This document provides information on osteomyelitis of the jaw, including its classification, etiology, pathogenesis, microbiology, clinical findings, imaging, and treatment. It discusses the different types of osteomyelitis (acute suppurative, secondary chronic, primary chronic, non-suppurative). It also covers osteoradionecrosis of the jaw, its definition, clinical findings, radiological features, treatment with hyperbaric oxygen therapy, and prevention. Microorganisms commonly involved include viridans streptococci and anaerobes such as Peptostreptococcus and Fusobacterium. Imaging tools like radiography, CT, MRI, and radionuclide bone scanning can aid in diagnosis

1. Prof. Dr.Ravi.S.Patil
Dept of OMFS
Navodaya dental college, Raichur.

2. Osteomyelitis of jaw
 Introduction
 History
 Classification
 Pre-disposing factors
 Etiology & Pathogenesis
 Microbiology of
Osteomyelitis
 Clinical findings
 Imaging
 Treatment
 Types of Osteomyelitis
Osteoradionecrosis of jaw
– Definition
– Clinical findings
– Radiological Features
– Treatment hyperbaric
Oxygen Therapy
– Prevention of
Osteoradionecrosis
– Bisphosphonate induced
Osteoradionecrosis of
Jaw(BIOJ)

3.  The word “osteomyelitis” originates from the ancient Greek words osteon (bone)
and muelinos (marrow) and means infection of medullary portion of the bone.
 Nelaton (1834) –coined the term Osteomyelitis.
 It is inflammatory process of the entire bone including the cortex and the periosteum.
 It can be considered as an inflammatory condition of the bone, that begins as an
infection in the medullar cavity and haversian systems of the cortex and extends to
involve the periosteum of the affected area.
 The infection becomes established in calcified portion of the bone when pus and
edema in the medullary cavity and beneath the periosteum obstructs the local blood
supply.
Following ischemia, the infected bone becomes necrotic and leads to sequester
formation, which is considered a classical sign of osteomyelitis (Topazian 1994,
2002).

4.  Osteomyelitis of the jaws is a disease that has affected mankind
since prehistory.
 1.6 million- year-old fossil find of “Turkana Boy” documents
this. As a 12-year-old prehuman hominid (homo erectus) his
nearly complete skeleton clearly showed an osteomyelitis arising
from an odontogenic infection around one of his first molar teeth
 The prevalence, clinical course, and management of
osteomyelitis of the jawbones have changed profoundly due to
the introduction of antibiotic therapy, specifically penicillin.
 After the introduction of antibiotics, acute phases were often
concealed by these antimicrobial drugs without fully eliminating
the infection

5.  ACCORDING TO Hudson JW (1993)
1. ACUTE forms of Osteomyelitis ( suppurative or non-
suppurative)
a. Contagious focus – i. Trauma
ii. Surgery
iii. Odontogenic infections
b. Progressive – i. Burns
ii. Sinusitis
iii. Vascular insufficiency
c. Hematogenous (Metastatic) – i. Developing skeleton
ii. Developing dentition.

6. 2. CHRONIC forms of Osteomyelitis
a. Recurrent Multifocal - Developing Skeleton
- Escalated Osteogenic Activity
b. Garres Osteomyelitis - Unique Proliferative Subperiosteal Reaction
- Developing Skeleton
c. Suppurative Or Non-suppurative - Inadequately Treated Forms
- Systemically Compromised Form
- Refractory Forms (Chronic Recurrent multifocal osteomyelitis)
d. Sclerosing
i. Diffuse - Fastidious microorganisms
- Compromised host/ pathogen interface
ii. Focal - Predominantly odontogenic
- Chronic localised injury

7.  ACCORDING TO Cierny, Mader ,
Pennick (1985)
I . Anatomic type
Stage I – Medullary Osteomyelitis - involved medullary bone
without cortical involvement, usually hematogenous
Stage II – Superficial Osteomyelitis - less than 2cm bony
defect without cancellous bone
Stage III- Localized Osteomyelitis - less than 2cm bony defect
on radiograph, defect does not appear to involve both the cortices.
Stage IV – Diffuse Osteomyelitis - defect larger than 2cm,
pathologic fracture, infection, non-union.
II. Physiologic type
a. Host – normal host
b. Host – systemic compromise & local compromise
c. Host – treatment is worse than disease
III . Systemic or Local factors that
affect immune surveillance,
metabolism and local vascularity-
a. Systemic
- Malnutrition
- Renal or Hepatic failure
- Diabetes Mellitus
- Chronic hypoxia
- Extremes of age
b. Local
- Venous stasis
- Extensive scarring
- Radiation fibrosis
- Loss of local sensations
- Small vessel disease.

