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1. Alveolar osteitis
INDIAN DENTAL ACADEMY
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2. Clotting
 Intrinsic
& Extrinsic pathway- clotting cascade
 Stabilized clot
 Clotting cascade
Thrombin

 Fibrinogen
Fibrin
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3. Fibrinolytic System
 Plasminogen

Plasmin
tPA (Plasminogen activator)


Soluble
Fibrin fragments



tPA- Tissue plasminogen activator, secreted by endothelial cells
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4. Role of Fibrinolytic system
A
fibrin clot is not designed to last for ever .
 I t is a transitory device until permanent repair of
the vessel occurs.
 The fibrinolytic system is the principal effector of
clot removal.
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5. Normal Extraction Site Healing
 1.
Socket fills with blood- clot
 2. First 24 hrs a fibrin covered clot becomes fixed
in the alveolus by the gingival tissues, which
collapses into the clot filled alveolus.
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6. 3
. Fibroplasia- During the first 5 days there is an
in growth of fibroblasts and capillaries from the
remnants of tissue in the alveolar walls, and the
epithelium continues to migrate down the socket
walls until it contacts either granulation tissue or
epithelium. Fibroblasts have grown in to stabilise
the clot by the 3rd or 4th day.
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7.  By
early second week- new capillaries have fully
penetrated the clot and Osteoid can be detected
extending outward from the alveolar wall .
 At 31 days the alveolar socket is filled with new
bone.
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8. Terminology
 Alveolar
osteitis
 Localized osteitis
 Alveolitis sicca dolorosa
 Alveolitis
 Localized alveolitis
 Localized alveolar osteitis
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9.  In
which there is loss of blood clot from the socket
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10. Factors implicated in the development
of AO
 1.
Smoking . 2. Women on OCP
 3. Surgical trauma. 4. Inexperience of the Surgeon
 5. Preexisting infection ( pericoronitis)
 6. Poor infection control ( increased bioburden)
 7. Increased Pt age
 8. Lack of copious saline irrigation during surgery
 9. Gender F > M
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11. Pathophysiology of Alveolar Osteitis
 Fibrinolytic
theory
 According to Birn in 1963- 1977 the trauma of
surgery, or existing inflammation causes the
alveolar bone or adjacent tissues to release tPA
which convert plasminogen to plasmin, a
fibrinolytic agent.This dissolved the blood clot ,
releasing kinins from kininogen which causes pain.
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12.  Little
or no evidence in
 1. Flap design
 2. Use of vasoconstrictors
 3. Saliva
 4. Role of bacteria
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13. Diagnosis
 1.
An empty alveolus 2 to 3 days after the
extraction
 2. Severe pain often radiates
 3.
Fetid odour, halitosis
 Increased temp is hardly ever encountered.
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14. Prevention of Alveolar Osteitis
 1.
Prerinsing with CHMW
 2. Copious intraoperative saline lavage
 3. Improved OH and plaque control
 4. Metronidazole after surgery !!!
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15. Treatment
 1.
CHMW
 2. ZnOE pack ( Obtundent dressing)
 3. Alvogyl ( analgesic and antiseptic; iodoform,
PABA, eugenol )
 4. Topical application of an emusion of
oxytertracycline and hydrocortisone cream.
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16. Dressing to Alveolar Osteitis- Purpose
 1.
Close the opening of the alveolar socket so that
food debri is kept out
 2. Local pain relief
 3. Keep the socket disinfected
 4. Promotes healing
 5. Suppress bad odour
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