Osteomyelitis (OML) is an inflammation of bone or bone marrow, primarily affecting the mandible in the maxillofacial region, resulting from infections, trauma, or hematogenous routes. It often presents as a polymicrobial disease, with risk factors including host resistance, vascular integrity, and specific organisms like aerobic and anaerobic streptococci. Management involves debridement, antibiotic therapy, and addressing underlying causes to promote healing and prevent complications such as necrosis or neoplastic transformation.

1. PRESENTED BY:
SACHITA

2. The words, “osseous” in latin means bony, and
“osteon” in Greek means “bone”, and ‘‘myleos’’
means marrow; and “itis” in Greek means
inflammation.
In 1834, Nelaton first coined the word
“Osteomyelitis”.
By definition osteomyelitis (OML) is an
inflammation of medullary portion of bone or bone
marrow or cancellous bone.

3.  Osteomyelitis is an extensive inflammation of a
bone. It involves the cancellous portion, bone
marrow ,cortex and periosteum. ( Laskin1989)

4. The inflammation may be acute, subacute or
chronic.
It may be localized ; or may involve a larger portion
of bone.
It may be suppurative or nonsuppurative.

5. The factors that predispose to osteomyelitis are:
1. Conditions affecting host resistance or defenses
2. Compromised vascular integrity and perfusion in
the host bone, at the local, regional or systemic level
3. Virulence of microorganisms

6. 1. Conditions that alter host defenses would
include chronic debilitating diseases, such as
diabetes mellitus, agranulocytosis, leukemia ,
severe anemia, malnutrition, drug abuse, chronic
alcoholism, sickle cell disease, and febrile
illnesses such as typhoid, tuberculosis.
2. Conditions that alter vascularity of bone include
therapeutic irradiation, osteoporosis, Paget’s
disease, fibrous dysplasia, peripheral vascular
disease, bone malignancy, metallic bone necrosis
(caused by mercury, bismuth, and arsenic).

7. 3. Virulence of organisms: Certain organisms precipitate
thrombi formation by virtue of their destructive
lysosomal enzymes (Hudson 1993). Lysosomal and
enzymatic degradation of host tissue, along with
microvascular thrombosis brought about by pathogen
borne bioactive peptides and chemoattracted leukocytic
purulence, forms a protective barrier for the infectious
foci, allowing organisms to proliferate in an enriched
host medium, while protected from the host immunity.

8. Osteomyelitis of the jaws is caused by:
Odontogenic infections: Primarily odontogenic infections
originating from pulpal or periodontal tissues,
pericoronitis, infected socket, infected cyst, tumor, etc.
Trauma: Is the second leading cause : (a) Especially,
compound fracture and (b) Surgery – iatrogenic cause.
Infections of orofacial regions derived from : Periostitis
following gingival ulceration, lymph nodes infected from
furuncles, lacerations, peritonsillar abscess.

9. Infections derived by hematogenous route: Furuncle on
face, wound on the skin, upper respiratory tract infection,
middle ear infection, mastoiditis, systemic tuberculosis.
The medications linked to osteomyelitis are steroids,
chemotherapeutic agents and bisphosphonates. Local
conditions that adversely affect the blood supply can also
predispose the host to a bony infection.

10. Osteomyelitis is initiated from a contiguous focus of
infection or by hematogenous spread
Primary hematogenous osteomyelitis is rare in the
maxillofacial region , generally occurring in the very young
patients
The adult process is initiated by an inoculation of bacteria
into the jaw bones

11. The initial causative insult results in a bacteria induced
inflammation or cascade
In normal healthy patient, this process will be self-limiting
Osteomyelitis is an infectious process of the medullary
myeloid cavity of bone
In the craniofacial skeleton , only the mandible and the
calvarium have myeloid compartments

12. The important factor in the establishment of osteomyelitis
is the compromise in the blood supply .

15. Primary supply: The mandible is supplied by inferior alveolar
artery, except coronoid process, which is supplied by
temporalis muscle vessels.
Secondary supply: It is periosteal supply, which generally
runs parallel to cortical surface of bone, giving off nutrient
vessels, those penetrate cortical bone and anastomose with
the branches of inferior alveolar artery.
Venous drainage of mandible: There are two routes: (1) Via
inferior alveolar vein ; it runs upwards, and joins pharyngeal
plexus, and (2) It runs downwards, and joins external jugular
veins.
Waldron(1943) , gave an exhaustive morphologic description
of vascular morphology of mandible and associated structures

