H o w Ca n We D i a g n o s e

a n d Tre a t O s t e o m y e l i t i s
of the Jaws as Early
as Possible?
Gerard F. Koorbusch, DDS, MBA, FICDa,*,
Joseph R. Deatherage, DMD, MDa, Joel K. Curé, MDb

KEYWORDS
 Osteomyelitis  Maxilla  Mandible  Jaws

Maxillofacial osteomyelitis is an uncommon condi- CLASSIFICATION

tion encountered in the clinical practice of oral and
maxillofacial surgery, which presents an enigma The focus of this article is the discussion of acute
for the clinician in terms of diagnosis and treat- and chronic suppurative osteomyelitis. Acute oste-
ment. Delayed recognition of the infection may omyelitis is the early phase of the disease, which is
result in a protracted course of treatment and in- usually a suppurative (pus forming) condition.3 The
creased surgical morbidity. acute phase may lead to the chronic phase of
The scientific literature is replete with case reports the disease, which has been arbitrarily defined as
and retrospective studies related to osteomyelitis of osseous infection lasting at least 1 month.4 Chronic
the jaws, which do not always give a structured forms of osteomyelitis may be suppurative or
protocol for the early diagnosis and treatment of nonsuppurative.
the disease. The function of this article is to eluci- Other forms of osteomyelitis of the jawbones
date that structured protocol to enable the timely include osteoradionecrosis (ORN), bisphosphonate-
management of the condition. related osteonecrosis of the jaws (BRONJ), Garrè
Osteomyelitis of the jaws is defined as an inflam- osteomyelitis, chronic recurrent multifocal osteomye-
matory process of the medullary portion of the litis of children, and chronic sclerosing osteomyelitis.
affected bone. Osteomyelitis of the jaws is predom- ORN is the death of osseous tissue associated
inantly a disease of the mandible, whereas the with a radiation injury to the mandible in most cases.
maxilla by virtue of its vascularity and thin cortical This condition is the result of radiation therapy to the
plates is less frequently involved. In the mandible, maxillofacial region for the treatment of malignant
the inflammatory process begins with an infection tumors. The tissue injury is represented by a chronic
of the medullary portion of the bone and eventually nonhealing wound of the affected jaw, typically
extends to include the haversian systems and the with exposure of bone. The progressive radiation
periosteum. Osteomyelitis is truly an infection of injury evolves in chronic hypovascularity, hypocellu-
bone.1–4 larity, and ultimately hypoxemia. Cell death and
Demographically, the infection is more frequently nonhealing osseous lesions ensue. ORN represents
found in the mandible, predominantly in men, with avascular necrosis of bone rather than a primary
a wide reported age range.5 infection of bone.6
oralmaxsurgery.theclinics.com

The authors have nothing to disclose.

a
Private Practice, Face and Jaw Surgery Center, 1140 West Capitol Avenue, Bismarck, ND 58501, USA
b
Department of Radiology, University of Alabama at Birmingham, West Pavilion, Room P150, 619 18th Street
South, Birmingham, AL 32533, USA
* Corresponding author.
E-mail address: [email protected]

Oral Maxillofacial Surg Clin N Am 23 (2011) 557–567

doi:10.1016/j.coms.2011.07.011
1042-3699/11/$ – see front matter Ó 2011 Elsevier Inc. All rights reserved.
558 Koorbusch et al

