The document discusses the sequelae of dental caries, detailing definitions, types of caries, and related conditions such as pulpitis and periapical abscesses. It explains the progression from enamel caries to dentinal caries and associated inflammatory conditions like osteomyelitis. Treatments for these conditions vary from root canal therapy to extractions, highlighting the importance of addressing dental infections to prevent severe complications.

1. SEQUELAE OF DENTAL CARIES
-DR.SUGUMARI V
MDS FIRST YEAR

2. CONTENT
• Dental caries-definition
• Sequelae of dental caries
• Enamel caries-types
zones
• Dentinal caries-zones
• Pulpitis
• Apical periodontitis
acute
chronic
• Periapical granuloma
• Periapical abscess
• Periapical cyst
• Osteomyelitis
• Conclusion

3. DENTAL CARIES
• Definition of dental caries by Sturdevant
Dental caries is an oral infectious microbiologic
disease of the teeth that results in localized dissolution and
destruction of calcified tissues

4. • Definition of dental caries by Shafers
Dental caries is a microbial disease of the
calcified tissues of the teeth, characterized by
demineralization of the inorganic portion and
destruction of the organic substance of the tooth.

5. SEQUELAE OF DENTAL CARIES
ENAMEL CARIES
DENTINAL CARIES
PULPITIS
APICAL PERIODONTITIS
PERIAPICAL ABSCESS PERIAPICAL GRANULOMA
OSTEOMYELITIS
PERIOSTEITIS
PERIAPICAL CYST
ABSCESS
CELLULITIS
ACUTE
CHRONIC
ACUTE
CHRONIC
ACUTE CHRONIC

6. ENAMEL CARIES
• Initiation-by formation of dental plaque.
TYPES OF ENAMEL CARIES
SMOOTH
SURFACE CARIES
PIT AND FISSURE
CARIES

7. ZONES OF ENAMEL CARIES
ZONES FEATURES
1.Translucent zone Present at advancing front of lesion
1%mineral loss
2.Dark zone Superifical to translucent zone
Formed as a result of demineralization
2-4% mineral loss
3.Body of the lesion Superifical to dark zone
Area of greatest demineralization(5-25%
mineral loss)
4.Surface zone Relatively unaffected
Greater resistance of surface layer maybe
due to greater degree of mineralization
1%mineral loss

9. DENTINAL CARIES
• Begins from DEJ (dentinoenamel junction) and rapid
involovement of great number of dentinal tubules
each of which acts as a tract leading to dentinal pulp
along with micro organisms.

10. ZONES OF DENTINAL CARIES
Zones of
dentinal
caries
Zone of fatty
degeneration of
tomes s fibres
Zone of
decomposed
dentin Zone of
bacterial
invasion
Zone of
decalcified
dentin
Zone of
dentinal
sclerosis

11. REACTIONARY CHANGES IN DENTIN
1.Tubular sclerosis Peritubular dentin reduces the size of
dentinal tubules ,preventing bacterial
peneration and generating a more heavily
mineralized dentin.
2.Regular reactionary dentin Forms at pulp dentin and interface and
retains tubular structure of dentin .
3. Irregular reactionary dentin Forms in respone to moderate to severe
insult by caries nd ranges from dentin with
irregular tubules to a disorganized bone
like mineralized tissue (eburnoid)
4.Dead tracts If peritubular dentin formation was
extensive before odontoblast death ,the
dead tracts may be sclerotic and inhibit
advance of caries.if not,it may allow more
rapid progress.

12. PULPITIS
• Inflammation of pulp,most common cause of dentinal
pain and loss of teeth in younger persons.
• Caused by infection or irritation of pulp,most
commonly by dental caries .
• Pupal pain is poorly localized.

13. FOCAL REVERSIBLE
PULPITIS
ACUTE PULPITIS CHRONIC PULPITIS
Early mild transient pulpitis Extensive acute
inflammation of the dental
pulp
Arises on occasion through
quiescence of previous
acute pulpitis ,but more
frequent the chronic type
of disease the onset
Localized chiefly to the
pulpal ends of irritated
dentinal tubules
Immediate sequela of focal
reversible pulpitis
The signs and symptoms
are considerably milder
than those in the acute
form of the disease.
Application of ice or cold
fluids to the tooth result in
pain ,but this disappear
upon removal of the
thermal stimuli or
restoration of normal
response
Severe pain is elicited by
thermal
changes,particularly when
taking ice or cold drinks
Mild ,dull aching pain
which is more often
intermittent than
continous

14. APICAL PERIODONTITIS
• Apical periodontitis is the inflammation of the
periodontal ligament around the root apex.
• This process may be acute or chronic depending upon
the virulence of the microorganisms involved, the
type and severity of the physical or chemical irritants,
and host resistance.