16. to account for spread of OML. He described mandibular
vascular support as being provided through multiple
arterial loops from a single major vessel, which renders
large portion of bone susceptible to necrosis with the
occurence of major vessel infectious thrombosis.
 Waldervogel (1970): described its relationship to vascular
support of long bones of developing and adult human
skeleton . He made several conclusions :
There tends to be segregation of vascular channels, which
act like “end organs”, due to lack of terminal collateral
anastomosis, ultimately, leading to vascular plugging by
bacteria, microthrombi or both.
When afferent vessels anastomose with medullary
channels

17. , there is a possibility of a decrease in venous flow with
associated areas of greater turbulence.
 There may be a reduction in host immune defense
mechanism associated with these vascular channels in
calcified tissue.

18. A true osteomyelitis infectious process does not occur in
the maxilla despite the presence of tooth follicle or
anatomic respiratory sinus cavities, including the nose.
It is rare , due to: (1) Extensive blood supply and
significant collateral blood flow in midface,
(2) Porous nature of membranous bone,
(3) Thin cortical plates, and
(4) Abundant medullary spaces. These preclude
confinement of infections within bone ; and permit
dissipation of edema and pus into soft tissues and
paranasal air sinuses.

20. The process of leading to OML is initiated by acute
inflammation, hyperemia, increased capillary permeability
and infiltration of granulocytes. Tissue necrosis occurs, as
proteolytic enzymes are liberated and as destruction of
bacteria and vascular thrombosis continues, there is a pus
formation.
The pus is a combination of necrotic tissue and dead
bacteria and white blood cells accumulate. When pus
accumulates, the intermedullary pressure increases
resulting in vascular collapse, venous stasis, and ischemia.

21. Subsequently, pus travels through Haversian and
nutrient canals and accumulates beneath the periosteum,
elevating it from the cortex ; and thereby further
reducing vascular supply. Compression of neurovascular
bundle accelerates thrombosis, ischemia, and infarction,
later resulting in paresthesia and sequestrum formation.
A sequestrum is defined as a portion of bone that
becomes separated from sound bone during the process of
necrosis.
Radiographically, the bone surrounding sequestrum
appears less densely mineralized than sequestrum itself,
since vascularity of vital bone creates relative
demineralization.

22. In the past, etiology of OML was associated with skin
surface bacteria, Staphylococcus aureus, and to a lesser
extent Staphylococcus epidermidis, or hemolytic
streptococci. However, the picture of S.aureus as primary
offending pathogen does not hold true with regard to OML
of tooth bearing bone.
Most of the cases are caused by aerobic Streptococci (alpha
hemolytic streptococci, Streptococcus viridans), anaerobic
streptococci; and other anaerobes, such as
Peptostreptococci, fusobacteria, and Bacteroides.

23. Other organisms, such as M. tuberculosis , T. Pallidum,
and Actinomyces species produce their respective specific
forms of OML.
Hence, established acute OML is usually a polymicrobial
disease and includes : Streptococci, Bacteroides,
Peptostreptococci and Fusobacteria.

24. A variety of classifications of various forms of the disease
are:
 Historically accepted classification : It is based on clinical
course. (A) Acute, (B) Chronic. The arbitrary time limit, to
identify acute from chronic form is of 1 month (Koorbusch
et al. 1992, Marx; 1992, and Mercuri ; 1992) .

26. Classification based on presence or absence of
suppuration:

27. Cierny et al. (1985) and Vibhagool (1993) developed a
classification and staging system; based on:
1. Anatomic location of infectious process,
2. Physiological status of the host,
3. Systemic or local factors affecting immune system,
metabolism, and local vascularity.

29. It may have the appearance of a typical
odontogenic infection. It can be localized and
widespread, with extensive sequestration and
possible pathological fracture.

30. It is caused by pyogenic organisms. OML in the tooth
bearing area, is polymicrobial in nature. The most
commonly found organisms in odontogenic OML is
Staphylococcus aureus, and Streptococcus pyogenes.