9. Incidence of osteomyelitis of the jawbones can be explained by four primary factors which are
responsible for deep bacterial invasion into the medullar cavity and cortical bone and hence
establishment of the infection:
1. Number of pathogens
2. Virulence of pathogens
3. Local and systemic host immunity
4. Local tissue perfusion- compromised
local blood supply.
Periodontal diseaseleads to breakdown of the periodontal
barrier membraneFacilitating deep invasions of
pathogens Leading to osteomyelitis(51% of the cases)

10. CONDITIONS
COMPROMISING THE HOST
DEFENSE-
1. Diabetes
2. Anemia/sickle cell
anemia
3. Tuberculosis
4. Malnutrition
5. Agranulocytosis
6. Leukemia
7. Chronic alcoholism
8. Febrile illness
CONDITIONS
COMPROMISING JAW
VASCULARITY –
1. Radiation
2. Paget’s disease,
osteopetrosis ,
osteoporosis
3. Fibrous dysplasia
4. Peripheral vascular disease
5. Malignancy
6. Sickle cell anemia

11. Odontogenic infections
Trauma
Infections derived from periostitis following gingival ulcerations, lymph nodes
infected from furuncles, lacerations and peritonsillar abscess
Infections derived by hematogenous route furuncle on face, wound on the
skin, URTI, middle ear infection , mastoiditis, systemic tuberculosis.

12. Acute and secondary chronic osteomyelitis are intiated by a contagious focus of
infection or by hematogenous spread.
The route of infection is considered by most clinicians to be hematogenous
Streptococcus viridans has been implicated as the organism responsible for this type of
osteomyelitis (Peterson 1999)
Trauma - especially compound fractures, if not treated or treated inadequately,
facilitates the development of osteomyelitis.
The different anatomy of maxilla and mandible is probably the most important factor
explaining the distribution of osteomyelitis involving the jawbones. The maxillary
blood supply is more extensive than in the mandible.

13. Additional thin cortical plates permit dissipation of edema and pus into the soft
tissues of the midface and the paranasal sinuses .
Acute and secondary chronic osteomyelitis of the mandible affects most commonly
the body of the mandible followed by the symphysis angle ascending
ramus condyle
In mandibular osteomyelitis, the increased intramedullary pressure also leads to
direct compression of the neurovascular bundle, accelerating thrombosis and
ischemia resulting in dysfunction of the inferior alveolar nerve, known as
Vincent’s symptom.

14. CHRONIFICATION OF BONE INFECTION :
 The chronification of the disease reflects the inability of the host to
eradicate the pathogen due to lack of treatment / inadequate treatment
resulting in failure to re-establish the carefully balanced equilibrium
between host factors and pathogens found in a healthy oral environment.
PATHOGENESIS

15. Compression of neurovascular bundlethrombosis
& ischemia osteomyelitis induced nerve
dysfunction(IAN in case of mandible)
Pus travelshaversian & nutrient canal
accumulates beneath the periosteum elevating it
from the cortex reduces vascular supply
Pus composed of necrotic tissuesintramedullary
pressure increasesvascular collapsevenous
stasisischemia.
Tissue necrosis  vascular thrombosis follows
Acute inflammation hyperemia, increased
capillary permeability and infiltration of
granulocytes

16. Occasionally. Involucrum is penetrated by channels i.e. cloacae through which pus escapes to an
epithelial surface.
Small sectionslysed completely, larger onesisolated by a bed of granulation tissue encased in a
sheath of new bone i.e. involucrum.
Thus separating fragments of necrotic bone(sequestra) from viable bone
Inflammation regressgranulation tissue formsnew blood vessels lyse bone
Depending on host defense & therapyosteomyelitis may become chronic.
More pus accumulation penetration of periosteum mucosal & cutaneous abscess fistulas

17. Bone surrounding a sequestrum sometimes appears radiologically as less densely
mineralised than the sequestrum itself because increased vascularity of adjacent vital bone
creates a relative demineralisation.
The lifting of the periosteum at the edges of the bony defect produces a triangular
elevation called the Codman’s triangle
The sequestra formation leads to undermining of the bone and render it weak, which
is liable to fracture even during functional movements or on application of mild
stress.(pathological fracture.)

