This document discusses various types of bone infections including osteomyelitis. It describes acute suppurative osteomyelitis as a rapidly destructive inflammatory bone lesion caused by bacteria. Chronic suppurative osteomyelitis results from unresolved acute osteomyelitis and involves bone destruction. Diffuse sclerosing osteomyelitis is characterized by pain, inflammation and bone sclerosis or destruction. Focal sclerosing osteomyelitis occurs in response to localized dental infections. Proliferative periostitis involves periosteal bone formation in response to chronic infections. Alveolar osteitis or "dry socket" results from loss of a blood clot following tooth extraction.
Night 7k to 12k Navi Mumbai Call Girl Photo 👉 BOOK NOW 9833363713 👈 ♀️ night ...
Bone infection causes and treatment
1. Bone infection
4TH YEAR /DENTAL COLLAGE
AL HADI UNIVERSITY
DR. MAHA MOHAMMED
ORAL PATHOLOGIST
1
2. Osteomyelitis
• An acute or chronic inflammatory process within the medullary ( trabicular )
bone , that involves the marrow spaces or the cortical surfaces of bone , that
extends away from the initial site of involvement ( usually a bacterial infection )
• Mandible most commonly affected ( especially in adult males ) because the
mandible is dense and less vascular than the maxilla
• Maxillary involvement mainly in pediatric patients
2
3. Periapical infection Bone Infection
Predisposing factors
Systemic
Local
Infection chronic systemic diseases
Tobacco , alcohol , intravenous drug abuse
Diabetes Mellitus Malnutrition
Malignancy AIDS
Predisposing factors
Fractures including gunshot wounds
Radiation damaged
Hypovascularized bone ( as in late -
Paget's disease or Osteopetrosis )
3
4. 1- Acute Suppurative Osteomyelitis:
• : A rapidly destructive lesion of the trabecular bone and bone marrow spaces of
an acute inflammatory origin .
• It usually contains virulent strains of bacteria and there has been insufficient
time for the body to react to the presence of the inflammatory infiltrate due to
the reduction of the systemic resistance .
• It is most commonly caused by direct extension of an untreated periapical
abscess , or by minor traumatic incident involving a mandible that has a
compromised blood supply by previous exposure to high doses of radiation for
the treatment of malignancies .
4
5. 1- Acute Suppurative Osteomyelitis:
Clinically
• : patients with acute osteomyelitis characteristically have signs and symptoms of an acute
inflammatory process as :
• *Sever intense pain as early complain with fever ,
• *leukocytosis and soft tissue swelling of the affected area .
• * Associated teeth are tender and loose and the gingival is red and swollen .
• *Regional lymphadenopathy
• *Occasionally alteration in the sensation ( paresthesia ) of the lower lip when the
inflammatory exudate with it's accompanying bacterial toxins and lytic enzymes may
involve the inferior alveolar canal , producing alteration in the conductivity of the nerve
5
6. Sequestrum
• Exfoliation of fragments of necrotic bone may be discovered . A fragment of
necrotic bone that has separated from the adjacent vital bone is termed a
Sequestrum Sequestra often exhibits spontaneous exfoliation .
• Involucrum
• On occasion , fragments of necrotic bone may become surrounded by vital bone ,
and the mass of encased nonvital bone is called an Involucrum
6
7. Pathologically
• , necrotic bone is formed when the acute inflammatory reaction in bone and
marrow spaces with suppuration spread , the necrosis is wide because of
thrombosis of blood vessels , marrow spaces become filled with pus , extension
of suppuration through cortical bone to involve the periosteum occurs , stripping
of periosteum compromises the blood supply to the cortical plate and predispose
to further bone necrosis
7
8. 1- Acute Suppurative Osteomyelitis:
Radiographically
• . : The radiographic features of acute osteomyelitis are usually unremarkable
until 10 days , then there will be significant loss of trabecular bone which appear
radiographically as radiolucency .
• These radiolucent areas are with ill - defined margins and therefore referred to
as ( moth - eaten appearance )
• Islands of fragments of dead bone are often visible in the central areas of
radiolucency .
8
10. 10
Acute Osteomyelitis with Sequestrum.
Radiolucency of the right body of the
mandible with central radiopaque mass
of necrotic bone.
11. 1- Acute Suppurative Osteomyelitis:
Histopathologic Features :
• Generation of biopsy material from patients with acute osteomyelitis is not common
because of the predominantly liquid content and lack of a soft - tissue component .
• The histopathological picture of the submitted material consists predominantly of
necrotic bone ( sequestrum ) .