15. • The common causes of apical periodontitis include
spread of infection following pulp necrosis, occlusal
trauma from a high restoration or biting suddenly on a
hard object, inadvertent endodontic procedures such
as over instrumentation, pushing the infected material
into the apical portion or chemical irritation from root
canal medicaments.

17. ACUTE APICAL PERIODONTITIS
• Give the history of previous pulpitis.
• Thermal change does not induce pain as in pulpitis.
• Due to the collection of inflammatory edema in the
periodontal ligament, the tooth is slightly elevated in
its socket and causes tenderness while biting or even
to mere touch.

18. • The external pressure on the tooth forces the edema
fluid against already sensitized nerve endings and
results in severe pain.

19. • RAGIOLOGIC FEATURES:
Radiographic appearance is essentially normal at
this stage except for a slight widening of periodontal
ligament space.

20. HISTOLOGIC FEATURES :
• The periodontal ligament shows signs of
inflammation characterized by vascular dilatation and
infiltration with polymorphonuclear leukocytes.
• Initially, these changes are localized around the root
apex, as this area is richly vascular.
• The inflammation is transient if it is caused by acute
trauma.

21. TREATMENT AND PROGNOSIS:
• If the inflammation is caused by occlusal trauma, it
should be relieved by selective occlusal grinding.
• If the periapical periodontitis occurs due to
the spread of pulpal infection, the tooth should be
extracted.

22. CHRONIC APICAL PERIODONTITIS
• Chronic apical periodontitis, also known as periapical
granuloma, is a low-grade infection and one of the
most common of all sequelae of pulpitis or acute
periapical periodontitis.
• If the acute process is left untreated, it is
incompletely resolved and becomes chronic.

23. • The acute inflammatory process is an exudative
response whereas the chronic one is proliferative.
• Periapical granuloma is essentially a localized mass
of chronic granulation tissue formed in response to
the infection.

24. Clinical features:
• The involved tooth is usually nonvital and may be
slightly tender to percussion, and percussion may
produce a dull sound instead of a normal metallic
sound because of the presence of granulation tissue
around the root apex.
• Patients may complain of mild pain on biting or
chewing on solid food.

25. Histologic features
• The typical periapical granuloma shows the delicate
fibrillar stroma with intense lymphocytic and plasma cell
infiltration and sometimes polymorphonuclear
leukocytes as well as many small capillaries
• collections of macrophages that are often filled with
lipoid material and cholesterol slits in the tissue The
typical granuloma is usually surrounded by a connective
tissue ‘capsule’

26. Treatment and Prognosis
• The treatment of the periapical granuloma consists in
extraction of the involved teeth, or under certain
conditions, root canal therapy with or without
subsequent apicoectomy.
• If left untreated, the periapical granuloma may
ultimately undergo transformation into an apical
periodontal cyst.

27. PERIAPICAL CYST
• Also known as apical periodontal
cyst ,Radicular cyst,root end cyst.
• It is most common odontogenic cyst it is an
inflammatory .

28. • PATHOGENESIS
Toxins at the apex of the infected tooth leads to
periapical inflammation
stimulates the cell rests of malassez that are in the
apical periodontal ligament
a periapical granuloma is formed.it may be infected
or sterile
the epithelial proliferation follows an irregular
pattern of growth.

29. the epithelial mass increases in size if by the division of
the cells in the periphery corresponding to the basal layer
of the cell in the surface epithelium.
cells in the centre becomes separated from their source of
nutrition
cell in the centre degenerates become necrotic and liquefy
This creates an epithelium lined cavity filled with fluid the
apica;l periodontal cyst

30. CLINICAL FEATURES:
• mostly asymptomatic
• Most commonly involved tooth maxillary anteriors
followed by premolars and molars.
• Expansion of cortical plate are uncommon

31. TREATMENT
• Root canal therapy of the involved teeth with periapical
surgery or extraction of involved tooth followed by
curretage.
• The cyst do not recur if the surgical removal in
thorough.