19.  The establishment of an infection in bone is related to the
i. Virulence of an organism
ii. Integrity and effectiveness of host defences
iii. Anatomical and structural factors.
 Findings help in recognition of pure anaerobic or mixed aerobic infections
i. Presence of foul smelling exudate
ii. Sloughing of necrotic tissue
iii. Gas in soft tissue
iv. Black discharge from the wound.
The most frequent microorganisms are
1.Viridans streptococci,
2. Peptostreptococci,
3. Eikenella corrodens,
4. Fusobacterium spp.,
5. Actinomyces spp
In case of implant-associated osteomyelitis,
5. S. aureus and
6. Coagulase-negative staphylococci
Accordingly, empirical therapy should include the spectrum of
these microorganisms

20.  Osteomyelitis of jaw is now recognised as a disease
caused primarily by streptococci(α-haemolytic) and
oral anaerobes, particularily Peptostreptococcus,
Fusobacterium & Prevotella (Bacteroides) , the
organisms responsible for odontogenic infections.
 The viridans streptococci can be divided into-
i. The mitis group
Ii. The mutans group
Iii. The salivarius group
Iv. The anginous group ( aka Strep milleri group)  this
group is found in abscesses but often with mixed anaerobic
flora.
Therefore, antibiotic therapy should be directed towards
streptococci and anaerobes and not the staphylococci.

21. Microbiological Procedures for Detection of Bacteria Found in Osteomyelitis
of the Jaws
• Swab cultures of pus and putride exudate often contain mostly dead
microorganisms
• Cultures from the sinus tracts may be misleading
• Aspiration and drainage from deep tissue samples provides the preferred
specimen
• Because acute and especially secondary chronic osteomyelitis of the jaws is
associated with anaerobes in a polymicrobic mixture,
• Culture specimens must be sent to the microbiology laboratory immediately.

22. Principles for bone biopsy for microbiological assessment of osteomyelitis of the jaws
(Modified after Eyrich et al. 1999; Marx et al. 1996)

23. Most frequently found bacteria in samples taken from patients with osteomyelitis of the jaws.

24.  Four types of osteomyelitis of jaws are
observed clinically
i. Acute suppurative
ii. Secondary chronic- a form that begins as
acute osteomyelitis and becomes chronic
iii. Primary chronic – a form that has manifested
no acute phase previously, having always been a
low grade
iv. Non-suppurative
Note – A sub-acute stage also exhibits - acute symptoms such as
1.elevated temperature
2. WBC count are nearly normal
3. Production of pus and extension into adjacent bone continues

25.  Characterised by four findings
i. Deep intense pain
ii. High intermittent fever
iii. Constitutional signs of acute infections such as
bodyache, malaise, leucocytosis , raised ESR.
iv.Paresthesia or anesthesia of the lowr lip (IAN)
v. Clearly identifiable cause, usually deep caries in an
involved tooth
Treatment : Antibiotic therapy at this stage may
prevent progression to involvement of periosteum
(subperiosteal osteomyelitis)
 Laboratory results : Leukocytosis .

26.  If the disease is not controlled within 10-14days
after onset, subacute suppurative osteomyelitis is
established.
Clinical features –
i. deep pain, malaise, fever (101degreesF - 102degreesF)
and anorexia are present
ii. Loose teeth with sensitive to percussion
iii. Fetid odor
iv. Firm cellulitis of the cheeks
v. Expansion of bone from increased periosteal activity

27. SECONDARY CHRONIC
OSTEOMYELITIS
 Clinical findings are limted to :
i. Fistulas & sequester formation- classical sign
ii. Induration of soft tissues
iii. A thickened or “wooden” character to the
affected area with dull pain and tenderness on
palpation
PRIMARY CHRONIC OSTEOMYELITIS
 It is the form not proceeded by an episode of
acute symptoms, insidious in onset &
periodic episodes of onset and slight pain.
 Slow increase in jaw size
 Gradual development of sequestra often
without fistulas.

28. 1. ‘moth-eaten’
2. ‘islands’ of sequestra.
3. Stippled or granular densification.

29.  Imaging of suspected osteomyelitis of mandible is accomplished by
i. Conventional Radiography
ii. Computed Tomography
iii. Magnetic resonace Imaging
iv. Radionuclide Bone Scanning.

30. SCINTIGRAPHY (BONE SCANNING)
In skeletal scintigraphy, the basic principle
consists of  injecting a radioactive tracer
into the circulation system.
99Tc labelled methylene diphosphonate is administered
intravenously and consists of 3 phases:
• Flow study: consists of serial 3-4seconds images taken during
the first 1-2mins after injection of the radionuclide.
• Blood-pool-study: consists of a single image obtained 5-
10mints after injection.
• Delayed study or bone study: include multiple views
obtained 2-4 hours after injection.
- The tracer is embedded
into the newly formed bone
tissue, hence, uptake is
directly
proportional to
osteoblastic activity.
- Demonstrates the relative
regional differences of
activity

31. A rectilinear scanner or scintillation camera ,both
of which contain sodium iodide, crystal nuclide that
emits light, is then used to obtain images of isotope
containing area.
The resulting image shows the distribution of
radionuclide in areas of increased bone activity.
Positive Tc scan results confirm the diagnosis of
acute OML, although bone scan finding maybe
negative very early in the disease.

