1. Inflammatory lesions of the jaws are the most common pathologic condition and can have various causes, presentations, and radiographic features. 2. Acute lesions typically present with pain, fever and swelling while chronic lesions present with less pain, intermittent fever and swelling. 3. Radiographically, lesions may appear radiolucent indicating bone destruction, radiopaque indicating increased bone formation, or mixed. Early lesions may not be visible on conventional radiographs.

1. 1
Inflammatory
lesions of the jaws
PREPARED BY:
Enas Anter Abd El-ghffar
Assistant lecturer of Oral Radiology
Faculty of Oral and Dental Medicine
Cairo University

2. 2
Inflammatory lesions of the jaws
- Inflammatory lesions are the most common pathologic condition of the
jaws. The jaws are unique from other bones of the body in that the
presence of teeth creates a direct pathway for infectious and inflammatory
agents to invade bone by means of caries and periodontal disease.
-The body responds to chemical, physical, or microbiologic injury with
inflammation, the inflammatory process is a responseof the body that aims
to destroy the injurious stimulus and repair the damaged tissue.
-Now speaking about the bone in the jaws: normally the bone metabolism
is balanced between the action of osteoblasts and osteoclasts. However,
mediators of inflammation (cytokines, Prostaglandins, and many growth
factors) can tip this balance to favor either bone resorption or bone
formation.
-according to the source of the infection which initiate the inflammatory
condition:
 When the initial source is a necrotic pulp and the bony lesion is just
around the tooth, it’s called periapical inflammatory lesion
 When the infections spreads to bone marrow and is no longer
contained in the area of the root apex, it’s called osteomyelitis.
 When the infection comes into the bone from the overlying soft
tissues; this type of lesions includes periodontal lesions and
pericoronitis.
 However other sources of infection could participate in inflammatory
response of jaw bones as hematogenous infection, extraction
sockets, opened fractures, and systematic infection as in syphilis, TB
and actinomycosis.
 General clinical features
Inflammatory lesions of the jaws have two main clinical presentations
either acute or chronic signs and symptoms

3. 3
Acute Chronic
Onset Recent , rapid Longer insidious onset
symptoms Pronounced pain , fever
, swelling
Less pain, low grade
and intermitted fever,
swelling may gradually
occur, however Some
chronic infections may
not produce any
significant clinical
symptoms.
 General Radiographic Features:
1. Location
-periapical inflammatory lesions, the epicenter is at the apex of a tooth.
However, lesions of pulpal origin in general may be also located anywhere
along the root surface because of accessory canals or perforations caused
by root canal therapy or root fractures.
- Periodontal lesion, the epicenter is at the alveolar crest, if periodontal
bone loss is severe, the inflammation may extend to the root furcation or
even to the root apex.
- Osteomyelitis, a diffuse uncontained inflammation of the bone, most
commonly found in the posterior mandible, the maxilla is rarely involved.
-pericoronities, most commonly at the area of partially erupted lower third
molar, near the follicular space of the embedded part of the molar.
2. Periphery
Most often the periphery is ill defi ned, with a gradual blending of normal
trabecular pattern into a sclerotic pattern, or the normal trabecula pattern
may gradually fade into a radiolucent region of bone loss.

4. 4
3. Internal structure
Cancellous bone may respond to an insult by tipping the bone metabolic
balance either in favor of resorption (giving the area a radiolucent
appearance) or toward bone formation (resulting in a radiopaque or
sclerotic appearance). Usually there is a combination of these two
reactions. In acute disease, resorption typically predominates; with chronic
disease, excessive bone formation leads to an overall radiopaque, sclerotic
appearance.
4. Effects on surrounding structures
 On the bone
-The effect on cancellous bone includes stimulation of bone formation or
bone resorption
-The periosteal component of the bone (on the surfaceof the jaw or lining
the floor of maxillary sinus) also responds to inflammation as inflammatory
exudates fromthe inflamed bone can penetrate the cortex , lift up the
periosteum fromthe surfaceof the bone and stimulate the periosteum to
producenew bone which is almost parallel to the bone surface.
-cortical boundaries as that of buccal or lingual cortices, inf. Alv. Canal or
max. sinus may be resorbed specially with chronic infection
 On the teeth
-The periodontal ligament space will be widened; the widening is greatest
at the source of inflammation, as with periapical lesions the widening is
greatest around the apex, whereas in periodontal lesions, the widening is
greatest at the alveolar crest.
-In chronic cases root resorbtion could occur, and sometimes
hypercementosis is found