32. PERIAPICAL ABSCESS
• Dentoalveolar abscess, alveolar abscess)
• Periapical abscess is an acute or chronic suppurative
process of the dental periapical region.
• It may develop either from acute periapical
periodontitis or more commonly from a periapical
granuloma.

34. • Acute exacerbation of a chronic periapical lesion is known as
Phoenix abscess.
• It usually arises as a result of infection following carious
involvement of the tooth and pulp infection, but it also does
occur after traumatic injury to the teeth, resulting in necrosis of
the pulp, and in cases of irritation of the periapical tissues either
by mechanical manipulation or by the application of chemicals
in endodontic procedures.
• It is a mixed infection with the culture of pus yielding to a wide
range of different bacterial species.

35. Clinical Features
• The acute periapical abscess presents the features of an
acute inflammation of the apical periodontium.
• The initial stages produce tenderness of the tooth,
which is often relieved by application of pressure. In
time, the tooth is extremely painful and is slightly
extruded from its socket
• regional lymphadenitis and fever may be present.

36. • The chronic periapical abscess generally presents no
clinical features, since it is essentially a mild,well-
circumscribed area of suppuration that shows little
tendency to spread from the local area.

37. Radiographic Features:
• The acute periapical abscess is such a rapidly
progressive lesion that, except for slight thickening of
the periodontal ligament space, there is usually no
radiographic evidence of its presence.
• The chronic abscess, developing in a periapical
granuloma, presents the radiolucent area at the apex of
the tooth described previously or the radiolucency may
be ill-defined.

38. Histologic Features:
• The area of suppuration is composed chiefly of a central
area of disintegrating polymorphonuclear leukocytes
surrounded by viable leukocytes, occasional
lymphocytes, cellular debris, necrotic materials and
bacterial colonies.
• There is dilatation of the blood vessels in the periodontal
ligament and adjacent marrow spaces of the bone.

39. • These marrow spaces also show an inflammatory cell
infiltrate.
• The tissue around the area of suppuration contains a
serous exudate

40. Treatment and Prognosis:
• The principle of treatment of the periapical abscess is the
same as for any abscess, drainage must be established.
• This can be accomplished by either opening the pulp
chamber or extracting the tooth.
• Under some circumstances, the tooth may be retained and
root canal therapy is carried out if the lesion can be
sterilized.

41. • If the periapical abscess is not treated, it may lead to
serious complications through the spread of the
infection.
• These include osteomyelitis, cellulitis, and bacteremia
and the ultimate formation of the fistulous tract
opening on the skin or oral mucosa.
• Cavernous sinus thrombosis has also been reported.

42. OSTEOMYELITIS
• Osteomyelitis is defined as the inflammation of bone
and its marrow contents.
• Changes in the calcified tissue are secondary to
inflammation of the soft tissue component of the
bone.

43. • Though the pathologic changes of periapical abscess
can even be considered as osteomyelitis as there is
involvement of bone, the term ‘osteomyelitis’ is
reserved for infections which spread through the bone
to a larger extent.

44. • Predisposing factors include fractures due to trauma and
road traffic accidents; gunshot wounds, radiation
damage, Paget’s disease, and osteopetrosis.
• Systemic conditions like malnutrition, acute leukemia,
uncontrolled diabetes mellitus, sickle cell anemia, and
chronic alcoholism may also predispose to osteomyelitis.
• The disease may be acute, subacute, or chronic and
presents a different clinical course, depending upon its
nature.

45. ACUTE SUPPURATIVE OSTEOMYELITIS
Acute suppurative osteomyelitis of the jaw
is a serious sequela of periapical infection that often
results in a diffuse spread of infection throughout the
medullary spaces, with subsequent necrosis of a
variable amount of bone.

46. Clinical features :
• this form of osteomyelitis, which arises from a dental
infection, are the same as those present after infection
due to a fracture of the jaw, a gunshot wound, or even
hematogenous spread.
• Dental infection is the most frequent cause of acute
osteomyelitis of the jaws. It may be a rather well-
localized infection of one involving a great volume of
bone.

47. • A periapical infection (usually an abscess), if it is a
particularly virulent one and not walled off, may
spread spontaneously throughout the bone.
• In other instances, a chronic periapical infection such
as a granuloma, or even a cyst that is walled off, may
undergo an acute exacerbation, especially if the area is
traumatized or surgically disturbed without
establishing and maintaining drainage.