32. Addition of GALLIUM 67
to TECHNETIUM(Tc) 99
aids in distinguishing OML
from malignancy and trauma
Positive findings on both the
test usually confirm the
infectious nature of the
disease.
When the Tc scan result is
positive and the Ga scan
results are negative, OML is
not the primary disease.
Ga uptake that exceeds Tc
upake indicates active
inflammatory disease.
Indium-111 in leucocyte
scintigraphy may also been
useful in determining when a
lesion is inactive.

33. Compared with conventional radiographs, the following additional information can
be gathered with bone scintigraphy (Hardt and Hofer 1988; Hardt 2000, 2003):
1. High level of activity with a mixed pattern of osteolysis and sclerosis or in cases
where the clinical course of the disease leads to the assumptions of an underlying
aggressive pathology.
2. Scintigraphy is positive as soon as regional osteoblastic activity is increased. The
latency period compared with conventional imaging is therefore reduced
3. Information is obtained from the whole skeleton- thus clinically silent lesion maybe
detected at an early stage.
Adult-onset primary chronic osteomyelitis with insinuating osteolysis in the symphyseal area
An increased uptake is noted in the entire symphysis as well in anterior portion of right mandibular corpus

34. Because osteoblastic activity is detected much earlier in bone scans, the dimension of the lesion can be
determined more accurately .
The changes are seen as early as 3 days after the onset of
symptoms of OML
Approximately one third to half of the bone mineral must be
altered before changes are observed on conventional radiographs.
These changes usually require atleast 10−14 days or even longer
after onset of the infection.
In a study of 18 patients, conventional radiographs were definitely
diagnostic of osteomyelitis in all patients only after 4 weeks
(Schuknecht et al. 1997).
Since radiopharmaceuticals in bone scans give particularly useful
information on osteoblastic bone activities, rather than
demineralization, changes may be seen as early as 3 days after
onset of symptoms of osteomyelitis (Topazian 2002). This
allows diagnosis of the disease in an early stage.

35. Summarized when
interpreting a bone scan, the
following criteria must
always be addressed:
1.Look for
symmetrical
uptake within the
corresponding
skeletal regions
2.Regions with
increased or
decreased uptake
compared with
surrounding and
corresponding bones
are suspicious and
may need further
radiological
investigation
3.Increased uptake
is a sign of
increased metabolic
activity
4.A physiological or
decreased uptake
indicates a normal
osteoblastic bone
activity or may be
the result of a very
aggressive lesion
with failure of local
bone repair

36. Because of its sensitivity, high resolution CT detects early bone changes before they
can be seen on conventional films
Changes visible on CT scans include:
i. Increased attenuation in medullary cavity
ii. Destruction of cortical bone
iii. New bone formation
iv. Appearance of sequestra
Advatages :
i. Extent of lesion
ii. Extent of cortical erosion
iii. Identification of sequestra.

37. The corresponding MRI (same patient as in)
demonstrates a hypointense bone marrow in
the symphysis and the anterior mandibular
body on both sides as a sign of marrow
fibrosis/sclerosis
The corresponding axial CT scan shows a more
distinct pattern with sclerosis and osteolysis
and cortical defects of the entire right
mandibular body as well the left anterior
mandible

38. Principles of Treatment of Osteomyelitis
 Evaluation and correction of host defence deficiencies
 Gram staining, culture and sensitivity
 Administration of empirical antibiotics.
 Imaging to rule out bone tumors
 Removal of loose teeth and sequestra
 Adminsistration of culture- guided antibiotics
 Possible placement of irrigation drains /polymethylmethacrylate- antibiotic
beads
 Sequestrectomy, debridement , decortication , resection and
reconstruction.
 Hyperbaric Oxygen Therapy

39. In the early border line cases with atypical
presentation ,the evaluation of the cases
should be undertaken as
1.Disrupt the infectious foci
2.Debride any foreign bodies, necrotic tissues or
sequestra for eventual definitive antibiotic treatment
3. Drain and irrigate the region
4.Begin empiric antibiotics based on gram stain
5.Stabilize calcified tissue regionally
6. Adjunctive treatment to enhance microvascular
reperfusion- Trephination, Decortication , Vascular
flaps and HBO Therapy
7. Reconstruction – as necessary following
resolution of infection.
Treatment Guidelines For Acute And
Chronic Osteomyelitis (MARX 1992)

40. Is usually diagnosed by the findings of
i. Deep intense pain
ii. Parethesia of the IAN
iii. Fever
iv. Identified cause
v. Positive bone scan findings
Initial management
i. Hospitalisation administration of high dose IV
antibiotics
ii. Identify and correct host compromised factor
iii. Biopsy of bone, granulation tissue and fistulas
iv. After acute stage subsides, Sequestrectomy and
Saucerization , Debridement and direct placement of
antibiotics , resection or late bone reconstruction .