5. 5
Periapical inflammatory lesions
Periapical inflammatory lesions have been called:
- Acute apical periodontitis.
- Chronic apical periodontitis.
- Periapical abcess.
- Periapical granuloma.
Radiolucent presentations have been called "rarefying osteitis", whereas
Radiopaque presentation have been called "sclerosing osteitis
A periapical inflammatory lesion is defined as local response of the bone
around the apex of the tooth that occurs as a result of pulp necrosis or
through destruction of the periapical tissues by extensive periodontal
disease.
The pathogenesis could be summarized as following:
 Caries & trauma causes pulp necrosis, which will lead to
inflammation around the apex (apical periodontitis), which has two
forms, acute and chronic.
 The inflammatory infiltrate is composed of lymphocytes, mixed with
PMN neutrophils, depending on the severity of the response,
neutrophils may collect to form pus, resulting in an apical abscess.
(acute inflammation)
 Alternatively , and in an attempt to heal from apical periodontitis ,
the body stimulates the formation of granulation tissue mixed with a
chronic inflammatory infiltrate composed of lymphocytes , plasma
cells , histiocytes , giving rise to periapical granuloma ( chronic
inflammation )
 Entrapped epithelium (rests of malassez) may proliferate to form
radicular cyst or apical cyst.
 Acute exacerbation of the chronic lesions may occur intermittently

6. 6
 The periapical abscess may transform into osteomyelitis if the
pyogenic organisms spread into bone marrow.
However Progression from PA lesion to OM is rare, and factors such us
decrease in the host defense and increase in the virulence of pathogenic
microorganisms can play a role in this progression.
 Clinical features
The periapical inflammatory lesions have broad spectrum of symptoms
ranging from being asymptotic to an occasional toothache to severe pain
(with or without facial swelling) and lymphadenopathy. However it is
important to understand that the clinical presentation does not necessarily
correlate with the histological or radioghrapical finding.
In acute cases: as acute apical periodontities or acute periapical abscess
there is usually severe pain, mobility and sometimes elevation of the
involved tooth, Tenderness to percussion, and in acute pperiapical abscess
swelling occurs and may makes spontaneous drainage into the oral cavity
through a fistula which relieves the acute pain .
In chronic cases: which either arise in the chronic formde novo; in this case
it may be asymptomatic, or the acute lesion may evolveinto a chronic one
which may be asymptomatic, except for the intermittent flare-ups of
toothache pain, which marks the acute exacerbation of the chronic lesion
(Patients give history of intermittent pain)

7. 7
 Radiographic features (conventional and CT or
CBCT)
-The radiographic features of PA inflammatory lesions vary depending on
the time course of the lesion, as very early lesions may not show any
radiographic changes, so diagnosis of these lesions rely on the clinical
symptoms only.
-More chronic lesions may show lytic (radiolucent) or sclerotic (radiopaque)
or both radiographic changes.
-However recent studies proved that CBCT consider superior to intraoral
radiographs in detection of periapical inflammatory lesions especially the
early ones, because to be visible radiographically on the conventional
intra-oral radiographs the lesion should:
- reach nearly 30%–50% of bone mineral loss.
-Other conditions, such as apical morphologic variations, surrounding bone
density, x-ray angulations, and radiographic contrast, also influence
radiographic interpretation ( Estrela et al 2008)
(Fig 1) B, C periapical radiographsshowing just widening of PMS of upper right central incisor,
whereasonCBCT cross sectional images D,E lossof laminaduraand periapical radiolucency can
be seen

8. 8
1. Location
The epicenter of PA inflammatory lesion is found at the apex of the
involved tooth. However less often, because of accessory pulpal canals,
perforation of the root or fracture, the location of the center of the lesion
may not be centered on the apex but this is LESS OFTEN.
2. Periphery
-It is ill defined with gradual transition (blending) from normal
trabeculation pattern into the abnormal bone pattern of the lesion. Fig 2
- In rare cases, it may be well defined, with sharp transition zone and
appearance suggesting a cortical boundary as in case of granuloma.
A B C
Fig 2 Periapical infl ammatorylesions associated with a mandibular fi rst molar (A) and a maxillary lateral
incisor (B). Note that in both cases the epicenter of bone destruction is located at the apex of the root. Also,
note gradual widening ofthe periodontal membrane space (arrow) characteristic of an infl ammatory lesion.
C, This periapical image ofsclerosing osteitis related to the fi rst molar shows a gradual transition from thick
and numerous trabeculae (short arrow) to a normal trabecular pattern (long arrow).
3. Internal Structure
Early periapical inflammatory lesions may show no radiographic change in
the normal bone pattern, or the changes could be limited to just decreased
bone density in the apical area on periapical radiograph Fig 3, however the
CT and CBCT images can reveal early inflammatory changes more
accurately than intraoral radiographs (Estrela et al 2008)Fig 1, Fig 6.