31. 1. Odontogenic infections
2. Local traumatic injuries
3. Peritonsillar abscess
4. Furunculosis
5. Hematogenous infections
6. Infected compounded odontoma
7. Compound fractures of jaws are complicated by OML.

32. These are the common local cause of OML. These
infections may result from: periapical disease secondary to
pulp pathology, periodontal disease, pericoronitis of long
duration, infected odontogenic cyst, and infection of an
extraction wound or fracture site.

34. Injuries of gingiva are usually insignificant;
however may become serious in patients with low
resistance (Ivy and Cook, 1942).
Instruments used for extraction of teeth.

35. PERITONSILLAR ABSCESS: It has been
recorded as a cause of OML of ascending ramus.
FURUNCULOSIS: Of skin is a rare cause of
OML.
HEMATOGENOUS INFECTION : It may
cause multiple sites of OML. The organisms enter
the bloodstream through a minor wound in the
skin, or infection of upper respiratory tract, or
infection of middle ear.

36. 1. Undernourished children
2. Lowered general resistance of body
3. Generalized body diseases, such as : diabetes,
leukemia and agranulocytosis
4. Acute illnesses such as influenza, measles,
scarlet fever, pertussis and pneumonia, etc.

37. OCCURENCE: In adults, it is more common in
mandible and involves alveolar process, angle of
mandible, posterior part of ramus and coronoid process.
OML of condyle is reportedly rare (Linsey, 1953).
 Early cases are characterized by :
Generalized constitutional symptoms: high
intermittent fever, malaise, nausea, vomiting,
anorexia.
Continuous intense pain in the affected area.

38. Intermittent paresthesia or anesthesia of the lower lip,
which helps the clinician to differentiate this condition
from alveolar abscess.
Facial cellulitis, or indurated swelling of moderate size,
which is more confined to the periosteal envelope and its
contents (I) Thrombosis of inferior alveolar vasa
nervorum, (II) Rise in pressure from edema in inferior
alveolar canal (III) Teeth are tender to percussion and
loose, and presence of trismus.
In children : fluminating, severe and serious, involvement
of maxilla or mandible, complicated by the presence of
unerupted developing teeth buds, which become necrotic

39. and act as foreign bodies and prolong the disease
process.
Long- term involvement of temporomandibular joint
(TMJ) can cause ankylosis of TMJ and subsequently
affect the growth and development of facial
structures.
Laboratory studies : Show mild leukocytosis [poly-
morphonuclear leukocytes (PMNL)] and
albuminuria.

40. Established cases are characterized by :
Deep pain, malaise, fever, dehydration, anorexia
Teeth in involved area begin to loosen and become
sensitive to percussion.
Purulent discharge through sinuses :
(a) Intraorally, around gingival sulcus or through buccal
vestibule, and
(b) Extraorally on the face, through cutaneous fistulae
Fetid odor is often present .
Dehydration, acidosis and toxemia.
Regional lymphadenopathy is usually present.

41. Laboratory studies show: moderate leukocytosis, slightly
elevated erythrocyte sedimentation rate (ESR) and C
reactive protien, anemia and albuminuria.
MANAGEMENT –
Removal of the cause and debridement with antibiotic
cover.

42. It can be primary: resulting from organisms which are less
virulent, and secondary occuring after acute OML, when
the treatment did not succeed in eliminating the infection

43. The clinical features are usually limited to :
Pain and tenderness : the pain is minimal
Nonhealing bony and overlying soft tissue wounds with
induration of soft tissues,
Intraoral or extraoral draining fistulae.
Thickened or “wooden” character of bone.
Enlargement of mandible because of deposition of
subperiosteal new bone .
Sterile abscess (Brodie’s abscess) , common to long bones
is rare in jaws.
Teeth in the area tend to become loose and sensitive to
palpation and percussion.

44. It is made on basis of : history, clinical examination and
radiological findings — 1) Presence of sequestra, (2)
Areas of suppuration involving the tooth –bearing area of
jaw bone, not responding to debridement and
conservative therapy, (3) Regional or systemic
compromise of immune response, microvascular
decompensation or both.