41. Requires surgical procedure such as
1.Sequestrectomy
2.Removal of foreign bodies such as wire, bone plates and screws
3.Repeated culturing
4.Improvement of host defences
 Treatment begins with IV therapy

42. Regimen I: For Hospitalised/Medically Compromised Patients Or When
Intravenous Therapy Is Indicated
 Aqueous penicillin, 2million U IV q4h + metronidazole, 500mg, q6h
when improved for 48-72hr, switch to
 Penicillin V, 500mg oral q4h, + metronidazole, 500mg oral q6h, for an additional
4-6 weeks
OR
 Ampicillin/Sulbactum, 1.5-3.0g IV q6h ,
when improved for 48-72 hours , switch to
 Amoxicillin+clavulanate (Augmentin), 875/125 mg PO bid for an additional
4-6weeks

43. Regimen II: for outpatient treatment
 Penicillin V, 2g + metronidazole, 0.5 g a8h PO, for 2-4 weeks after
last sequestrum removed and patient without symptoms
OR
 Clindamycin, 600-900mg q6h - IV
then
 Clindamycin, 300mg -450mg q6h - PO
OR
 Cefoxitin(mefoxin) 1.0g q8h IV or 2g q4h IM or IV.
Until no symptoms, then switch to
 Cephalexin(Keflex),500mg q6h PO, for 2-4 weeks

44. LOCALANTIBIOTIC THERAPY
1. Closed Wound Irrigation Suction
2. Antibiotic Impregnated Beads.
Closed wound irrigation suction
- Placement of the tube against the bone is done to
 allow drainage of the pus and serum
 and to provide a route for irrigation. Thus, reducing
the number of remaining organisms
- Irrigation without surgical debridement to the
point of bleeding bone is unlikely to be effective,
prolongs the process and delays definitive treatment.

45. The soln is evacuated by suction through the efferent drain every 24h
1-2L of soln is instilled through the afferent tube
The irrigating solution is introduced through one tube while the other tube is
connected to low pressure suction
Tubes flushed with saline solution
Water tight closure of wound is achieved
Alterrnatively, 2 tubes exit from one stab incision for instillation & suction
Drains held into skin by suture or tape
Tubes placed into bone bed affixed with catgut sutures through hole drilled in the
bone
After intraoral debridement, polyethylene irrigation tubes 3-4mm in diameter and 6-
10inches in length are perforated along a distance of 3-4cm from the tip
TECHNIQUE

46. The drug is left in place for 3hours , then low-pressure intermittent suction is used
for 9hours followed by culture of specimen.
Wound should not be overfilledvolume should decrease gradually to allow for
filling of the wound by healthy granulation tissue and avoid neomycin toxicity
Systemic antibiotics should be continued throughout irrigation for atleast
2months after cessation of clinical evidence of disease.
Various antibiotic used are ( placed in direct contact with bone manually or with
implantable pump)
i. Clindamycin
ii. Neosporin G.U. irrigant
iii. 1% neomycin with 0.1% polymyxinB in equal volume instilled on a 24 hour cycle

47. NEGATIVE PRESSURE HEALING: OCCURS BY THREE MECHANISMS
1. Altered blood flow-
Vaccum increases the vascularity of wound edges by increasing blood flow diameter,
velocity, blood volume, endothelial proliferation and angiogenesis and thus promoting
healing
2. Mechanical deformation-
Because of negative pressure there is stretching of the cell which causes disturbances in
the extracellular and intracelllualr skeleton. To overcome this, there is increased mitotic
activity which inturn promotes healing
3. Pressure gradient-
Pressure itself pulls cytotoxic substances, bacteria, normal cells towards infected site,
reduces interstitial edema and thus promotes healing

48. Used to deliver high conc. of antibiotics into the wound bed and in immediate
proximity to the infected bone.
Antibiotics used
i. Tobramycin
ii. Gentamycin
iii. Clindamycin
Uses-
i. in Chronic sclerosing OM refractory to systemic antibiotics.
ii. In Chronic Sclerosing OM after decortication
Duration 10-14days and removed through a small incison with adminstration of
systemic antibiotics
Advantages high local conc. but low systemic conc., thus reducing risk for toxixcty
.