9. 9
Fig 3 A veryearlylesioninvolvingthe pulpof the second bicuspid without signifi cant change in
the periapical bone (arrow). Incontrast,note the loss of the lamina dura and periapical bone at
the apex of the mesial root of the second molar. Also note the subtle halo of sclerotic bone
reaction around this apical radiolucency
Letter on loss of lamina dura may be seen, however with the disease
progress areas of radiolucency can be seen indicating bone destruction, or
areas of increased bone formation (sclerosis), any way mixture of sclerosis
and rarefaction could be seen with variable percentage of these two bone
reactions. Fig 2, Fig 4
Fig 4 croppedCBCT reconstructedpanoramashowingbothrarifyingandcondensingostitis
apical to lowerfirstmolar
4. Effects on Surrounding Structures
-The lamina dura around the apex of the tooth usually is lost
-The sclerotic reaction of the cancellous bone may be limited to a small
region around the tooth apex or in some cases may be extensive Fig 5
-In chronic cases external resorption of the apical region of the root may
occur Fig 5
-If the lesion is long standing, the pulp canal may appear wider than
adjacent teeth due to death of odontoblasts and subsequent cessation of
the formation of secondary dentin

10. 10
-These lesions are capable of producing an inflammatory periosteal
reaction, mostnotably in the adjacentfloor of the maxillary antrum. A
regional mucositis may be presentwithin the adjacent segment of the
maxillary antrum (Scheinfeldet al 2012) Fig 5
Fig 5 the most leftperiapical radiographshowingexyensive formof condensingostitiesapical to
the distal root of lower first molar, and root resorbtion in mesial root of the same tooth, the
middle radiograph is perapical film showing Periostitis and mucositis In the floor of the
maxillaryantrum,The mucositisischaracterizedbyaslightradiopaque band(arrow) next to the
periosteal bone formation, the most right image is coronal cut CT showing periapical lucency
nearone of the right maxillarymolars(yellow arrow). Note the mucosal thickening in the right
maxillary sinus (green arrow) as a result of the adjacent inflammation
Fig 6 (A) The patientis complainingaboutapainful sensationinherleftmaxillaryfirst molar. No
periapical lesion can be detected on the periapical radiograph.(B) A small apical lesion was
diagnosedwiththe sagittal CBTimage atthe distobuccal rootof the left maxillary first molar. In
addition, a slight thickening of the sinus membrane can be seen.

11. 11
MRI imaging of periapical inflammatory lesions
The teeth and dento-alveolar area are always visible on MRI of the lower
one third of the head but are usually ignored by radiologists and clinicians.
However there has been a paucity of literature studying dental pathology
using MRI.
First we should know how dentition and alveolar bone appear on the MRI
scan; the enamel and dentine of the teeth appeared black owing to a lack
of unbound protons. The dental pulp chamber, containing nerves, blood
vessels and connective tissue within the teeth, appeared white or grey on
T1 weighted and STIR images. Cortical bone was seen as a black zone
outlined by moderate signal from external soft tissues and high signal
internal fatty marrow, on fat annulled scans (STIR), fatty marrow had low
signal and appeared dark grey(Tutton and Goddard 2002)
-In case of inflammatory lesions associated with destruction of alveolar
bone it will appear on T1 weighted image as area different from the
surrounding normal bone showing either high signal (white) or moderate
signal (grey), and also on STIR images it appear either with high signal
(white) or moderate signal (gray), the difference is related to the amount
of the inflammatory exudates contained in the lesion and its composition as
on STIR images high cellular or protein content of the lesion gives higher
signal, whereas higher water content gives moderate signal.
-In case of inflammatory lesions associated with sclerosis of alveolar bone
It will appear on both T1 weighted image and STIR images as thick black
area of low signal, due to thickening of the bone trabecule in this area
(Tutton and Goddard 2002) Fig 8

12. 12
Fig 8. A scan taken 3 mm inferior to Figure 7 shows a distinct circular area of slightly lower
signal than surrounding marrow around the root apex of the upper left central incisor (red
arrow).There isno cortical bone on the labial aspectof the root surface (blue arrow),whichisat
the level of the dischargingsinusasascertainedclinically. There isathickblack line of low signal
on the palatal aspectthat indicatessclerosisandthickeningof the palatal cortex(white arrow) of
the dentoalveolar ridge, probably in response to the chronic infection
Fig 9 Short tau inversion recovery (STIR) sequence at comparative levels to Figure 7 shows a
mottledgreyappearance of mixed signal from the same area, indicating high water content in
the lesion.Thisheterogeneityandthe moderate signal onT1 weightedimaging, is not typical of
a simple cyst but of chronic infection.
Figure 10. Periapical radiographs of lower central incisors showing a large radiolucency at the
apices of both central incisors and extending to the margins of the mesial root surface of the
lateral incisors, with loss of the lamina dura of all teeth involved. The radiolucency extends
inferiorly into the mandible and has a ragged and uneven inferior margin