• The bone shows loss of the osteocytes from their lacunae , peripheral resorbtion of
bone in scalloped eroded borders .
• The periphery of bone and the haversian canals contain necrotic debris and
inflammatory infiltrate consisting of polymorphonuclear leukocytes .
• This necrotic bone may undergo resorption by osteoclastic activity or may be
exfoliated through a sinus if they are small , or they have to be removed surgically
11
12. 12
Acute Osteomyelitis. Nonvital bone
exhibits loss of the osteocytes from the
lacunae. Peripheral resorption, bacterial
colonization,
and surrounding inflammatory response
also can be seen.
13. 1- Acute Suppurative Osteomyelitis:
Treatment :
• acute Essential measures : -
• Bacterial sample for culture and sensitivity test .
• - Heavy antibiotic treatment . Analgesics to relief pain .
• - Drainage
• -Debridement: Remove the source of infection ( if possible ) .
• Adjunctive Measures :
• * Sequestrectomy .
• * Decortication
13
14. 1- Acute Suppurative Osteomyelitis:
Treatment :
• Hyperbaric oxygen used in patients who does not respond to
standard therapy or for disease arising in hypovascularized ( as in
osteoradionecrosis ) .
• Resection and reconstruction .
• Immobilization of weakened bones
14
15. 2- Chronic Suppurative Osteomyelitis :
• This type is either a sequela of unresolved acute osteomyelitis , or
the process may arise primarily without a previous episode . It is a
low grade infection associated with bone destruction
• Chronic osteomyelitis exists when the defensive response leads to
the production of granulation tissue which subsequently forms
dense scar tissue in an attempt to wall off the infected area
15
16. 2- Chronic Suppurative Osteomyelitis :
Clinically
• Clinically :There may be
• swelling ,
• pain ,
• sinus formation , purulent discharge ,
• sequestrum formation , or
• pathologic fracture .
• Patients may experience acute exacerbation or periods of decreased pain .
16
17. 2- Chronic Suppurative Osteomyelitis :
Radiographically
• Radiographs : reveals
• a patchy , ragged radiolucency that often
• contains central radiopaque sequestra .
17
18. Chronic Osteomyelitis. A, Ill-defined area of radiolucency of the right body of the mandible adjacent to a
recent extraction site. B, After the initial intervention, the patient failed to return for follow-up because of
lack of significant pain. An enlarged, ill-defined radiolucency of the right body of the mandible was
discovered 2 years after the initial surgery.
19. 2- Chronic Suppurative Osteomyelitis :
Histopathology
• Histopathology :
• Biopsy material demonstrates a significant soft - tissue component that consists
of :
• chronically inflamed fibrous connective tissue filling the intertrabecular areas of
bone .
• Scattered sequestra and pockets of
• abscess formation are common
19
20. 2- Chronic Suppurative Osteomyelitis
Chronic Osteomyelitis. Chronically
inflamed and reactive fibrous connective
tissue filling the intertrabecular spaces
21. 2- Chronic Suppurative Osteomyelitis :
Treatment
• Treatment : Chronic osteomyelitis is difficult to be managed medically , because
pockets of dead bone and organisms are protected from antibiotics by the
surrounding wall of fibrous connective tissues .
• The best treatment is by:
• surgical intervention and
• high doses of antibiotics to be given intravenously .
• For the small lesions , curettage , removal of necrotic bone are sufficient , while
in patients with extensive osteomyelitis , decortication combined with
transplantation of cancellous bone chips
21
22. 3- Diffuse Sclerosing Osteomyelitis :
• This diagnosis is highly controversial which involve a group of presentations that are
characterized by pain , inflammation and various degrees of periosteal hyperplasia , sclerosis
and bone destruction .
• These can be grouped under three major categories :
• A - Diffuse sclerosing osteomyelitis
• B- Primary chronic osteomyelitis (no suppuration or sequestration )
• C- Chronic tendoperiostitis (due to over use of masticatory muscles)
• D - SAPHO syndrome (Synovitis, Acne, Pustulosis, Hyperostosis, and Osteitis)
autoimmune disease
22
23. A - Diffuse sclerosing osteomyelitis
• This term should be used when an infectious process is directly responsible for
sclerosis of bone Classically , this condition defectively caused by bacterial
spread through cancellous bone which creates a mass of chronically inflamed
granulation tissue , then by extension of inflammation perforation of the cortex
occur .
• At this site the periosteum is elevated from the cortical surface with localized
deposition of periosteal new bone .