BRONJ is a necrosis of bone related to the long- abscess, or adjacent soft issue infection; contami-
term use of bisphosphonate drugs. In this condi- nated facial fractures; or foreign bodies such as
tion, the osteoclasts are poisoned by ingestion of implants, wires, or bone plates and screws.2,4,5
the bisphosphonate during normal bone remodel- Comorbidities are varied and include malnutrition,
ing, resulting in diminished bone loss, which is alcoholism, substance abuse, smoking, human im-
beneficial in conditions such as osteoporosis. munodeficiency virus infection, sickle cell anemia,
The drugs are also beneficial in the treatment of malignancy, myeloid disorders, hypertension, pulmo-
certain malignancies because they help reduce nary disease, immunosuppression, diabetes mellitus,
the spread of the malignancy to bone. Alveolar steroid use, heavy metal toxicity, fibrous dysplasia,
bone undergoes more rapid bone turnover than Paget disease, and osteopetrosis.1,2,5,9,10
skeletal bone; however, in the aftermath of bi-
sphosphonate administration, senescence and CLINICAL FINDINGS
death of osteocytes, which cannot be resorbed
by osteoclasts, results in necrosis.7 Acute osteomyelitis is characterized by intense
Garrè sclerosing osteomyelitis was first des- pain, swelling that is frequently firm and indurated,
cribed in 1893 and describes an osteomyelitic fever, paresthesia or anesthesia of the inferior
condition secondary to a proliferative periostitis. alveolar nerve, and a clearly identifiable cause.
The result is a hard swelling of bone often noted Over time, loosening of the teeth, fistula formation
in the mandibular first molar region in response transorally or facially, lymphadenopathy, and pa-
to a carious first molar. Radiographs reveal a focal thologic fracture may be consequences of the
area of cortical-layered thickening, which has infection.1–3
been termed onionskin appearance. The disease Chronic osteomyelitis has as its primary clinical
is usually seen in patients younger than 25 years, expression deep pain, fever, malaise, and anorexia.
and the treatment consists of removal of the of- The infection is usually attributable to long-standing
fending tooth.1,2 odontogenic infection or inadequately treated facial
Chronic recurrent multifocal osteomyelitis of fractures. Once again, loose teeth, intraoral or facial
children refers to a condition characterized by an fistula formation, trismus, malocclusion, sequestra,
inflammatory process, which presents with find- and potentially pathologic fracture may be antici-
ings similar to infectious osteomyelitis; however, pated. Indurated swelling and lymphadenopathy
no infectious source is identifiable. The condition is often associated with chronic osteomyelitis.
affects individuals in their preteenage and teenage Exposure or exfoliation of infected bone fragments
years. The disease is polyostotic and may affect may be seen in the course of the disease.1,2,4
the mandible. The treatment is controversial, and
the disease may resolve spontaneously.2 RADIOLOGIC CONSIDERATIONS
Chronic diffuse sclerosing osteomyelitis is a con-
dition characterized by an intermedullary osseous Roles for imaging in maxillofacial osteomyelitis
infection, which induces the sclerosis. Marx and include disease detection and staging, differential
colleagues8 demonstrated a bacterial cause for diagnosis, and monitoring of treatment response.
the disease, especially Actinomyces species and Because pretherapeutic symptom duration is one
Eikenella corrodens. The disease is predominantly of the most significant factors influencing the
found in women and appears radiographically as curability of mandibular osteomyelitis,11 accurate
medullary sclerosis with little cortical expansion. early diagnosis is critical in the management of
Inferior alveolar canal widening may occur over maxillofacial osteomyelitis.
time. The disease is often painful in affected Available modalities for imaging evaluation of
patients. The therapy includes antibiotic therapy patients with maxillofacial osteomyelitis include
and surgical debridement. In some refractory cases, plain and orthopantomographic radiographs,
hyperbaric oxygen therapy may be indicated.2,4 computed tomography (CT), magnetic resonance
The remainder of this article is devoted to the imaging (MRI), and radionuclide imaging (scintig-
discussion of acute and chronic suppurative oste- raphy). Given its frequent odontogenic origin, the
omyelitis of the jaws. initial imaging manifestations of acute osteomye-
litis are often observed on plain dental or panorex
ETIOLOGY radiographs. Because they require a loss of up to
50% of bone mineral density to reveal disease,
Osteomyelitis of the jaws is caused by some incit- these studies may be normal for up to 8 days or
ing focus that enables the infection to propagate. even as long as 3 weeks from symptom onset.12,13
Specific causative factors include odontogenic infec- Radiographic findings in acute osteomyelitis reflect
tion, whether from periodontal disease, periapical demineralization and destruction of trabeculae
 Osteomyelitis of the Jaws 559