13. 13
A B
Figure11. A T1 weightedcoronal image throughmidline of teeth shows a diamond shaped area
of moderate signal (lightgrey) aroundthe rootsof the lowercentral incisors,extendingfromthe
mesial aspect of the lower lateral root apices to a point 1 cm lower in the midline. This
corresponds to the abnormal area previously demonstrated on transverse MR images. It is
demarcatedarounditssidesandbase by a thindark grey/blackline of low signal due tosclerotic
bone. The lower right central incisor root apex is displaced laterally away from the midline by
about0.75 cm. B Coronal short tau inversionrecovery(STIR) (fatsuppressed)image comparable
to (A).Itshowsthe area describedabove asbright white, which indicates that it has high water
contentand may be oedematousinnature.The correspondingmoderate signal on T1 weighted
scans shows that it is not a solitary bone cyst. It must either contain a high protein or high
cellular content. The appearances are not typical of blood and were considered likely to be
owingtoinfection,which,basedonthe history,waschronic.The diagnosis of infectedperiapical
cyst wasconfirmedbydrainage of pusand bloodstainedexudate viathe rootcanalsof the lower
central incisors, and was successfully followed by root filling of these teeth.
 Differential diagnosis
 Periapical cemental dysplasia PCD
 Enostosis
 Metastic lesions of malignancy
Pericoronitis
It is Inflammation of the tissues surrounding the crown of a partially
erupted tooth. The gingiva surrounding the erupted portion of the crown
becomes inflamed when food or microbial debris becomes trapped under
the soft tissue. The gingiva subsequently becomes swollen and may
become secondarily traumatized by the opposing occlusion. This
inflammation may extend into the bone surrounding the crown of the
tooth.

14. 14
 Clinical Features
It is most often seen in association with the mandibular third molars in
young adults; however it can affect patients at any age.
It is manifested as Pain, swelling and truisms is a common presentation
when the affected tooth is the mandibular third molar; usually the pain is
felt on occlusion. An ulcerated operculum is usually the source of the pain
(Yamaoka et al 2009)
 Radiographic Features(conventional and CT or
CBCT):
On conventional periabical radiograph it range from no changes when the
inflammatory lesion is confined to the soft tissues, to localized rarefaction
and sclerosis to osteomyelitis in the most severecases, however with CT, or
CBCT the extension of the inflammatory process could be estimated more
accurately, as even when it is confined to the soft tissues it is demonstrated
on the CT images with soft tissue window, and it also help in differentiation
between myositis-fascitis and abscess formationFig 13, Fig 12
Any way the limiting factor of the diagnostic accuracy of CT images in case
of pericoronitis is the metallic streaks produce from adjacent metallic
restoration (Scheinfeld et al 2012) Fig 13
1. Location:
The mandibular third molar region is the most common location. When
bone changes are associated with pericoronitis, they are centered on the
follicular space or the portion of the crown still embedded in bone or in
close proximity to bone.
2. Periphery:
Illdefined, with a gradual transition of the normaltrabecular pattern into a
sclerotic region

15. 15
3. Internal Structure:
Itmay appear as an area of bone loss or radiolucency immediately adjacent
to the crown that enlarges the follicular space around the embedded part
of the tooth; however the bone adjacent to the folliculare space most often
is sclerotic with thick trabeculae. Fig 12, Fig 13
4. Effects on Surrounding Structures:
Like other periapical inflammatory lesions, pericoronitis may cause the
typical changes of sclerosis and rarefaction of surrounding bone. In
extensive cases periosteal new bone formation may be seen at the:
-Inferior cortex (Fig 12)
-The posterior border of the ramus
-Along the coronoid notch of the mandible (Yamaoka et al 2009)
5.DifferentialDiagnosis
 Enostosis
 Fibrous dysplasia.
 The sclerotic formof osteosarcoma
 Squamous cell carcinoma in older patients

16. 16
Figure 13. Pericoronitis in two patients. (a) Coronal CT image obtained with bone window
settingsina 24-year-oldman shows an impacted left third mandibular molar and expansion of
the buccal coronal follicular space (arrow). (b) Coronal CT image obtained with soft-tissue
window settings in the same patient shows an adjacent abscess in the masticator space
(arrows).Streakartifactfromdental amalgamextendsthroughthe abscess. (c,d) Sagittal (c) and
axial (d) CT imagesobtainedwithbone window settingsina31-year-oldmanshow distocoronal
chronic pericoronitis (arrow) involving the bone posterior to the mandibular third molar. A
widened distocoronal follicular space and adjacent bone sclerosis are also seen, common
changes, especially in young adults, that are most often accompanied by a partial soft-tissue
covering(operculum) of the third molar that becomes intermittently inflamed, traps food and
debris,andleadstothe gradual destructionof andadjacentsclerosisinthe bone adjacenttothe
crown of the tooth.