45. Several sequalae/complications can occur as a result of
OML of jaws.
Neoplastic transformation: With chronic OML,
neoplastic conversion of inflammatory metaplasia to
squamous cell carcinoma is noted. The incidence
reported is 0.2-1.5%.
Discontinuity defects: The defects can be (a)
spontaneous (b) surgically induced, necessitating jaw
reconstruction ; once infection is resolved.

47. Progressive diffuse sclerosis : It involves the medullary
and cortical portions of maxillofacial skeleton, especially
mandible, over a period of time.

48. The overall treatment modalities include:
1. Conservative treatment
2. Surgical treatment
 The goal of the treatment is to:
1. Attentuate and eradicate proliferating pathological
organisms
2. Promote healing
3. Re-establish vascular permeability.

49. Successful treatment is based on the following
fundamental principles :
1. Early diagnosis with radiographic evaluation and tissue
histopathology diagnosis
2. Bacterial culture and sensitivity testing
3. Adequate, appropriate and prompt antibiotic therapy
4. Adequate pain control
5. Proper surgical intervention
6. Reconstruction, where indicated.

50. Complete bed rest
Supportive therapy: It includes – nutritional support, in
the form of high protein and high caloric diet, and
adequate multivitamins
Dehydration: Hydration orally or through
administration of IV fluids
Blood transfusion : In case, RBCs and hemoglobin is
low
Control of pain: It is controlled with analgesics.
Sedation may be employed for keeping patient
comfortable and allow to sleep.

51. Antimicrobial agents : Begin with empiric dual drug
therapy— Penicillin and metronidazole or single drug
Clindamycin. Definitive antimicrobial therapy can be
started after final culture and sensitivity test results are
obtained.
Antibiotics of value in treatment of OML include:
penicillins, penicillinase-resistant penicillins, clindamycin,
cephalosporins and erythromycins. Some of the newer
antibiotics which provide effective coverage include:
metronidazole, clindamycin, ticarcillin, clavulanic acid,
cephalosporins, vancomycin in combination with other
antibiotics, and fluoroquinolones.

52. Recommended antibiotic regimens for OML of jaws are as
follows:
Regimen I (1st choice) : As empirical therapy, penicillin
(penicillin V) is given.
Aqueous penicillin: 2 million units IV every 4 hourly.
Oxacillin: 1g IV every 4 hourly.
When the patient has been asymptomatic for 48-72 hours,
then switch to—penicillin V orally 500mg every 4 hourly,
with dicloxacillin 250 mg orally every 4 hourly for 2-4 weeks.
 Regimen II: It is based on culture and sensitivity results.
Penicillinase penicillinase-resistant penicillins, such as
oxacillin, cloxacillin, dicloxacillin, or flucloxacillin may be
given.

53. In case of allergy to penicillin, the following antibiotics are
prescribed, in order of preference: (i) Clindamycin 300-600
mg orally 6 hourly, (ii) Cephalosporin 250-500mg orally
every 6 hourly: (a) Cefazolin 500 mg 8 hourly, or (b)
Cephalexin 500 mg 6 hourly, (iii) Erythromycin 2g every 6
hourly IV, then 500 mg every 6 hourly orally.
Second choice: Clindamycin: It is effective against
penicillinase producing staphylococci, streptococci and
anaerobic bacteria including Bacteroides. It is used because
of its ability to diffuse widely in bone. It is nkt
recommended as first choice; as it is bacteriostatic, and
causes diarrhea due to pseudomembranous colitis.

54. Third choice : Cefazolin or Cephalexin : It is effective
against most cocci including penicillinase –producing
staphylococci, Gram-negative aerobic bacilli viz. E. coli ,
Klebsiella, and Proteus.
Cephalosporins are not recommended as first choice
because these are moderately effective against anaerobes
and because of broad spectrum coverage, which increases
antibiotic complications.
Fourth choice: Erythromycin : These drugs cannot be used
as first choice, as these are : (i) Bacteriostatic, and (ii)
rapidly develop resistant strains.

55. Over the last several decades, HBO therapy has
emerged as :
(i) a potent alternative to surgical reperfusion, and
(ii) as an adjunctive enhancement to host –immune
response.
Its use has increased in the treatment of refractory OML
and osteoradionecrosis (ORN) .
The hyperbaric oxygen therapy is indicated in cases of
osteomyelitis , which do not respond to routine
treatment due to presence of certain associated
conditions like irradiated jaw , osteosclerosis ,
osteoporosis , and geriatric patients.