within cancellous bone and include ill-defined bone phase images (obtained approximately 3
lucency adjacent to either an extracted tooth hours after the blood pool images) demonstrate
socket (Fig. 1) or a carious or restored tooth with increased uptake in both acute and chronic osteo-
a lucent periapical inflammatory lesion.14 Addi- myelitis. Uptake on blood pool images reflects
tional findings may include widening of the peri- altered vascular permeability, whereas persistent
odontal ligament space, loss of the lamina dura, uptake on delayed images reflects increased oste-
and loss of sharp margination (with apparent oblastic activity at sites of inflammation (Fig. 2).
widening) of the mandibular nerve canal and In addition to poor spatial resolution, routine
mental foramen. Subacute findings may include radionuclide bone scans have low specificity,16
sequestra (radiodense intraosseous necrotic problems that may be mitigated with the addition
bone fragments) and periosteal new bone forma- of single photon emission CT methodology and
tion, but these are often difficult to appreciate on use of alternative radionuclide agents. Increased
plain radiographs. In chronic suppurative osteo- uptake on blood flow phase images may be seen
myelitis, plain radiographs demonstrate variably with soft tissue infection, and increased uptake
mixed mandibular lucency and sclerosis and on bone phase images occurs in healing fractures,
bone enlargement related to cortical thickening dental extraction, or surgical sites and within
by appositional periosteal new bone formation.14 osseous neoplasms and other osseous diseases
Radionuclide scintigraphy using 3-phase (eg, Paget disease, fibrous dysplasia). Prolonged
imaging and technetium Tc 99m (99mTc)-labeled uptake of radionuclide during bone healing may
bisphosphonates demonstrates abnormal radio- confound interpretation of radionuclide studies
nuclide accumulation in mandibular osteomyelitis used to monitor treatment. However, decreasing
because of inflammation and pathologic bone uptake on serial scans correlates with treat-
turnover. Findings may be abnormal as early as 2 ment response, whereas renewed uptake signals
to 3 days after symptom onset.15 Early blood disease recurrence. Specificity of radionuclide
flow phase images obtained during the intrave- examinations is better (especially in patients
nous infusion of radionuclide demonstrate in- with indwelling surgical hardware) when using
creased uptake as a result of hyperemia in the white blood cells (WBCs) tagged with indium In
affected area.16 Uptake during this blood flow 111 or 99mTc hexamethylpropyleneamine oxime
phase is not usually observed in chronic mandib- (HMPAO).18 Because WBCs accumulate in normal
ular osteomyelitis.17 Blood pool phase images marrow, the specificity of 99mTc HMPAO–tagged
(obtained within 5 minutes of the injection) and WBC studies can be improved still further by

Fig. 1. Subacute suppurative mandibular osteomyelitis after dental extraction. (A) Right hemimandible, panorex
radiograph. Arrowhead indicates site of persistent pain at tooth number 32 extraction site. Extraction socket and
mandibular nerve canal margins are well defined. (B) Follow-up panorex image demonstrates diffuse lucency in
bone mesial to the extraction site (white arrowhead). Margins of the mandibular nerve canal and mesial wall of
the extraction socket are now obscure (outlined arrowhead). Early periosteal new bone formation is indicated by
the white arrow.
560 Koorbusch et al

artifacts that adversely affect MRI quality), scintig-

raphy is an excellent alternative for treatment
surveillance. Whole-body radionuclide bone scans
are also useful for detection of multifocal involve-
ment in cases of nonsuppurative primary chronic
mandibular osteomyelitis associated with sys-
temic diseases known as synovitis, acne, pustulo-
sis, hyperostosis, and osteitis or chronic recurrent
multifocal osteomyelitis.
MRI is sensitive for soft tissuepathology but is
relatively insensitive for bone and dental pathology.
Because of their low mobile proton density, healthy
cortical bone, teeth, and sequestra yield weak
signal and therefore appear as dark signal voids.
Alteration of the normal signal generated by
fatty marrow elements in the medullary compart-
ment of the bone is a useful marker for the patho-
logic condition. Normal fat appears “bright” on
T1-weighted (short pulse repetition time, short
echo time) MRI. Inflammatory exudate, marrow
fibrosis, trabecular thickening, or tumors decrease
Fig. 2. Right mandibular osteomyelitis on 99mTc radio- this marrow signal by altering or replacing normal
nuclide bone scan (bone phase image, anteroposte- fat. Short tau inversion recovery MRI depicts tissues
rior projection). Arrowhead indicates intense uptake with increased water content as bright and nulls
in the right mandibular body. signal from fat. This sequence is valuable for
demonstrating exudate and edema within bone or
in the perimandibular soft tissues, including the
correlation with scans using 99mTc-labeled nano- subperiosteal and masticator spaces. Contrast-
colloids that accumulate in normal marrow.16 In enhanced T1-weighted imaging in conjunction
treatment-responsive disease, abnormal uptake with fat suppression techniques helps define hyper-
on these studies resolves earlier than CT abnormal- vascular tissue in both inflammatory and neoplas-
ities. In patients who have contraindications for tic disease. Both abnormal signal and contrast
MRI (eg, cardiac pacemakers or other implanted enhancement within the bone and adjacent soft
ferromagnetic materials) or those with surgical tissues is maximal in acute osteomyelitis and
hardware in the maxillofacial region (which creates decreases with chronic disease (Fig. 3). Contrast