17. 17
MRI imaging of pericoronities
-Due to absence of any paper showing the MRI images of pericoronitis, so
this is a T1 image of impacted third molar normal appearance in MRI
images (Fig 14)
-- The crown and the roots showing low signal, and high signal from their
pulp chamber can be seen, and a band of high signal immediately
surrounding the crown, demarcated by a lower signal edge of bone. This
band or ‘‘halo’’ enveloping the crown is an eruption follicle (Tutton and
Goddard 2002).
-in case of partially erupted wisdom:
-- The low signal band (the bony crypt wall) will be inturrupted at the part
of the crown emerging in the oral cavity, and widening in the follicular
space (area with high signal above the crown) could also be seen, however
the sorrunding bone may show eithera bright area with high signal due to
inflammatory exudate formation, or low signal area due to sclerosis of the
bone
Fig 14 Coronal T1 weightedscanshowing the normal appearance of impactedlower third molar
(H) are seenwiththeircrowns angledlinguallyandrootsangledbuccallyin close approximation
withthe buccal cortex of the mandible.There ishighsignal from their pulp chambers and there
isa bandof highsignal immediately surroundingthe crown, demarcated by a lower signal edge
of bone. This band or ‘‘halo’’ enveloping the crown is an eruption follicle (Q)
Osteomylitis
It is inflammation of bone and bone marrow; begins in the medullar cavity
and havarian systems 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 compromises or 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. Many

18. 18
classification systems have been postulated for osteomylitis of which we
will mention the following:
 Classification based on pathogenesis. FromVibhagool 1993 (Hudson
1993)
I. Hematogenous osteomyelitis
II. Osteomyelitis secondary to a contiguous focus of infection
III. Osteomyelitis associated with or without peripheral vascular disease
 Classification based on clinical picture, radiology, pathology, and
etiology ( Topazian 1994)
I. Acute suppurative osteomyelitis (rarefactional osteomyelitis)
II. Chronic suppurative osteomyelitis (sclerosing osteomyelitis)
III. Chronic focal sclerosing osteomyelitis (pseudo-paget, condensing
osteomyelitis)
IV. Chronic diffuse sclerosing osteomyelitis
V. Chronic osteomyelitis with proliferative periostitis (Garre's chronic non
suppurative sclerosing osteitis, ossifying periostitis)
VI. Specific osteomyelitis
1. Tuberculous osteomyelitis
2. Syphilitic osteomyelitis
3. Actinomycotic osteomyelitis
 Classification based on clinical pictureand radiology (Bernieret al
1995)
I. Suppurative osteomyelitis
1. Acute suppurative osteomyelitis
2. Chronic suppurative osteomyelitis
II. Nonsuppurative osteomyelitis
1. Chronic focalsclerosing osteomyelitis
2. Chronic diffuse sclerosing osteomyelitis
3. Garre'schronic sclerosing osteomyelitis (proliferative osteomyelitis)
III. Osteoradionecrosis
 The Zurich Classification Systemof jaw osteomylitis based on
clinical course (Baltensperger andEyrich2009)
I. Acute osteommylitis
II. Secondarychronic osteomylitis
III. Primary chronic osteomylitis

19. 19
However in talking about clinical and radiographic features of osteomylitis
for the sake of simplicity, we group them into two major phases, acute and
chronic, recognizing that these represent two ends of a continuum without
a definite separating boundary in the process of bone inflammation. Other
forms of osteomyelitis have been described as separate and distinct clinic-
pathologic entities with unique radiographic features including Garre’s
osteomyelitis and diffuse sclerosing osteomyelitis. We consider them as
part of the same continuum. The features expressed by each subtype
represent only variations in the type and degree of bone reaction (White
and Pharoah 2006)
Acute phase of osteomylitis
 Clinical features
-It is characterized by rapid onset, pain, swelling of the adjacent soft
tissues, which may lead to trismus and limitation of jaw function.
-Fever, lymphadenopathy, and leukocytosis can also be seen with general
malais.
-The associated teeth may be mobile and sensitive to percussion.
-Purulent drainage also may be present -in acute suppurative form
-parathesia of the lower lip may also be seen (Vincent’s symptom),
indicating involvement of the inferior alveolar nerve.
However the clinical appearance of acute osteomyelitis of the jaws may
show a great variety, depending on the intensity of the disease and the
magnitude of imbalance between the host and the microbiological
aggressors (Baltensperger and Eyrich 2009)
 Radiographic Features(conventional and CT or
CBCT):
1-Location
Maxilla is rarely affected which is not the case in mandible, because the
distribution of blood vessels is poorer in the mandible than in the maxilla
and the cortical bone of the mandible is thicker and more compact than
that of the maxilla so the mandible is the common site for jaw osteomylitis ,
the posterior body of which is most commonly affected followed by the

20. 20
symphesis, angel, and ascending rami, and rarely the condyl and coronid
process.
2-Periphery:
An ill-defined periphery with a gradualtransition to normaltrabeculae Fig
15, 16
3-Internal Structure:
-Initially: a slight decrease in the density of the involved bone, with a loss of
sharpness of the existing trabeculae can be seen on intra-oral or panoramic
radiograph, however with CT images at this stage the bone lytic changes is
more clear Fig 15, 16,17
-With time: the bone destruction becomes more profound, resulting in an
area of radiolucency in one focal area or in scattered regions throughout
the involved bone which can be seen in both conventional radiographs and
CT images Fig 18
-Later: the appearance of sclerotic regions becomes apparent. Sequestra
may be present but usually are more apparent and numerous in chronic
forms, however it is better to discuss the appearance of sequestra in
chronic phase.
Fig. 15 Acute osteomyelitis involving the body of the right mandible, with initial blurring of
bony trabeculae.