56. It facilitates the healing of the bone and also helps in
combating the infection .
The HBO therapy involves the intermittent ,twice daily,
inhalation of 100% humidified oxygen under 2 atmospheric
pressure for 90 minutes .
HBO reduces the hypoxia within the affected tissues and
stimulates angiogenesis in the hypovascular tissues.
It enhances phagocytic activity of leukocytes to stimulate
fibroblast growth , increase in collagen formation and
promote growth of new capillaries.

57. Hyperbaric oxygen chamber : The patient is placed in a
chamber. Oxygen is given by mask or by hood .It is given for
5 days per week for 30, 60, or more dives at 2.4 ATA for 90
minutes , while breathing 100% oxygen twice daily.
 Marx protocol (1983 ):
• 30 initial dives, if improved then 60 dives completed
• Otherwise , sequestrectomy +30 dives
• If wound dehiscence , resection + 60 dives and 20 dives after
10 weeks
• Patient with pathological fracture , orocutaneous fistula are
given 30 dives more prior going to resection.

59. The surgical treatment modalities include:
1. Incision and drainage
2. Extraction of loose or offending teeth
3. Debridement
4. Decortication
5. Continuous or intermittent indwelling close catheter
irrigation

60. 6. Sequestrectomy
7. Saucerization
8. Resection of jaw
9. Trephination
10. Immediate or delayed reconstruction with bone
graft.
Surgical intervention is done under antibiotic cover,
started atleast, 1-2 days prior to the procedure.

61. It should be done as soon as possible. It relieves the
pressure and pain caused by the accumulation of pus.
Incision of abscesses should be carried out intraorally or
extraorally depending upon the location. Evacuation of
pus by drainage, lessens absorption of toxic products and
prevents further spread of infection in the bone, thus,
helping in its localization. The consistency, color and odor
of the pus may provide important clues to the diagnosis
and initial treatment. Patients with compromised
systemic conditions or toxemia, surgical interference may
be postponed for 2-3 days.

62. The various methods employed for causing drainage from
the bone include: (i) Opening up the pulp chamber, (ii) By
making fenestration through cortical plate over the apical
area with a drill, (iii) In an edentulous area, especially,
posterior maxilla or maxillary tuberosity region, by making
an incision over the alveolar crest, and by making a
window, pus is evacuated and (iv) OML at the angle of
mandible or ascending ramus, drainage can be achieved by
a small incision made over the point of the greatest
tenderness, or just below the mandible.
 Extraction of loose or offending teeth: Sometimes,
drainage is achieved by extraction of offending teeth.

63. Debridement : followed by incision and drainage, thorough
debridement of affected area should be carried out. The area
may be irrigated with hydrogen peroxide and saline. Any
foreign body, necrotic tissue or small sequestrum should be
removed.
Decortication: Removal of dense chronically infected and
poorly vascularized, lateral and inferior cortical plates of
bone 1-2 cm beyond the area of involvement. Thus, an access
is provided to medullary cavity. Obwegeser (1960) advocated
this procedure, as it shortens healing time.
Decortication and mobilization of muscle flaps to achieve or
improve regional and systemic vascular supply to the involved
area have been used to bring the overlying vascular soft
tissue envelope to a closer proximity to infected spongiosa.

64. This will increase the blood supply and healing of the affected
area.
The steps in decortication are:
Creation of buccal flap by crestal incision extending along the
necks of the teeth.
Reflection of mucoperiosteal flap to the inferior border.
Removal of teeth in the involved area.
Removal of cortical plates —lateral and inferior border, with
chisel in one piece. Bone must be cut back to uninvolved
areas.
Bony bed should be thoroughly debrided and flaps should be
closed primarily and dead space is eliminated by applying
pressure bandage placed to keep vascularized soft tissue in
contact with bony bed.