49. Establish correct diagnosis, based on history, clinical evaluation, and imaging studies
Biopsy in unclear cases to rule out other pathology (e.g.. malignancy)
Determine extent of infected bone and soft tissue
Evaluation and correction of host defense deficiencies when possible
Removal of source of infection, usually a dental focus, foreign bodies/implants
Local incision and drainage of pus
Local curettage with removal of superficial sequestra and saucerization if necessary
Collection of specimens for Gram stain, culture and sensitivity, histopathology
Begin with empiric broad-spectrum antibiotic therapy and change to culture-guided antibiotics as
soon as possible
More extensive surgical debridement if necessary (e.g., decortication, resection)
Possible adjunctive hyperbaric oxygen therapy

50. Establish correct diagnosis, based on history, clinical evaluation, and imaging studies
Biopsy in unclear cases to rule out other pathology (e.g., malignancy)
Determine extent of infected bone and soft tissue
Evaluation and correction of host defense deficiencies when possible
Surgical debridement of infected tissue dictated by extent of the lesion (removal of affected teeth
and foreign bodies/implants,
sequestrectomy, local curettage, saucerization, decortication, resection
Collection of specimens for Gram stain, culture and sensitivity, histopathology
Begin with empiric broad-spectrum antibiotic therapy and change to culture-guided antibiotics
as soon as possible
Possible adjunctive hyperbaric oxygen therapy
More extensive surgical debridement if necessary (e.g., repeated decortication, resection)

51.  The most performed procedures in acute and secondary chronic
osteomyelitis are
1. Sequestrectomy
2. Saucerization
3. Decortication
4. Resection and Reconstruction

52.  Sequester formation is a classical sign of secondary chronic
and advanced acute osteomyelitis cases
 Starts 2 weeks after onset & persist for several months
 Resorption of sequester is achieved by lytic activity of the
osteoclast cells in the surrounding granulation tissue
 sequester are avascular, they are poorly penetrated by
antibiotics or HBO and hence are ideal breading grounds
for bacteria. – Sequestrectomy adviced.

53. Intraoral incision should be placed. Ofending
tooth should be removed.
Intraoral wound – packed with iodoform
gauze soaked in betadine.
If sequestrum is encased by involucrum –
window must me created with a curette/
chissel/ drill around the natural perforation.
Cavity exposed – granulation tissue – curetted
out until healthy bone is exposed.
If suppuration present – partly closed with
sutures & rubber drain is inserted through
skin.
Sequestrectomy – helps in
establishment of local microvascular
proliferation.

54. Step 4: Removal of the odontogenic focus, the teeth in the affected
region and removal of sequester

55. Definition : Saucerization is the ‘unroofing’ of the bone to expose the medullary
cavity for thorough debridement
The margins of
the necrotic
bone overlying
the focus of
osteomyelitis
are excised
allowing
visualisation
of sequestra
and excision of
the affected
bone
Timing : can be performed as soon as acute infection has
resolved
Aim : to decompress the bone & allow ready extrusion of
pus, debris and avascular fragments.

56. Place it for 3-4 days  replace several times until bed of granulation tissue
epithelised and margins healed.
Place the pack firmly(without pressure) retain using interrupted sutures from
lingual to buccal flap
The buccal flap is trimmed and packed with idoform gauze  to achieve
hemostasis & maintain flap in a retracted position until intial healing occurs
All granulation tissues and loose bonesremoved using curettes and irrigated
(this area is usually hypermic but can be controlled by packing)
The lateral cortex of the mandible is reduced using burs until bleeding bone is
encountered at all margins app. to the level of the unattached mucosa thus
producing saucer like defect
The buccal periosteum flap is reflected to expose the infected bone

57.  Decortication was first advocated for treatment of osteomyelitis of the
mandible in 1917 and further described by Mowlem (1945). The
application of this surgical procedure in conjunction with antibiotic
therapy was later well described by Obwegeser (1960), Hjorting-
Hansen(1970).
Definition : Decortication of the mandible refers to the removal of
chronically infected cortex of bone
Purpose of the decortication procedure is
1. to remove the chronically infected cortex
2. meticulous surgical debridement under direct visualization.
3. Furthermore, this procedure allows bringing well-perfused tissue in
contact with bone – promoting healing.

