Regressive alterations

1. DR. SUHASINI GP
SENIOR LECTURER
DEPT. ORAL &MAXILLOFACIAL PATHOLOGY AND MICROBIOLOGY
SUBHARTI DENTAL COLLEGE AND HOSPITAL
SWAMI VIVEKANAND SUBHARTI UNIVERSITY
MEERUT. UP
Subject: Oral Pathology

2.  Clinically normal tooth
 Normal vitality test
 Symptomless
 H/P-
 Large vacuolated spaces in the pulp
 Reduction in the number of cellular elements
 Degeneration and disappearance of odontoblasts

6.  Artefact brought about by autolysis of pulp
tissue
 Improper fixation
 Pulp after exraction
 Does not occur invivo

7.  Histologically - 87%
 Radiographically -15%
 10-20 years - 66%
 50-70% - 90%

10.  Three types-
I. Denticles - Denticles are formed as a result of
an epitheliomesenchymal interaction within the
developing pulp.
II. Pulp stones- pulp stones are developed around
the central nidus of pulp tissue
III. Diffuse linear calcifications- they exhibit areas
of fine, fibrillar, irregular calcification that often
parallel the vasculature.

11. Local metabolic
dysfunction
Hyalinization
of injured cells
fibrosis
Trauma
Vascular
damage
Mineralization
PULP STONE

12. Clinical & radiographic features
• Denticles and pulp stones are detected on intraoral
radiographs as radioopaque enlargements within
the pulp chamber or canals
• May interfere with root formation leading to early
periodontal destruction and tooth loss

14. Histopath features
• Denticles (true pulp stones) – consist of tubular dentin
surrounding a nest of epithelium , central epithelium
degenerates with time and tubules undergo sclerosis.
• Pulp stones (false denticles) –a central amorphous
mass of irregular calcification surrounded by concentric,
lamellar rings of regular calcified material.
• Diffuse linear calcification (calcific degeneration) –
consist entirely of fine, fibrillar and irregular calcification
that develop in the pulp chambers and canals
• Amorphous, linear strands or columns paralleling
blood vessels

15.  True- pulp chamber
 False, diffuse linear calcifications - root canal

19.  Interstitial denticles
 False denticles- eventually becomes surrounded by
sec. dentin

20.  Pulp irritation, inflammation
 Cholelithiasis
 Renal lithiasis
 Arteriosclerosis
 Gout
 Acromegaly
 Osteitis deformance
 Hypercementoses
 Torus
 Streptococcal microorganisms

21.  Pain
 Difficulty in pulp extirpation

22.  Defn
destruction of teeth by cells located in
the dental pulp (internal resorption) or in
the PDL (external resorption).

26. osteodentin
radiopaque
dentin
dentin

27. •Balloon like radiographic dilatation of canal
in internal resorption
•asymptomatic
•Internal resorption appears as pink
discoloration in crown (pink tooth of mummery)

30. Histopath
Internal resorption – increased vascularity,
cellularity, collagenization of pulp tissue.
numerous multinucleated dentinoclasts
adjacent to dentinal wall.
Inflammatory infiltrate by lymphocytes,
histiocytes and PMNL

34. Internal
resorption
resulting in
perforation of
the root

35. External resorption

38. external resorption of
impacted canine

39. Chronic apical periodontitis and apical cyst showing
early external root resorption.

40. H/P
External resorption –
•Numerous multinucleated odontoclasts
are located in the area of structure loss.

41. Cervical external root resorption

42. Cervical external root resorption

43. Multiple idiopathic root resorption.
Extensive invasive cervical resorption of
several anterior mandibular teeth.
•Moth eaten appearance of
external resorption
radiographically

44. Treatment
Internal resorption : endodontic treatment
External resorption : elimination of accelerating
factor, removal of soft tissue from defects and
restoration of lost tooth structure

47. I. Calcification of nests of epithelial cells – circular
lamellated structure formed
II.Focal calcification of connective tissue between
sharpey’s bundles with no central nidus – appear as
small round or ovoid globules of Ca
III.Small spicules of cementum torn from root surface
i.e. cemental tears
IV.Calcification of thrombosed capillaries in PDL

50.  Def
It is a non neoplastic condition in which
excessive cementum is deposited in continuation
with the normal radicular cementum.

51. •Calcinosis
•Rheumatic fever
•Gardener syndrome
•Vit. A deficiency
•Repair of vital root #

53. Clinical features
Asymptomatic
When tooth is extracted the roots appear larger
in diameter and present rounded apices
Radiographic features
Thickening and blunting of roots
Rounding of root apex

54. Histologic features
Excessive amount of
secondary or cellular
cementum is deposited over
primary acellular cementum
Secondary cementum
(osteocementum) is
arranged in concentric layers
around roots

55. Dr Manish Bhargava
 Diffuse/ circumscribed; single/all teeth/parts
of single teeth
 Improvement of functional quality c/as
HYPERTROPHY
 Non functional teeth c/as HYPERPLASIA
 Decrease in number of Sharpey's fibers

56. Dr Manish Bhargava
 Localized hypertrophy
 Spur/ prong like extension
 Teeth exposed to stress
 Localized hypercementosis
 Single location anywhere on the root
 Chronic periapical infection
 Appear as a rounded projection that develop by
deposition of cementum over degenerated epithelial
rests
 Generalized hypercementosis
 Paget’s disease
 Non functional teeth without antagonist

57. Treatment
No t/t needed
Extraction is
difficult

60. Gingival hemorrhage

61. trauma
Localised rbc breakdown