65. Irrigation tubes should be placed through separate stab
incision and closed suction should be employed.

66. Continuous or intermittent indwelling closed catheter
irrigation : After intraoral sequestrectomy and
saucerization or decortication, two small pediatric
nasogastric feeding tubes, catheters or polyethylene drain
tubes, 3-4 mm in diameter and 6-10 inches long in length,
are placed against the bony bed through separate skin
incisions at some distance and secured with sutures. One
tube is connected to the low – pressure suction to allow
drainage of pus and serum and another is kept patent to
provide a route through which locally antibiotics may be
instilled in very high concentrations. Daily, first saline
irrigation followed by antibiotic instillation should be
repeated, until negative cultures are obtained. Systemic
antibiotics are also continued for atleast 2-3 months
following cessation of clinical evidence of disease.

67. Sequestrectomy: An integral part of definitive therapy. It helps
in establishment of local microvascular proliferation. It should
be undertaken through an intraoral incision; or extraoral (
submandibular) approach, depending upon the site of
sequestrum.
Saucerization: Excision of margins of necrotic bone overlying a
focus of OML. It is useful in chronic form, since it permits
removal of formed and forming sequestra with better
visualization. It is performed when removal of sequestrum
leaves a large cavity, and to eliminate the dead space to avoid
reinfection of extensive clot. It is performed with a large round
bur, so that when wound is closed, the soft tissues eliminate a
dead space. The buccal cortex is reduced to the level of
unattached mucosa, producing a saucer like defect.

70. Sequestrectomy and saucerization are to be carried out after
the acute phase has subsided; and the defense mechanism of
host and antimicrobial therapy have overcome the virulence
of organisms. In certain circumstances, after performing the
necessary surgical procedures, where the soft tissues cannot
be closed without leaving dead space, or because of rigid
fibrosis ; the wound may be packed with 2” ribbon gauze
soaked with Whitehead varnish.
Trephination Or fenestration is the creation of bony holes or
windows in the overlying cortical bone adjacent to the
infectious process for tissue ammoniation and
decompression of the medullary compartment. Drilling of
holes into the cortex and reaching medulla provides multiple

72. surgical transcortical ports, that allow vascular
communication between the periosteum and the medullary
cavity.
 Resection : It is rarely required. When full thickness of
segment of jaw is involved and a conservative approach
has failed to cure, resection of the part should be
considered. However, while exposing the affected area, the
only soft tissue related to the necrotic bone should be
elevated, to avoid devitalization of the adjoining cortex.

74. Immediate and/or delayed reconstruction : It has been
used successfully in cases of: (i) pathological fracture, (ii)
persistence of infection after decortication, and (iii) when
both cortical plates are markedly diseased . Iliac crest is
a desirable graft. A block of corticocancellous iliac crest
can be used or cancellous marrow is used. Stabilization
may be achieved with vitallium or titanium mesh that
also serves as a tray to contain the graft. Immediate
reconstruction offers the obvious advantage of shortening
the period of illness and speeding recovery and
rehabilitation. In cases, where immediate bone grafting
is contraindicated, a reconstruction plate is fixed as a
spacer.

75. Secondary bone grafting: This should be considered when
the wound has healed completely and is free of infection.
Postoperative care: It includes the following :(i) Continued
use of antibiotics, analgesics, and hot saline mouth rinses,
(ii) Adequate hydration, complete rest, removal of
sequestra, in case they are in the alveolar part of bone. The
wound is closed preferably primarily, with a drain.
Prognosis : If proper aggressive and comprehensive
therapy is instituted on time, then, the recovery of acute
and chronic OML is always good. But, in cases of chronic
refractory or diffuse sclerosing OML, associated with
regional or systemic disease, such as microvascular or
immunosuppressive disorders, the treatment may be worse
than the disease itself.

76. In these cases, attempt should be done to provide long – term
conservative therapy than major surgical debridement. Long
term use of salicylates, nonsteroidals or steroids with
laboratory monitoring is advised in some of these cases.
The treatment regimen will have to be modified depending
on the status of general health of the patient.