Fig. 3. Right mandibular osteomyelitis on coronal short tau inversion recovery MRI. Images were acquired (from
left to right) at presentation, 2 months, and 1-year follow-up. Initial image demonstrates edema in masseter
muscle and mandibular medullary compartment (arrowheads). On follow-up, soft tissue changes have decreased
markedly. There is a persistent high signal in the buccal subperiosteal region (arrow) and within the mandible
(outlined arrowhead). At 1-year follow-up, the findings are essentially normal.
 Osteomyelitis of the Jaws 561

enhancement highlights periosteal/subperiosteal a bone window to optimally depict fine trabecular

inflammation (Fig. 4), which may require surgical detail and periosteal new bone formation. Post-
resection. MRI demonstrates disease when CT contrast images are reconstructed in a soft tissue
results are negative, demonstrates more extensive algorithm and viewed in soft tissue windows that
disease (including subperiosteal disease) than is de- optimize visualization of paramandibular soft
picted by CT, and may more accurately guide tissue swelling and pathologic contrast enhance-
debridement.14 Absence of enhancement helps ment (Fig. 6). Coronal images are automatically re-
distinguish osseous sequestra from normal bone. formatted from the axial data. Additional oblique
Decreasing enhancement in chronic osteomyelitis planes and volume-rendered 3-dimensional images
probably reflects obliteration of marrow spaces and are routinely generated on 3-dimensional worksta-
reduced vascularity of the fibrotic/sclerotic cancel- tions. Oblique sagittal and axial images parallel to
lous bone. the mandibular body are very useful for evaluating
Marrow signal changes may take up to 6 months extension of disease along the mandibular body
to return to normal after successful therapy. This and evaluating tooth displacement and apical
prolongation limits the usefulness of MRI for erosion. True coronal imaging oriented perpendic-
treatment monitoring during the first 6 months. ular to the long axis of the mandibular body is
However, as with radionuclide examinations, useful for evaluating periapical disease, buccolin-
normalization of imaging abnormalities suggests gual extent of disease, sinus tracts, and periosteal
treatment success. After 6 months, MRI is more new bone formation. These conditions are typically
specific than CT for detecting ongoing infection more pronounced along the buccal and lingual
or recurrence. Interpretation of MRI in patients surfaces of the mandibular body and angle in which
with osteomyelitis and underlying bone diseases it is difficult to visualize on plain radiographs.
(eg, sickle cell disease) and maxillofacial surgical Given its cross-sectional methodology, CT can
hardware may be difficult because of abnormal demonstrate early features of impending cortical
baseline bone appearance and artifacts (Fig. 5), perforation (cortical bone thinning) and the full
respectively. extent of intramedullary disease to better advan-
CT is more sensitive than plain radiographs for tage than plain radiographs. Although osseous
subtle early trabecular demineralization in acute sequestra and periosteal new bone formation may
osteomyelitis. Maxillofacial CT examinations can be detected as early as the third or fourth symptom-
be performed with a helical high-resolution CT atic week, these findings are more typically encoun-
(HRCT) technique using submillimeter (0.67 mm) tered in the chronic phase (>4 weeks) of mandibular
slice thickness. Precontrast images are recon- osteomyelitis. Cortical interruption is said to be
structed in a bone algorithm and viewed in unusual in acute osteomyelitis. However, in the
authors’ population, cortical interruption is often
encountered in patients presenting with acute peri-
apical dental abscesses that have extended into the
paramandibular soft tissues. Associated soft tissue
abnormalities (masticator space edema, regional
adenopathy, abscesses, sinuses, and fistulae) are
much better depicted with CT than radiography.
Foreign bodies or retained tooth fragments are
usually obvious on CT. The severity of swelling
and contrast uptake on CT decreases in the chronic
phase. Late-developing swelling or increased
enhancement of muscles suggests disease recur-
rence or exacerbation.
On CT, chronic suppurative osteomyelitis is
characterized by a mixture of lucency and scle-
rosis (Fig. 7A). Medullary bone sclerosis is charac-
teristic, and its extent correlates with disease
duration.14 Expansion of cortical bone due to
periosteal new bone formation may increase the
buccolingual width of the bone as well as narrow-
Fig. 4. Left mandibular chronic osteomyelitis. Marked ing of the medullary cavity. Periosteal new bone
periosteal thickening is well demonstrated on this formation tends to be more prominent in children
axial fat-suppressed contrast-enhanced T1-weighted and adolescents than in adults. Periostitis ossifi-
magnetic resonance image (arrowheads). cans is a multilaminated pattern of periosteal
562 Koorbusch et al

Fig. 5. MRI pitfalls in mandibular osteomyelitis. (A) Axial short tau inversion recovery (STIR) image from a patient
with sickle cell anemia and recent sickle cell crisis, with right mandibular osteomyelitis. The left hemimandible
was clinically normal. The area of infected bone on the right (solid white arrowhead) is difficult to distinguish
from the baseline abnormal bone on the left (outlined arrowhead). (B) Axial STIR image shows left mandibular
osteomyelitis with metallic hardware in place. Note that the artifacts generated by the hardware obscure the
mesial left mandibular body (outlined arrowhead). Marrow edema (solid arrowhead) is evident distally. The
extent of the disease mesially is difficult to evaluate.