58. The Classical Decortication Procedure
Odontogenic secondary chronic osteomyelitis of the left mandible

59. Step 1: buccalflap - crevicular incision reflection
affected bone
(dashed curve)

60. Step 2: Subperiosteal dissection and exposure of the affected region

61. Step 3: exposure of the affected mandibular corpus

62. Step 5: The margins of the intended area of decortication are marked
with a burr

63. Step 6: After demarcation of the intended area of decortication,a long Lindemann burr is used to
perform multiple monocortical decortication osteotomies on the buccal cortex of the mandible
leaving a distance of approximately 1 cm between the decortication osteotomies

64. Step7: The buccal cortical bone and the inferior border are then removed
with a chisel, lane by lane, until bleeding bone is encountered

65. Step8 : Mobilization (neurolysis) of the inferior alveolar nerve is performed to allow access to
the surrounding deeper areas of affected bone. The nerve may be marked with a vessel loop

66. An intraoperative view of this step of the decortication the inferior alveolar nerve is liberated and
mobilized (lateralization)  allowing further surgical debridement

67. Step 9: Meticulous removal of affected bone and granulation tissue is performed

68. Step 10: Mandible after completed decortication and surgical debridement. The
remaining bone represents the remaining vital bone tissue

69. Step 11: If necessary, additional burr holes and perforations can be performed to facilitate
contact better in vascularized deeper bone compartments or to the lingual periosteum

70. An intraoperative view after surgical debridement (decortication) of the anterior mandible and
perforations of the lingual cortical bone

71. Step12:Resection of affected buccal periosteum with areas of neoosteogenesis

72. Step 13:If extensive debridement was required and the remaining bone is suspected to be
prone to fracture, appropriate stabilization and reconstruction should be performed.

73. The surgical site after completed decortication and stabilization of the anterior mandible
with reconstruction plate

74. Step 14:Primary closure is achieved to ensure close contact of the bone bed to the well-
vascularized soft tissue.

75. Step 15:Maxillary−mandibular fixation may be performed if additional
stabilization and immobilization is required

76. Maxillary−mandibular fixation may be performed if additional stabilization and
immobilization is required. Postoperative OPG of a patient with extensive secondary
chronic osteomyelitis of the left mandible after surgical decortication

77. Marx (1991) advocates a two-stage procedure to reconstruct continuity
defects resulting from surgical debridement of osteomyelitis with
reconstruction of the bone commencing as Early As 3 Months After
Debridement, provided that skin and mucosa are intact and the tissue is
free of contamination and infection.
Regardless of the preferred protocol, a meticulous debridement is always
the prerequisite for successful treatment of advanced acute and secondary
chronic osteomyelitis cases.
SMALLER BONE DEFECTS free autologous bone graft through oral
approach
LARGER DEFECTS microvascular bone (and soft tissue) grafts
through extraoral approach.

78. 1. Osteomyelitis associated with fracture
Causes :
- Failure to use effective methods of reduction, fixation and
immobilisation as microorganisms gain access to the fractured site
- Overzealous use of intraosseous wiring, bone plates or screws that
devascularises bone segments
Treatment :
- IMF
- Loose teeth and foreign materials removal
- High dose of antibiotic therapy (6weeks – absence
of internal fixation,
3 months – presence of internl fixation)

79. 2. Infantile Osteomyelitis: (Osteomyelitis Maxillaries Neonatorum)
rare but risk of
- Involvement of eye
- Extension to dural sinuses
- Potential for facial deformities
Time of occurrence : Few weeks after birth and affects maxilla
Mode of spread :
- Hematogenous spread from perinatal trauma of the oral mucosa from the obstetrician’s finger
- Infection involving maxillary sinus
- Contaminated human or artificial nipple
Treatment :
- Prevent permanent optic damage
- IV antibiotics and drainage of abscess
- Antipyretic fluids/ proper diet

80. 3. Chronic recurrent multifocal osteomyelitis in
children (CRMO)
- Affects children averaging 14years of age
Site:
- Tibia , Clavicle Fibula , Spine , Femur
- Mandible – lesion are bilateral, irregular, mottled - ramus
region
Characterised by:
- Periods of exacerbations and remissions over many years.
 In correlation with advanced age, there seems to be an
increased association with SAPHO syndrome (Shilling et
al. 2000).
Treatment :
- Antibiotics
- Debridement

81. 4. Proliferative Periostitis ( Garre’s Osteomyelitis )
- First described in 1893 By Carl Garre “as an irritation
induced focal thickening of the periosteum and cortical
bone of the tibia.’’
Clinical features:
- localised, hard & non-tender, unilateral bony swelling of
the lateral and inferior aspect of the mandible – peripheral
subperiosteal bone deposition.
- skin overlying the swelling is normal
- Absent  lymphadenopathy, fever
- Associated with carious lower first molar tooth with history
of past toothache
Radiological features:
- A focal area of well-calcified bone proliferation with
smooth laminated or ‘onion-skin’ appearance
- Radiolucency associated with apices of involved tooth.