78. Infantile OML( OML Maxillaries Neonatorum,
Maxillitis of infancy) :It is a rare type of OML seen in
infants involving maxilla. Wilensky (1932) described
OML in infants in a comprehensive manner.
ETIOLOGY: (1)Trauma: The access may be through a
break in the mucosa. Perinatal trauma caused to oral
mucosa during delivery. (2) Infection of maxillary sinus
(3) Paunz (1926) and Ramon et al. (1977) believe that
the disease is caused by infections from the nose. (4)
Hematogenous invasion by streptococci and
pneumococci

79. Clinical features-
Almost seen a few weeks after birth. There is sudden
onset and acute course. The disease may also have slow
onset and a chronic course. In acute stage , severe pain
and high fever ; and with chronic course there is moderate
pain and slight fever.
General constitutinal manifestations : Pyrexia, anorexia,
dehydration, convulsions, or vomitting may occur.
Treatment-
The treatment should be prompt and aggressive.
Antibiotics preferably be given by IV route. Penicillins or

80. penicillinase – resistant penicillins like flucloxacillin, or
broad – spectrum antibiotics may be given for 2-4 weeks.
 Incision and drainage of fluctuant areas : It is indicated
in the presence of of periosteal or palatal abscesses.
Irrigations: In case of sinus tracts, irrigations are done
frequently.
Supportive therapy: (i) Analgesics and antipyretics, (ii)
fluids (iii) Proper diet.
Sequestrectomy or removal of necrotic tooth germs:
Removal of sequestra is undertaken when they are
completely separated, and on the basis of clinical and
radiological findings. Surgical interference should be
conservative; as loss of bone and teeth leads to severe
deformities later in life.

81. Children who have undergone sequestrectomies, should be
followed up by an orthodontist to aid in the development of
the arch and maintenance of occlusion.
Garre’s Sclerosing Osteomyelitis: Also known as chronic
nonsuppurative sclerosing OML, chronic OML with
proliferative periostitis, and periostitis ossificans . It was
first described Carl Garre (1893) , as irritation induced focal
thickening of periosteum and cortical bone of tibia. It is a
nonsuppurative inflammatory process; where there is
peripheral subperiosteal bone deposition caused by mild
irritation and infection.
Pathogenesis : The etiological agents can be a carious tooth,
or the overlying soft tissue infection. The infectious process
localizes in periosteum or beneath the periosteal covering of

82. cortex and spreads slightly into the inferior of bone .
 Clinical features: It is characterized by: (i) localized hard,
nontender bony swelling of lateral and inferior aspects of
mandible, (ii) lymphadenopathy, hyperpyrexia and
leukocytosis usually not found
Treatment: It is directed towards removing sources of
inflammation : (a) Removal of infected tooth and curettage
of socket, (b) Surgical recontouring : This is done to
recontour the cortical expansion of the jaw. This is
attempted only if there is obvious expansion, (c)
Endodontic therapy , (d) Antibiotics : If signs of infection
are present and (e) follow – up.

83. Chronic Sclerosing OML (focal and diffuse) :
The various other names are sclerosing osteitis, ossifying
OML, sclerosing cementoma, gigantiform cementoma,
and sclerotic cemental masses.
Focal form: (I) Below the age of twenty, (II) More common
in mandible, (III) Associated with infected pulp of lower
molars /premolars, (iv) Appears as circumscribed
radiopaque mass of sclerotic bone associated with tooth
roots, (v) Margins may be distinct or may blend into
surrounding bone.
Treatment: Endodontic therapy or Extraction.

84. Multiple form: These occur in both maxilla and mandible
(resembles chronic suppurative OML). Pain is a prominent
feature. Suppuration is usually absent.
Treatment: Debridement, antibiotic therapy, alveolectomy,
and HBO2, etc.
Actinomycotic OML of jaws : It is a chronic infection
manifesting both granulomatous and suppurative features ;
and usually involved soft tissues and occasionally bone.
Pathogenesis: Organisms gain entry into soft tissues directly
or by extension from bone through (i) Periapical, or (ii)
Periodontal lesions and (iii) Fractures, or (iv) Extraction
sites.

85. Clinical features:
Soft or firm tissue masses on the skin ; which have
purplish, dark red, oily areas with occasional small zones
of fluctuation.
Spontaneous drainage of serous fluid containing granular
material. These granules are yellowish substances called
sulfur granules , and represent colonies of bacteria.
Regional lymph nodes are occasionally enlarged.
Trismus: Not common ; unless secondary infection
Pyrexia

86. Management: In the past, many therapeutic agents and
techniques were used including: (a) Iodides (b)
Radiation (c) Incision and drainage (d) Excision of soft
tissues and bone. Currently, iodides and radiotherapy
are considered to be ineffective.