new bone formation that is inappropriately con- chronic osteomyelitis also lacks CT features of
nected with Garrè, who never described this cortical breakthrough and sequestrum formation.
process (see Fig. 7B). Cortical erosion, seques-
trum, and involucrum (periosteal new bone envel-
oping a sequestrum) formation are commonly LABORATORY FINDINGS
encountered on CT in chronic suppurative man-
dibular osteomyelitis but not with primary nonsup- Patients with acute osteomyelitis may present with
purative chronic mandibular osteomyelitis. Three leukocytosis or even a normal white cell count,
CT patterns may be observed in patients with whereas those with chronic osteomyelitis may have a
chronic osteomyelitis.19 These patterns include completely normal laboratory profile throughout the
a bone defect pattern that histologically correlates course of the disease. Laboratory testing of serum
with fiber-rich granulation tissue, a frosted glass parameters does not frequently aid in the diagnosis
pattern corresponding to formation of tiny osseous and treatment of either form of osteomyelitis.
trabeculae, and a compact bone pattern that The microbiology of the facial bone osteomye-
correlates with thickening of osseous trabeculae. litis is consistent with the spectrum of odontogenic
CT findings in successfully treated chronic man- infection: polymicrobial.3,5 Culture and sensitivity
dibular osteomyelitis may progress from the testing of specimens from the affected osseous
bone defect pattern to the frosted glass and ulti- sites may be diagnosed as normal oral flora if the
mately compact bone patterns before returning laboratory is not specifically warned of the need
to normal. Conversion of the frosted glass or for more extensive evaluation of the specimen to
compact bone pattern to the bone defect pattern determine the spectrum of organisms in the spec-
in a given area of bone suggests disease recrudes- imen and in directing the administration of appro-
cence. These features may be helpful when using priate antibiotic therapy.5 Contemporary laboratory
CT to monitor treatment of mandibular osteomye- techniques using DNA and RNA identification of
litis, although normalization of CT abnormalities microorganisms establish the causative agents of
lags behind clinical response. The CT appearance infection more accurately and definitively. Well-
of the mandible in chronic suppurative osteomye- analyzed specimens may show predominant organ-
litis eventually returns to normal or near normal. isms and, with antibiotic sensitivity testing, may
This appearance does not occur in nonsuppura- substantially focus antibiotic therapy to shorten
tive chronic osteomyelitis (Fig. 8). Nonsuppurative the overall course of the disease.20
 Osteomyelitis of the Jaws 563

Fig. 6. Acute left mandibular osteomyelitis CT. (A) Axial contrast-enhanced CT image demonstrates marked left
masticator muscle swelling with masticator space abscesses (arrowheads). (B) Sagittal oblique image demon-
strates mottle lucency distal to the left third molar extraction socket (arrowheads). (C) True coronal CT image
(perpendicular to long axis of mandibular body) demonstrates thinning of the lingual bone (arrowhead, compare
with the right side) and demineralization of the upper aspect of the mandibular nerve canal (arrow).

The histologic findings of acute osteomyeli- THE ROLE OF BIOFILMS

tis show an inflammatory exudate, decreased
osteoblasts, and increased osteoclasts. Necrotic Bacteria are found in both planktonic and biofilm
bone may present with an acellular histologic varieties. Costerton20 has defined a biofilm as
picture.6 a “multicellular community composed of prokary-
In chronic forms of the disease, chronic inflam- otic and/or eukaryotic cells embedded in a matrix
matory cells (lymphocytes and plasma cells) may composed, at least partially of material synthe-
be limited in number and venous thrombosis may sized by sessile cells in the community.” The
be noted. The development of septic thrombi in investigator has characterized the biofilm as
the mandible may explain the development of a combination of bacteria and slime. Bacteria
paresthesia in some cases. Organisms in the prefer the multicellular lifestyle of the biofilm both
specimen may be difficult to identify, and the in nature and in chronic infections versus the
histologic findings may be variable.6 planktonic form, in which the cells have rapid
growth and mobility. Planktonic bacteria are more
564 Koorbusch et al

Fig. 7. Chronic suppurative mandibular osteomyelitis CT. (A) Axial image demonstrates osseous sequestrum (solid
white arrowhead), lingual cortical erosion (outlined arrowhead), and periosteal new bone/involucrum (arrows).
(B) Right-sided proliferative periostitis. Axial CT image demonstrates lamellated buccal cortical periosteal new
bone formation (arrowheads) in a child with osteomyelitis caused by actinomycosis.