82. 5. Chronic Sclerosing Osteomyelitis
i.Chronic Diffuse Sclerosing OM( Diffuse & affects only mandible)
ii. Florid Osseous Dysplasia (Opaque mass limited to alveolar process of both jaws)
iii. Chronic Tendoperiostitis.

83. 5a. CHRONIC DIFFUSE SCLEROSING OM: IS
an inflammatory, non-suppurative, painful disease with a protracted course.
Site –
- Occurs only in the mandible and affects both the basal bone & the alveolar
process involves the entire height of mandible simultaneously and usually
unilateral
- Angle, ramus and even condyle
Clinical Features-
- Bone is mildly expanded and tender
- Episodes of recurrent swelling and pain occurs
- Common in 3rd decade
- 2/3rd of patients are women
Radiographical Features-
- Diffuse intramedullary sclerosis with poorly defined margins with
occasional focal areas of radiolucency and radio-opacity

84.  Cause –
i. Infectious & non-infectous
ii. Overuse of jaw
iii. Malocclusion
iv. Abnormal jaw positioning habits causing chronic osteomyelitis
 Treatment –
i. High dose of antibiotics for prolonged periods
ii. Removal of source of infection
iii. Repeated culture & sensitivity test
iv. Wound irrigation
v. Antibiotic impregnated beads
vi. Debridement
vii. Decortication
viii.HBO therapy

85. 5b. Florid Osseous Dysplasia :
- Multiple exuberant (florid) lobulated densely opaque masses are restricted to the alveolar
process in either both jaws
Clinical Features:
- Seen mostly in black women
- Cause :Infection  periapical, advanced periodontal disease, ulceration of mucosa when the
lesion becomes superficial as when residual ridge resorption proceeds, extraction of teeth,
attempts of surgical excision.
- Fistulas & sequestra may form
- Secondarily infected florid osseous dysplasia is a suppuraitve , mildly painful condition of
mandible without expansion.
Treatment :
- Lesion should be treated only -symptoms are present
- The masses, sequestra and associated granulation
tissue are excised and the wound is debrided and
irrigated followed by primary or secondary closure .

86. 6. CONDENSING OSTEITIS ( FOCAL SCLEROSING OM)
 Is a localised area of bone sclerosis associated with the apex of a carious tooth
 This causes more bone production rather than bone destruction in the area (most common site is near
the root apices of premolars and molars).
Radiological Features :
 Radiopacity in the periapical area hence the sclerotic reaction.
( The sclerotic reaction results from good patient immunity and a low degree of virulence of the
offending bacteria. The associated tooth may be carious or contains a large restoration, and is usually
associated with a non-vital tooth.)
Treatment :
 Endodontic therapy /extraction
 Lesion then regresses or remain as a bone scar.

87. caused by Actinomyces israelii
 Actinomycosis is a chronic, slowly progressive infection with both granulomatous and suppurative
features
Clinical Features:
 It usually affects soft tissue and occasionally bone, no fever, delayed healing of extraction socket.
 Forms external sinuses that discharge distinctive sulphur granules and spreads unimpeded by
anatomical barriers.
 Tissues - invaded by hematogenous spread
 Spontaneous drainage of serous fluid containing granular material may occur
 Limited mouth opening due to fibrosis of one muscles of mastication  LUMPY JAW
Treatment :
 Antibiotics  4-6 weeks(PenicillinV 1g 6hrly) followed by
oral therapy for 6-12months(Doxycycline 100mg BD) .
 Penicillin & macrolides, Doxycycline and Clindamycin, Amoxicillin,
Ampicillin.
 Incision and Drainage
 Excision of soft tissue and bones.
7. ACTINOMYCOTIC OSTEOMYELITIS OF THE JAW:

88. Site : dorsal and lumbar vertebrae, epiphysis and diasphysis of long and flat bones including skull and
mandible which are rarely affected.
Age: more common in children
Sex : 5 times more common in males than in females.
Inovlvement of mandible by tuberculos infection rare
Treatment
1. Primarily with antitubercular drugs such as streptomycin, isoniazide , rifampicin , ethambutol and
pyrazinamide.
2. Surgical management  marginal and restricted to debridements and drainage after chemotherapy is
started.
8. TUBERCULOS OSTEOMYELITIS :

89.  Osteomyelitis Of Jaw –Robert E.Marx
 Textbook Of Oral And Maxillofacial Infections – Richard G.
Topazian
 Fonseca- Surgical Pathology Vol.5
 Petersons Principles Of Oral And Maxillofacial Surgery
 Oral Radiology – Principles And Interpretations- White
&Pharoah