• In the cancellous bone significant bone deposition and sclerosis occur around the
central zone of infection and bone resorption
23
24. A - Diffuse sclerosing osteomyelitis
clinically
• Mostly arises in adults without sex predominance .
• It primarily occurs in the mandible .
• There is increased radiodensity develops around sites of chronic infections
( e.g. , periodontitis , pericoronitis , periapical inflammatory disease ) .
• The affected area is restricted to a single site but may be multifocal or extend to
fill an entire quadrant .
• Pain and swelling are not typical , patient may experience vague pain .
24
25. A - Diffuse sclerosing osteomyelitis
Radiographically
• Radiographically :
• It appears as patchy diffused or nodular sclerosis ( cotton - wool ) appearance
Diagnosis :
• To make definitive diagnosis of chronic sclerosing osteomyelitis , microbiologic
cultures should be positive , and the infected sites respond to appropriate
antibiotics and surgical debridement
25
26. Diffuse Sclerosing Osteomyelitis. Diffuse area of
increased radiodensity of the right body of the
mandible in the tooth bearing area. No other
quadrants involved.
27. A - Diffuse sclerosing osteomyelitis
Histopathology
• Histopathology : Diffuse sclerosing osteomyelitis demonstrates
• dense irregular bone demonstrates sclerosis and remodeling , indicated by
repeated periods of resorption followed by repair , this is obvious by prominent
reversal lines .
• The haversian canals scattered widely and little marrow spaces can be found .
• Chronic inflammatory process may be seen in the soft tissue , like , proliferating
fibroblast and connective tissue fibers that show infiltration with chronic
inflammatory cells lymphocytes and plasma cells
27
28. Histopathologic feature
(Primary chronic osteomyelitis )
• Similar Histopathologic features are seen in primary chronic osteomyelitis,
SAPHO syndrome, and CRMO.
• Areas of sclerosis, numerous irregular trabeculae of pagetoid bone
• are present and demonstrate extensive evidence of remodeling
• with prominent reversal lines, osteoblastic rimming, and focal areas of
osteoclastic activity
• fibrosis is present, with scattered lymphocytes and plasma cells.
• micro abscess formation
30. 4-Focal Sclerosing Osteomyelitis ( Condensing
Osteitis )
• It's a bony reaction to low grade periapical inflammation
characterized by localized areas of bone sclerosis associated with
the apices of teeth with pulpitis ( either from a large carious lesion
or deep coronal restoration ) or pulpal necrosis
30
31. 4-Focal Sclerosing Osteomyelitis
Clinically
• Clinically :
• It arise almost in children and young adults , the teeth most
commonly involved is the mandibular first molar which presents a
large carious lesion .
• There may be no signs and symptoms other than mild pain
associated with an infected pulp .
31
32. 4-Focal Sclerosing Osteomyelitis
Radiographically
Uniform zone of increased radiodensity adjacent to the apex of a tooth that
exhibits a thickened periodontal ligament (PDL)space or an apical inflammatory
lesion
• lesion does not exhibit a radiolucent border, as is seen in cases of focal cemento-
osseous dysplasia
• the radiopacity is not separated from the apex as would be seen in idiopathic
osteosclerosis
• Bone Scar
• A residual area of condensing osteitis that remains after resolution of the
inflammatory focus is termed
32
36. 5-Osteomyelitis with proliferative periostitis
(Periostitis ossificans)
( Garre's osteomyelitis )
• It represents a periosteal reaction to the presence of
chronic periapical inflammation .
• The affected periosteum forms several rows of reactive
vital bone that parallel each other and cause expansion of
the affected bone
36
37. ( Garre's osteomyelitis )
Clinically
• Clinically :
• It affects usually the mandibular premolars and molar of children and young
adults .
• Mild pain and
• bony swelling along the lower and lateral borders of the jaw .
• Most cases are unifocal ,
• although multiple quadrants may be affected
37
38. ( Garre's osteomyelitis )
Radiographically
• Occlusal radiographs demonstrate radiopaque lamination of bone parallel to
each other and underlying cortical surface termed as
• ( onion - skin ) .
• A radiolucent separation often present between the new bone and original cortex
• these alteration are typically seen in
• *panoramic ,
• *posteroanterior , or
• * lateral oblique radiographs
38
39. Proliferative Periostitis. A, Firm swelling of the lateral and inferior border of the right
mandible that arose after traumatic injury. B, Computed tomography (CT) image demonstrating new periosteal
bone growth with onionskin laminations. C, Panoramic radiograph exhibiting new periosteal bone formation
along the right inferior border of the mandible.