likely to be expressed in disease states in the form However, they have been associated with infec-
of acute infection and are more susceptible to anti- tions of implantable devices such as artificial joints
biotic therapy.20 and mechanical heart valves, indwelling catheters,
Biofilms are not necessarily the cause of infec- periodontal disease, root canals, osteomyelitis,
tion in all cases and often are not pathogenic. prostatitis, endocarditis, and otitis media. When
biofilms are the source of infective bacteria, the
disease process is disseminated through the
release of planktonic bacteria causing the symp-
toms of acute infection and by inflammation
secondary to the biofilm itself involving large areas
of the affected tissue.20 High concentrations of
antibiotic agents potentially eradicate the plank-
tonic forms of bacteria but have little effect on
the long-term viability of the biofilm, which is highly
resistant to antibiotics.20 To effectively treat an
infection in bone caused by a biofilm, surgical
removal of all affected bone has been demon-
strated as the method of choice.20 Treatment
with antibiotic therapy alone may lead to continu-
ing osseous destruction during repeated thera-
peutic cycles, which may reduce the patient’s
symptoms but result in overall treatment failure.20

TREATMENT

Fig. 8. Chronic nonsuppurative osteomyelitis, pano- The standard surgical treatment regimen for oste-
ramic image from cone beam CT examination. Arrow- omyelitis has been well established in the scientific
head indicates thick periosteal new bone formation at literature. These principles remain as applicable
the mandibular angle and diffuse osseous sclerosis. today as they did when initially presented, and
Note absence of sequestra. There is a narrowing of they may be summarized as follows:
the medullary cavity because of marked cortical thick-
ening that extends to involved non–tooth-bearing 1. Early diagnosis
portions of the mandible, all characteristic of this 2. Elimination of the source of the infection
disease. 3. Establishment of surgical drainage
 Osteomyelitis of the Jaws 565

4. Bacteriologic identification and antibiotic sensi- a sheath or membrane of new bone, termed an
tivity testing involucrum. The removal of sequestra is important
5. Appropriate antibiotic coverage because it enables the penetration of high concen-
6. Surgical debridement trations of antibiotics into an area of previously
7. Supportive care poor vascularity. Saucerization is frequently per-
8. Reconstruction. formed in conjunction with sequestrectomy. This
procedure removes the margins of necrotic bone
The early diagnosis of osteomyelitis of the jaws to expose the medullary spaces for further explo-
is often predicated on the clinical suspicion of ration and removal of necrotic tissue. The proce-
the treating surgeon. A high index of suspicion dure is usually performed intraorally, giving direct
coupled with a thorough clinical examination and access to the infected bone. After the procedure
appropriate imaging leads the clinician to the pre- the wound may be packed open to allow irrigation
sumptive diagnosis. The establishment of surgical and examination during the early healing of the
drainage by transoral or extraoral exploration defect. Once a bed of healthy granulation tissue
enables the surgeon to obtain material for bacterial is formed, the packing may be removed.1,2
identification and antibiotic sensitivity testing, as Decortication is the removal of lateral and
well as removal of any pockets of purulence and inferior cortical plates of bone to gain access to
visual inspection of the extent of the disease. the infected medullary cavity. Avascular bone is
Antibiotic administration should always be insti- removed until a 1- to 2-cm margin of vital bone is
tuted after bacterial identification and sensitivity achieved.1 Besides removing devitalized bone
testing; however, delays in treatment should be and soft tissue, decortication also has the theoret-
avoided. This dilemma may be circumvented by ical advantage of shortening the time of antibiotic
the administration of penicillin with metronidazole therapy and decreases the risk of further formation
or clindamycin initially until bacterial identification of sequestra and abscesses.2 This procedure is
is available. Previous studies have shown that usually reserved for refractory osteomyelitis that
the polymicrobial nature of osteomyelitis presents is nonresponsive to more surgically conservative
with a microflora spectrum that is very respon- procedures.
sive to the therapeutic regimens normally used to Persistent chronic osteomyelitis may require res-
treat odontogenic infections.2,5 It is important for ection with bony margins prepared for immediate
the clinician to request identification of as many or delayed reconstruction. Long-term osteomyeli-
organisms as possible on the submitted specimens tic infections may lead to pathologic fractures, con-
to determine the microbial mix of the infection and tinuing infection after decortication, or persistent
thus select the most appropriate antibiotic regimen nonunion of facial fractures. In such cases, resection
for the patient. Consultation with an infectious and eventual reconstruction may be indicated to
disease consultant is often helpful in cases of oste- eradicate the disease. The resection margins should
omyelitis to aid identification of the causative org- be in a viable bone 1 to 2 cm from the site of infec-
anisms and selection of an appropriate antibiotic tion. Reconstruction bone plates or external pin fixa-
therapeutic regimen. tion may be placed where prolonged infection or
Surgical debridement of the osteomyelitic jaw lack of a viable tissue bed precludes bone grafting
may encompass a series of procedures. The in the short run.
removal of infected and devitalized teeth and In severe long-standing refractory cases of oste-
associated soft tissue is a preliminary treatment omyelitis, hyperbaric oxygen therapy may be indi-
of osteomyelitis, as is the stabilization of fractures cated. In such cases, surgical debridement has
with intermaxillary or external pin fixation and the been achieved, antibiotic therapy has been dir-
removal of any involved implants or hardware.6 ected by bacterial identification and antibiotic
Internal rigid fixation of fractures during the early sensitivity testing, and no further focus of infection
treatment of osteomyelitis is not recommended.6 has been identified. The protocol is well identified
The removal of necrotic and chronically infected in the literature.4
bone is essential to the successful management
of the infection. Multiple procedures over a period SPECIAL INFECTIONS
of days or weeks may be required to eradicate the
infection from the affected jaw. The procedures Actinomycosis is a rare infection of the oral-
include sequestrectomy, saucerization, decortica- cervicofacial region, which routinely involves both
tion, resection, and reconstruction. the soft tissue of the area and the mandible. The
Sequestrectomy is the removal of infected devi- organisms have characteristics of both bacteria
talized bony fragments in the infected area of and fungi but require treatment with antibiotics
the jaw. The sequestrum is often surrounded by and not antifungal agents. Actinomyces species
566 Koorbusch et al