21. 21
Fig 16 panoramic radiograph showing the source of infection appear in the incisor and canine
Region on both sides as well as in the molar region on the right side with rarefaction of the
neighboring bone
Fig 17 CorrespondingaxialCTscan to the panorama shown in Fig. 15 with a more detailed view
of the osteolysis in the anterior and right sided alveolar bone

22. 22
Fig 18 areas of bone resorbtion distributed through the lesion, note the ill defined borders of
the lesionasa whole (rarefaction)while the areas of bone resorbtion which appear as RL spots
have well demarcated borders
4-Effects on SurroundingStructures:
-the effect in bone appears as areas of rarefaction or destruction in bone
trabeculation, destruction of the cortical bone also could be seen with
formation of sinus tract to drain the pus (however at this point the lesion
usually turn chronic) Fig 19
-sub-periosteal new bone formation could be seen as when an
inflammatory exudate lift the periosteum it stimulate bone formation
which appear radiographically as a thin, faint, radiopaque line adjacent to
and almost parallel or slightly convex to the surface of the bone and a
radiolucent band separates this periosteal new bone from the bone surface
Fig 20
Fig 19 An axial CT image of osteomyelitiscase showscortical bone perforation(arrow) ,the
surroundingsofttissue shadowshowingswellingatthe area where the perforationfound

23. 23
Fig 20 Anaxial CT image of osteomyelitis reveals lamellated periosteal reaction (short arrows)
on the almost normal cortical bone around the perforated site (long arrow).
-the effect on teeth appears as widening of periodontal membrane space,
and loss of lamina dura at the involved teeth
5-Differentialdiagnosis
 Fibrous dysplasia
 Squamous cell carcinoma
 Osteosarcoma
 Leukemia
MRI imaging of acute osteomylitis
-Although (CT) is known to be the most effective tool for the evaluation of
osteomylitis bony changes, such as cortical bone lesion, sequestra, and
subperiosteal bone deposition, but it can hardly depict bone marrow
changes in the acute stage or evaluate the early response to the treatment.
- MRI can well demonstrate the bone marrow changes caused by edema or
inflammatory tissue due to increase of water content, which often replaces
the normal fatty marrow in the acute stage (Ariji et al 2008)
These changes appear as the following:
 On T1 weighted images it appears as low signal intensity (SI)
compared to the contralatteral normal bone Fig 21 C
 On T2 weighted images or short TI inversionrecovery (STIR) images
it appears as marked high (SI) area Fig 21 D, Fig 22

24. 24
Fig. 21 47-year-old man. The patient had dull pain in the cheek and the buccal gingiva of the
rightmandibularmolarregionfor 2 weeks.He complainedof paralysis in the lower lip from the
day before admission. A and B, Panoramic tomography and computed tomographic image did
not showany change of the cancellous and cortical bone in the right mandibular molar region.
On the nextday,MRI examinationwasdone. C,The T1-weightedimage showed a low SI area in
the molar to ramus region of the right mandible (arrow). D, The STIR image showed an
extremely high SI area in the same region (arrow).
Fig 22 (STIR) image of case of acute osteomylitis showing extensive high. SI at the posterior
body and ramus of the right area with erosion of the cortical bone (arrow) and the adjacent soft
tissue swelling with high SI

25. 25
Chronic phase of osteomylitis
The term chronic osteomylitis is very vague, it have been subcategorized
into many different terms in different classification, however The chronic
phase of osteomyelitis may be a sequela of acute osteomyelitis (secondary
chronic osteomylitis),as if acute osteomylitis left untreated or inadequately
treated after 3-4 weeks may turn to chronic phase, or it may arise de novo
(primary chronic osteomylitis), another differentiation of the chronic cases
based on suppuration (chronic suppurative osteomylitits, and chronic non
suppurative osteomylitis) was proposed as more helpful in clinical
differentiation between the lesions, their causes, and their response to
treatment however, some confusion may arise among clinicians in some
cases, because confirmation of the presence of suppuration is difficult in
some suppurative lesions and suppuration from a periodontal pocket may
be seen in nonsuppurative lesions (Baltensperger and Eyrich 2009)
 Clinical features
-Pain and swelling, are usually less extensive in the chronic than in the
acute stage.
-The deep and intense pain frequently observed in the acute stage is
replaced by a more dull pain.
-Painful swelling caused by local edema and abscess formation in the acute
stage is subsided by a harder palpable tenderness caused by periosteal
reaction
-A disturbed occlusion can sometimes be noted when teeth of an affected
region become more mobile and elongate due to rise of intraosseous
pressure or a fracture
- Pus, fistula, and sequestra are the typical clinical finding in case of
suppurative osteomylitis, however the nonsuppurative form lacks pus
formation, Topazian (1994) includes chronic sclerosing types of
osteomyelitis, proliferative periostitis, as well as actinomycotic and
radiation-induced forms to this group, whereas Bernier et al (1995)
advocate a more restrictive use of this term.
-parathesia of the lower lip may also be seen

