Dental caries leads to changes in the enamel and dentin, including tubular sclerosis, reactionary dentine, and dead tracts formation. Left untreated, dental caries can cause pulpitis, which involves inflammation of the pulp and can be reversible, acute, or chronic. Pulpitis and pulp necrosis can further lead to apical periodontitis, periapical abscess, osteomyelitis, or cellulitis as the infection spreads. Advanced stages include formation of a periapical cyst, bone destruction, and soft tissue infection.

1. Sequelae of Dental Caries
PBL
Group B
Date : 10th April, 2016
Sushant Pandey Tutor : Dr. Vinay Marla

2. Contents:
 Definition of caries
 Changes in enamel and dentin
 Pulpitis
 Periodontitis
 Summary

3. It is defined as “a progressive, irreversible microbial
disease of multifactorial nature affecting the
calcified tissues of the teeth, characterized by
demineralization of the inorganic portion and
destruction of the organic portion of the tooth.”
Dental Caries :

4. Sequelae of Dental Caries
Enamel Caries
Dentine Caries
Pulpitis
Apical Peridontitis
Periapical Abscess Periapical Granuloma
Osteomyelitis
Periosteitis
AbscessCellulitis
Acute Chronic
Acute
Chronic
Acute Chronic
Acute Chronic
Periapical cyst

5. Initially, caries presents as a painless white spot
(decalcification of the enamel, which may be
reversible), followed by cavitations and the
appearance of brownish discoloration.
Changes in enamel:

6. • Tubular sclerosis = Formed at halfway between pulp and DEJ.
Heavily mineralized.
• Reactionary dentine = Forms at pulp dentine interface.
• Dead tracts = Formed when odontoblasts die and their tubules
become sealed off.
Changes in dentin:

8. Changes in pulp:
Most common cause of dental pain.
Most cases of pulpitis are primarily a result of
dental caries in which bacteria or their
products invade the dentin and pulp tissue.
Within the rigid confines of the pulp chamber
this produces severe persistant pain and the
pulp eventually undergoes necrosis.

9. 1. FOCAL REVERSIBLE PULPITIS:
• due to dentinal and pulpal irritation
• pulp hyperemia
C/F:
• Tooth sensitive to thermal changes
• Responds to low current in EPT
• Application of ice results in pain but disappears
on removal

10. 2. ACUTE PULPITIS:
• extensive acute inflammation of pulp
• frequent sequel of focal reversible pulpitis
• Pain is due to pressure built up due to lack of
exudate escape
C/F:
• pain persists even after removal of thermal stimuli
• Lacinating or throbbing type pain
• Responds to low current in EPT

11. 3. CHRONIC PULPITIS:
• Due to quiescence of a previous acute
pulpitis or may be chronic from onset
• Reduced pain and reaction to thermal
change due to degeneration of nerves
• Granulation tissue formation
• Response to high current in EPT

12. Effects in the periapical tissue
1. APICAL PERIODONTITIS:
• Inflammation of the periodontal ligament around the root apex
• Due to spread of infection following pulp necrosis
• May be ACUTE or CHRONIC
A. Acute apical periodontitis:
• Tenderness on mastication
• May cause reabsorption of surrounding bone
• Widening of periodontal space

13. B. Chronic apical periodontitis (periapical granuloma):
• Common sequelae of pulpitis
• Localized mass of chronic granulation tissue at the
apex of non vital tissue
• Thickening of ligament at the root apex

14. 2. APICAL PERIODONTAL CYST (PERIAPICAL
CYST):
• Due to bacterial infection and necrosis of pulp
• Usual sequela of the periapical granuloma
• Lined by epithelium and fluid filled
• Lining epithelium is derived from epithelial rests of
Malassez

15. 3. PERIAPICAL ABSCESS (ALVEOLAR
ABSCESS):
• Acute or chronic suppurative process of the
periapical region.
• May develop from acute periapical periodontitis or
from periapical granuloma.
• Localized collection of pus in the alveolar bone at
the root apex following death of the pulp.

16. Osteomyelitis:
• Inflammation of bone and bone marrow
• Sequela of periapical infection resulting in diffuse spread of
infection throughout the medullary space
• Necrosis of jaw bone

17. Cellulitis:
• Inflammation of soft tissues which tends to
spread through tissue spaces and facial planes
• Caused by organisms producing hyaluronidase
and fibrinolysins
• Cellulitis of face and neck occurs as sequela of
an apical abscess or osteomyelitis

18. Summary

19. References:
 Shafer’s textbook of oral pathology, 7th
edition
 Cawson’s essentials of oral pathology and
oral medicine, 8th edition