are gram-positive, microaerophilic, non–acid-fast, nonspecific. The imaging technique with the best
non–spore-forming bacteria that are normal inhab- combination of sensitivity and specificity seems
itants of the mouth. The oral-cervicofacial form of to be CT (HRCT). Comparative studies of the vari-
the infection presents with a firm brawny swelling ous modalities are not currently available.
or mass usually associated with a dental extrac- Laboratory identification and antibiotic sensi-
tion or fracture. Rarely the disease may present tivity testing help in directed medical care of the
in the maxilla. The infectious lesion may be painful infection. Although a histopathologic diagnosis of
and is often a red to purple color. Facial fistulae osteomyelitis may be confirmatory, it is not in
are common, and lymphadenopathy is a late itself usually an early aid to the diagnosis of the
finding. Trismus, periosteal involvement, bony disease.5
destruction, and drainage of sulfur granules from Surgical intervention should be early and agg-
the fistulae are common. These sulfur granules ressive. Multiple surgical procedures may be
represent clumps of bacterial colonies when vie- required to remove all devitalized bone and nec-
wed microscopically.1,2 rotic soft tissue at the affected site. The early
The treatment of the disease is consistent with removal of foreign bodies (bone plates, screws,
that previously presented for osteomyelitis with implants) is essential in view of the contemporary
the following exceptions: identification of the org- concepts of the role of biofilms in infection.
anism may be difficult and the patient will require Although the knowledge base, technical expertise,
long-term antibiotic therapy. Antibiotic therapy and availability of advanced imaging have increa-
includes several weeks of intravenous antibiotics sed, suppurative osteomyelitis of the jaws remains
followed by months of orally administered drugs a surgical disease and surgical treatment modalities
to assure control of the infection. Specific antibiotic are virtually unchanged in recent decades.
regimens have included penicillin, doxycycline, or It is the clinical expertise of the surgeon using
ceftriaxone. the clinical signs and symptoms presented, aided
Nocardia species occasionally cause infection with appropriate imaging (HRCT), that result in the
in the head and neck. The organism is not normally early diagnosis of osteomyelitis. Surgical interven-
an inhabitant of the mouth and usually gains tion will then enable the surgeon to harvest mate-
access to the body via inhalation. Nocardia is rial for histopathologic diagnosis and bacterial
primarily a pulmonary disease but may spread identification. Antibiotic sensitivity testing helps in
hematogenously to virtually any organ system. the selection of the appropriate therapeutic agent,
The disease may be encountered in immunocom- whereas serial imaging may be required to monitor
promised patients. Nocardiosis is very similar in its the response of the patient to treatment and help
disease picture to actinomycosis. Chronic infec- determine its end point.
tions may present with fistulae, brawny swelling,
pain, and limited constitutional symptoms. Surgical REFERENCES
management is with debridement and drainage of
all abscesses. Identification of the organism is 1. Koorbusch GF. Infections of the orofacial region. In:
significant because antibiotic therapy with sulfon- Zambito RF, Cleri DJ, editors. Immunology and
amides for extended periods of time is recommen- infectious diseases of the mouth, head and neck.
ded in contradistinction to the treatment regimen St Louis (MO): Mosby Year Book; 1991. p. 334–41.
for actinomycosis.1,2 2. Topazian RG. Osteomyelitis of the jaws. In:
Topazian RG, Goldberg MH, Hupp JR, editors. Oral
and maxillofacial infections. 4th edition. Philadelphia:
A NEW PARADIGM FOR THE MANAGEMENT
OF MAXILLOMANDIBULAR OSTEOMYELITIS W.B. Saunders Company; 2002. p. 214–42.
3. Mercuri LG. Acute osteomyelitis of the jaws. Oral
The early diagnosis of osteomyelitis, especially in Maxillofac Surg Clin North Am 1991;3(2):355–65.
its chronic forms, is key to the establishment of 4. Marx RE. Acute osteomyelitis of the jaws. Oral Max-
antibiotic therapy and appropriate surgical inter- illofac Surg Clin North Am 1991;3(2):367–81.
vention. Clinical findings suggestive of osteomye- 5. Koorbusch GF, Fotos P, Terhark-Goll K. Retrospec-
litis along with a high index of diagnostic tive assessment of osteomyelitis: etiology, demo-
suspicion on the part of the treating surgeon are graphics, risk factors, and management in 35
the first step in the treatment path of the disease. cases. Oral Surg Oral Med Oral Pathol 1992;74(2):
Orthopantomographic imaging will undoubtedly 149–54.
offer some information in the diagnostic process. 6. Marx RE, Stern D. Oral & maxillofacial pathology:
More definitive imaging can be used, such as scin- a rationale for diagnosis and treatment. Carol
tigraphy, MRI, and CT, but which one is the best? Stream (IL): Quintessence Publishing Company,
Scintigraphy and MRI are both sensitive but Inc; 2003. p. 54–7, 388–94.
 Osteomyelitis of the Jaws 567