48. Clinical Features:
• Acute or subacute suppurative osteomyelitis may
involve either the maxilla or the mandible.
• In the maxilla the disease usually remains fairly
well localized to the area of initial infection.
• In the mandible, bone involvement tends to be
more diffuse and widespread. The disease may
occur at any age.

49. • A particular form of acute osteomyelitis, referred to as
neonatal maxillitis in infants and young children, is a
well recognized entity that is fortunately becoming
extremely uncommon nowadays because of antibiotic
drugs.
• In some instances, this osteomyelitis of infants is of
hematogenous origin, but at other times it seems to be a
result of local oral infection following some minor
injury or abrasion.

50. Radiographic Features:
• Acute osteomyelitis progresses rapidly and demonstrates
little radiographic evidence of its presence until the
disease has developed for at least one to two weeks.
• At this time diffuse lytic changes in the bone begin to
appear.
• Individual trabeculae become fuzzy and indistinct, and
radiolucent areas begin to appear .

51. Histologic Features:
• The medullary spaces are filled with inflammatory exudates .
• The inflammatory cells are chiefly polymorphonuclear
leukocytes, but may show occasional lymphocytes and plasma
cells.
• The osteoblasts bordering the bony trabeculae are generally
destroyed, and depending upon the duration of the process, the
trabeculae may lose their viability and begin to undergo slow
resorption.

52. Treatment and Prognosis:
• General principles of management includes
debridement, drainage, and antimicrobial therapy.
• When the intensity of the disease becomes attenuated,
either spontaneously or under treatment, the
sequestrum begins to separate from the living bone.
• If the sequestrum is small, it gradually exfoliates
through the mucosa.

53. • If large, surgical removal may be necessary, since
its removal by normal processes of bone resorption would
be extremely slow.
• Sometimes an involucrum forms when the sequestrum
becomes surrounded by new living bone.
• Unless proper treatment is instituted, acute suppurative
osteomyelitis may proceed to the development of
periostitis, soft-tissue abscess, or cellulitis .

54. CHRONIC SUPPURATIVE OSTEOMYELITIS
• Chronic suppurative osteomyelitis may develop in
inadequately treated acute osteomyelitis or may arise
from a dental infection without a preceding acute
stage.

55. Clinical features
• Similar to those of acute osteomyelitis except that all
signs and symptoms are milder.
• The pain is less severe; the temperature is still
elevated, but only mildly; and the leukocytosis is only
slightly greater than normal.

56. • Teeth may not be loose or sore, so that mastication is
at least possible even though the jaw may not be
perfectly comfortable.
• Acute exacerbations of the chronic stage may occur
periodically, and these present all features of acute
suppurative osteomyelitis.
• The suppuration may perforate the bone and
overlying skin or mucosa to form a fistulous tract and
empty on the surface

57. CHRONIC FOCAL SCLEROSING OSTEOMYELITIS
(CONDENSING OSTEITIS)
• Chronic focal sclerosing osteomyelitis is an unusual
reaction of the bone to infection: a reaction to mild
bacterial infection entering
• In either case, the radiopacity stands out in distinct
contrast to the trabeculation of the normal bone.

58. Histologic Features:
• Histologic examination reveals only a dense mass of bony
trabeculae with little interstitial marrow tissue .
• The osteocytic lacunae appear empty.
• The bony trabeculae exhibit many reversal and resting lines
giving pagetoid appearance.
• If interstitial soft tissue is present, it is generally fibrotic and
infiltrated only by small numbers of lymphocytes.
• Osteoblastic activity may have completely subsided at the time
of microscopic study.

59. Garres chronic nonsuppurative sclerosing osteitis, periostitis
ossificans:
• This is a distinctive type of chronic osteomyelitis in which
there is focal gross thickening of the periosteum, with
peripheral reactive bone formation resulting from mild
irritation or infection.
• It is essentially a periosteal osteosclerosis analogous to the
endosteal sclerosis of chronic focal and diffuse
sclerosingosteomyelitis.

60. CELULITIS
• Diffuse inflammation of soft tissue.
• Tends to spread through tissue space and
facial planes.
• Caused by organisms producing hyaluronidase
and fibrinolysins like streptococci.

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