26. 26
 Radiographic Features(conventional and CT or
CBCT):
The chronic phase of osteomylitis have more than one presentation
radiographically, for that it have been classified as diffuse sclerosing
osteomylitis, focal sclerosing osteomylitis, proliferativeperiostitis (Garre’s
), however they all share the hallmark of osteomylitis which is presence of
sequestra, the followings are the general radiographic features of chronic
osteomylitis as seen by CT and 2D plan radiographs, and latter each
subcategory will be features explained
1-Location
As in acute phase, the mandible is the common site for jaw osteomylitis ,
the posterior body of which is most commonly affected followed by the
symphesis, angel, and ascending rami, and rarely the condyl and coronid
process.
2-Periphery:
-The periphery may be better defined than in the acute phase, but it is still
difficult to determine the exact extent of chronic osteomyelitis.
-Usually a gradual transition is seen between the normal surrounding
trabecular pattern and the dense granular pattern characteristic of this
disease.
-When the disease is active and is spreading through bone, the periphery
may be more radiolucent and have poorly defined borders
3-Internal structure
-The internal structure comprises regions of greater and lesser radiopacity
compared with surrounding normal bone Fig 23, 24
-In older, more chronic lesions the internal bone density can be exceedingly
radiopaque and equivalent to cortical bone. In these cases no obvious
regions of radiolucency may be seen (Sclerotic osteomylitis).
-In other cases, small regions of radiolucency may be scattered throughout
the radiopaque bone. However A close inspection of the radiolucent
regions may reveal an island of bone or sequestrum within the center).

27. 27
Often the sequestrum appears more radiopaque than the surrounding
bone Fig 25
-This island of non-vital bone may vary in size from a small dot (smaller
sequestra usually are seen in young patients) to larger segments of
radiopaque bone.
-CT is superior for revealing the internal structure and sequestra, especially
in cases with very dense sclerotic bone. The bone pattern usually is very
granular, obscuring individual bone trabeculae, whereas on plain film
illumination of the radiolucent regions of the film with an intense light
source is needed to detect the sequestra.
Fig 23 AnOPG of a chronicosteomyelitis case demonstratesosteolysisinthe mandibular corpus
aroundthe alveolarregionof the right first molar. A sequester is noted at the base of the right
mandibular corpus
Fig 24 CT scans of a patient with secondary chronic osteomyelitis of the left mandible
developingagiant sequesteron the bases of the mandibular corpus. The progressive infection
has weakened the bone and hence a pathological fracture has resulted

28. 28
Fig 25 Panoramicradiographof leftmandible withosteomyelitis.Osteolyticareas(arrows) are
observed inareaswithsevere scleroticchanges(mixedpattern)
Some studies have classified the CT radiographic finding of osteomylitis to 3
different appearances: bone-defect pattern, frosted-glass pattern and
compact-bonepattern (Tanaka and Hayashi 2008) Fig 26
a b c
Fig 26 Three patterns of pathological CT findings of affected bone with mandibular chronic
osteomyelitis.the areas of (a) bone-defect pattern, (b) frosted-glass pattern and (c) compact-,
4-effect on the surrounding structures
-subperiosteal new bone formation as discussed previously in acute stage,
but as the lesion develop in to more chronic stage cyclic and periodic acute
exacerbations may produce more inflammatory exudate which again lifts
the periosteum and stimulates it to form a second layer of bone
Radiographically this looks like a second radiopaque line almost parallel to
the first and separated from it by a radiolucent band. This process may
continue and may result in several lines (an onion-skin appearance), and
eventually a massive amount of new bone may be formed. This is referred
to as proliferative periostitis Fig 27

29. 29
a b
Fig 27 (a) proliferative periostitis forming onion skin appearance at the bucal side of the
mandibularmolars, (b) Osteomyelitis of the mandible with a periosteal reaction located at the
inferiorcortex.Note the radiolucent line (arrow) between the inferior cortex of the mandible
and the firstlayerof periosteal new bone.A secondradiolucentline separates the second layer
of new bone from the first layer
-Resorbtion of the cortical bone, as when sinus tract is formed to discharge
the pus Fig 23, also pathological fracture of the mandible may result Fig 24
-The roots of teeth may undergo external resorption, and the lamina dura
may become less apparent as it blends with the surrounding granular
sclerotic bone.
5-differntial diagnosis
 Fibrous dysplasia
 Paget’s disease
 Florid cement osseous dysplasia
 Osteosarcoma
MRI imaging of chronic osteomylitis
-MRI imaging in chronic phase of osteomylitis is not as useful as in acute
phase, as the changes in chronic phase are well demonstrated on
radiographs and best seen by CT, however in case of acute exacerbation of
chronic case it could be early seen by MRI
-Itis characterized by low SI area on T1-weighted images and T2-weighted
or STIR images, the low SI is due to the sclerotic bone with thickened
trabecule Fig 28

