radiographs alone?

58. 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.

62. Periapical Inflammatory Lesions
Can you definitively differentiate between a periapical granuloma, abscess or radicular cyst on the basis of radiograph alone?

64. 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.

65. Sclerosing Osteitis

66. (Idiopathic) Osteosclerosis

67. 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.

68. Calcific Degeneration (Calcific Metamorphosis)
Secondary to Trauma to the Tooth

69. Calcific Degeneration

70. Calcific Degeneration

71. 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

72. 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.

73. 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.

77. Periapical Cemental Dysplasia
Stage I ( Osteolytic stage )
Stage II ( Osteo or cementoblastic stage)
Stage III ( mature stage )

78. Stage II

79. Stage III

80. Multiple

81. 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.

83. Apical Scar (Fibrous Scar )

84. Apical Scar (Fibrous Scar )

85. Apical Scar (Fibrous Scar )

86. Periapical Lesions (Bhaskar)
Periapical granuloma %
Radicular cyst %
Periapical abscess %
Residual cyst %
Apical scar %
Periapical cemental dysplasia %
Rare lesions %

87. Rare Periapical Lesions (Bhaskar)
Central giant cell granuloma
Traumatic (simple) bone cyst
Hyperparathyroidism

88. Periapical Lesions (LaLonde and Leubke)
Periapical granuloma %
Radicular cyst %
Periapical abscess %
Other periapical lesions %