40. ( Garre's osteomyelitis )
Histopathological
• Specimens often reveal parallel rows of highly cellular and reactive
woven bone in which the individual trabeculae are frequently
oriented perpendicular to the surface
• Resembling the pattern seen in immature fibrous dysplasia
• Sequestra, if included, demonstrate the typical features of bone
necrosis
40
41. ( Garre's osteomyelitis )
Proliferative Periostitis.
Interconnecting trabeculae of new bone
formation (top left) extending from the original
cortical surface (delineated by arrows).
42. ( Garre's osteomyelitis )
treatment
• After the focus of inflammation has been eliminated the layers of
bone will show gradual remodeling in 6 to 12 months by the action
of overlying muscle action
42
43. 6-Alveolar Osteitis
( Dry Socket : Fibrinolytic Alveolitis )
• After extraction of a tooth , a blood clot is formed at the site , with eventual
organization of the clot by granulation tissue , gradual replacement by coarse
fibrillar bone , and finally , replacement by mature bone .
• Destruction of the initial clot prevents appropriate healing and causes the
clinical condition known as alveolar osteitis .
• The clot is lost secondary to transformation of plasminogen to plasmin , with
subsequent lysis of fibrin and formation kinins ; these are potent pain mediators
( fibrinolytic alveolitis ) .
43
44. 6-Alveolar Osteitis
• Factors that stimulate fibrinolysins :
• Local trauma
• Estrogens
• Bacterial Pyrogens
• the socket, which reveals exposed and extremely sensitive bone.
• Typically, severe pain, foul odor, and (less frequently) swelling and
lymphadenopathy develop 3 to 4 days after extraction of the tooth.
• The signs and symptoms may last from 10 to 40 days.
44
45. 6-Alveolar Osteitis
Etiological
• Etiological factors of alveolar osteitis ( dry socket ) :
• 1- Excessive extraction trauma , mostly surgical removal of impacted mandibular
third molar ( 25 % -30 % ) .
• 2- Oral contraceptive use ,
• 3- Presurgical infection
• 4- Hypovascularized bone ( osteosclerotic diseases ) .
• 5- Radiotherapy
• 6- Local anesthesia with strong vasoconstriction .
45
46. 7- Osteoradionecrosis
• Osteoradionecrosis : It is one of the most serious complications of radiation of
head & neck , however , it is seen less frequently today because of better
treatment modalities & prevention .
• Although the risk is low , it increases dramatically if a local surgical procedure is
performed within 21 days of therapy irradiation or within 12 months of therapy .
• Although , most instances of osteoradionecrosis arise secondary to local trauma
a minority appear spontaneous .
46
47. 7- Osteoradionecrosis
• Osteoradionecrosis is believed to result from osseous endarteritis that induced
by radiation that lead to tissue hypoxia , hypocellularity and hypovascularity
which predispose to necrosis if a minor injury occurs .
• However , many now believe radiation damage to osseous cells causing these
cells lose their normal function , and bone turnover is suppressed , also affect
bone vascularity through a complex interaction of cytokines and growth factors
47
48. • Clinically : the mandible is involved most frequently , presenred by pain , cortical
perforation , fistula formation , surface ulceration and pathologic fracture may be
present
• Radiographically: affected areas of bone reveal ill - defined areas of radiolucency
that may develop zones of relative radiopacity as the dead bone separates from the
residual vital areas
48
49. 7- Osteoradionecrosis
Prevention :
• : Before radiation therapy , the following measures should be followed : .
• all questionable teeth should be extracted or restored .
• any oral foci of infection should be eliminated .
• Excellent oral hygiene should be initiated and maintained .
• A healing time of at least 3 weeks between extensive dental procedures and the
initiation of radiotherapy significantly decreases the chance of bone necrosis .
Extraction of teeth or any bone trauma is strongly contraindicated during
radiation therapy
49
50. 8-Bisphosphonate - Associated Osteonecrosis :
• Bisphosphonate is a unique class of medication used primarily to slow osseous
involvement in a number of cancers ( as multiple myeloma and metastatic breast or
prostate carcinoma ) , to treat Paget's disease and to reverse osteoporosis .
• This drug inhibit osteoclast and interfere with angiogenesis ( new blood vessels
formation ) .it can be administered orally or intravenously .
• Clinically : mandible commonly involved , in 60 % necrosis followed invasive dental
treatment the remainder occurring spontaneously .
• Affected patients have areas of exposed necrotic bone that may be asymptomatic
• All patients who take these medications should be warned of the risks and obtain
and maintain ultimate oral hygiene .
50