88. Mucormycosis is a rare opportunistic fungal infection with
high morbidity and mortality
3rd most common Angio- invasive fungal infection (after
candidiasis and aspergillosis)
 Majority of the patient has underlying risk factor
Immuno-compromised patient
Mucormycosis is caused by the fungal organisms of the
family of Mucorale (Mucor, Rhizopus and Absida).

89. Represents 8.3%-13% of all fungal infections
In developed countries, the disease remain uncommon is
mostly seen in patients with diabetes mellitus and
hematological malignancies undergoing chemotherapy.
In developing countries, especially in India,
mucormycosis cases although sporadic, occur mainly in
patients with uncontrolled diabetes or trauma.

90. Inoculation occurs when spores reach the nasal cavity
during inhalation.
Tiny spores then become airborne and land on the oral and
nasal mucosa of humans.
Angio-invasion
 Vessel thrombosis
Tissue necrosis
Hematogenous spread to other organs can occur.

92. Rhino-orbitocerebral
Cutaneous /subcutaneous
Gastrointestinal
Pulmonary
Dissiminated
Uncommon Presentation

93. Stage 1: Sino-nasal disease
Stage 2: Rhino-orbital disease
Stage 3: Rhino-orbital- cerebral disease

94. Sinusitis
Unilateral facial swelling
Periorbital cellulitis
Eye Or facial pain and facial numbness
Conjuctival suffusion
Blurred vision
Low-grade fever
Increased white blood cell counts

95. Opthalmoplegia
Chemosis

96. The nasal turbinates on the affected side may be dusky red
or necrotic black.

97. Palatal involvement is usually the result of direct
extension of disease from the maxillary sinus and in the
distribution of the nasopalatine and greater palatine
arteries.

98. Oral and skin ulcerations are present with pain and
swelling

99. Plain orbit or sinus radiography
CT
MRI
Early diagnosis: small, focal lesions can often be surgically
excised before they progress to involve critical structures.
Antifungal therapy:
Amphotericin B : Initially a test dose- 1mg in 20 ml of
5%dextrose in water is infused intravenously over 20-30
minutes

100. With careful monitoring for side effects (i.e, chills, fever, and
anaphylaxis) every 30 minutes for 2to4 hours.
 If this dose is well tolerated – An initial dose of 0.1 to 0.3
mg/kg/day is then prepared as a 0.1mg /ml infusion and
delivered slowly over 6-24 hours .
Gradually increased by 5 to 10 mg per day, upto a total
dose of 0.7to1 mg /kg/day.
But a single dose should exceed 1.5 mg/kg /day ; as
overdoses can result in cardiorespiratory arrest.
 Liposomal Amphotericin B:
 First line recommended agent
 Can be given as 5mg/kg/day to 10 mg/kg/day

101.  Surgery + Liposomal Amphotericin B increases survival
rates and cure rates.
Posaconazole :
Dose : 800 mg/day divided in 4
 Isavuconazole:
Available in oral and intravenous formulations.
Administered with a loading dose of 200 mg 3 times a
day for 2 days and 200 mg daily thereafter.
Fluconazole , voriconazole, and itraconazole do not have
reliable activity against mucormycosis.

102. Surgical debridement:Extensive and early surgical
debridement is necessary.
Therefore, debridement of necrotic tissues may be
important for complete eradication of mucormycosis.
Surgical management include:
Debridement of the necrotic part
Drainage of the sinuses
Total and subtotal maxillectomy
Palatectomy
Sphenoid and ethmoid sinusectomy

103. Exerts a fungistatic effect
Aids in neovascularization
Dose: exposure to 100% oxygen for 1 and ½ hours
at pressures from 2-2.5 atm with 1or 2 exposures
daily for a total of 40 treatments.

104. Mucormycosis is a fatal infection.
Early recognition will prevent further dissemination of
disease.
Medical as well as surgical management plays equal role
in its treatment.
Osteomyelitis, although uncommon, continues to be seen
and treated by dentists and oral and maxillofacial
surgeons.
Complete therapy involves both medical and surgical
approaches in an effort to achieve total care.