7. Marx RE. Oral and intravenous bisphosphonate- 14. Schuknecht B, Valavanis A. Osteomyelitis of the man-
induced osteonecrosis of the jaws. Hanover Park dible. Neuroimaging Clin N Am 2003;13:605–18.
(IL): Quintessence Publishing Company, Inc; 2007. 15. Reinert S, Widlitzik H, Venderink DJ. The value of
8. Marx RE, Carlson ER, Smith BR, et al. Isolation of magnetic resonance imaging in the diagnosis of
a Actinomyces species and Eikenella corrodens mandibular osteomyelitis. Br J Oral Maxillofac Surg
from patients with chronic diffuse sclerosing osteo- 1999;37:459–63.
myelitis. J Oral Maxillofac Surg 1994;51:26–33. 16. Gotthardt M, Bleeker-Rovers CP, Boerman OC, et al.
9. Hudson JW. Osteomyelitis of the jaws: a 50 year per- Imaging of inflammation by PET, conventional scin-
spective. J Oral Maxillofac Surg 1993;51:1294–301. tigraphy and other imaging techniques. J Nucl
10. Veaeau PJ, Koorbusch GF, Finkelstein M. Invasive Med 2010;51(12):1937–49.
squamous cell carcinoma of the mandible present- 17. Fukmitsu N, Utigawa K, Mori Y, et al. What can be
ing as a chronic osteomyelitis. J Oral Maxillofac identified by three phase bone scintigraphy in
Surg 1990;48:1118–22. patients with chronic osteomyelitis of the mandible?
11. Ida M, Watanabe H, Tetsumura A, et al. CT findings Ann Nucl Med 2010;24:287–93.
as a significant predictive factor for the curability of 18. Weon YC, Yang S, Choi Y, et al. Use of Tc-99m
mandibular osteomyelitis: a multivariate analysis. HMPAO leukocyte scans to evaluate bone infection:
Dentomaxillofac Radiol 2005;34:86–90. incremental value of additional SPECT images. Clin
12. Worth HM, Stonemen DW. Osteomyelitis, malignant Nucl Med 2000;25(7):519–26.
disease and fibrous dysplasia. Some radiographic 19. Tanaka R, Hagashi T. Computed tomographic find-
similarities and differences. Dent Radiogr Photogr ings of chronic osteomyelitis involving the mandible:
1977;50:1–9. correlation to histopathologic findings. Dentomaxillo-
13. Davies HT, Carr RJ. Osteomyelitis of the mandible: fac Radiol 2008;37:94–103.
a complication of routine dental extractions in the 20. Costerton W. The biofilm primer. Berlin: Springer-
alcoholic. Br J Oral Maxillofac Surg 1990;28:185–8. Verlag; 2007. p. 129–80.