30. 30
-Administration of gadolinium-DTPA may add very important information,
such as a noncalcified periosteal reaction, definition of the limit of the
sequestrum, and extension of the inflammation to soft tissue. However
these features were also detectable on STIR image, and therefore sequence
with gadolinium-DTPA was not always used for making of MRI diagnostic
criteria (Ariji et al 2008).
Fig 28 A, Panoramictomographyshoweddiffuselyscleroticchange inthe left mandibular molar
region (arrows). The range extended from the mandibular notch of the ramus to the lower
marginof the mandible.BothT1-weightedMRI image (B) andSTIR MRI image (C) showed low SI
in the widespread area of the ramus (arrows).
As we mentioned beforesome forms of chronic osteomylitis was popular as
showing unique radiographic features which gave them special attention in
the osteomylitis classifications and became a separate entity under the
main group of chronic osteomylitis they include:
 Garre’s osteomyelitis
-It was also called osteomyelitis with periosteitis (periosteitis ossificans).
These terms are used to identify lesions with a large amount of periosteal

31. 31
reaction, but periosteal reaction can be seen in any type of osteomyelitis
lesion; the amount or periosteal reaction depends on the activity of the
osteoblastic cells in the periosteum, Furthermore, Garre’s work was done
before the invention of radiography and Garre himself never used his name
as a diagnostic term (Suei et al 2005)
-It is chronic sclerosing form of osteomylitis affecting young ages, lack pus
formation (non suppurative) and due to the young age of the patient when
the periosteum is loosely attached to the bone surface and with powerful
osteogenic capability, so extensive subperiosteal bone formation may be
seen (onion skin appearance) Fig 27 a.
-however recent publications now used the term “juvenile chronic
osteomyelitis,” in describing the same clinical and radiographic appearance
of what was called Garre’s osteomyelitis (Heggie et al 2003)
 Diffuse sclerosing osteomylitis DSO
-It is form of chronic osteomylitis characterized by sclerosing dense radio-
opaque masses diffuse in the jaw, True diffuse sclerosing osteomyelitis,
however, is a rare disease of unknown etiology that can cause major
diagnostic and therapeutic problems.
-It characterized by absence of pus, fistula, and sequestration, has an
insidious onset, lacking an acute state. It is therefore considered to be
primary chronic and has been named primary chronic osteomyelitis by
several authors.
-Periods of onset usually last from a few days up to several weeks and may
demonstrate a cyclic course with symptom-free intervals. Pain, swelling,
and limitation of mouth opening, as well as occasional lymphadenopathy,
dominate the clinical picture.
-A further pathological disease entity has been confused with diffuse
sclerosing osteomyelitis, since it may mimic DSO radiographically by
presenting sclerosing opaque and dense masses it is florid osseous
dysplasia (FOD), however these masses are confined to the alveolar
process of either or both jaws.
Florid osseous dysplasia is mostly observed in black women and in many
cases lacks clinical symptoms Patients suffering from this disease, similar to
true DSO, may in some instances also experience cyclic episodes of
unilateral pain and mild swelling. This is usually the case when
superinfection occurs (Baltensperger and Eyrich 2009) Fig. 29

32. 32
Fig 29 . SclerosingosteomyelitisinCTscan showsdiffuse sclerotic changes with expansion
of the left mandibular body (arrows). Note the diffuse soft-tissue swelling (arrowheads).
 Focal sclerosing osteomylitis
Also known as periapical osteitis/osteomyelitis or condensing osteitis, it is a
rather common condition with a pathognomonic, well-circumscribed
radioopaque mass of sclerotic bone surrounding the apex of the root. The
infection in these cases is limited to the apex of the root with the absence
of deep bone invasion (Baltensperger and Eyrich 2009)
Two different types of osteomylitis were not mentioned in any of the
classifications proposed for jaw osteomylitis , they are osteomylitis in
SAPHO syndrome, and chronic recurrent multifocal osteomyelitis (CRMO)
 Chronic recurrent multifocal osteomyelitis (CRMO)
It is askeletal disorder of unknown cause, occurring primarily in children
and adolescents. It often occurs symmetrically in the long bones with
frequent involvement of the clavicle and often showing multifocality.
Clinically: it is characterized by the insidious onset of pain and swelling
corresponding to the involved bones The disease course is typically
prolonged over several years, punctuated by periodic exacerbations.
Symptoms may either recur at sites affected previously or involve new
areas with subsequent flare-ups, low-grade fevers and generalized malaise
may also be found, it also showed association with pustulosis and

33. 33
palmoplantaris, Itis characterized by lack of causativeorganism; no abscess
formation, fistula, or sequestra
-NSAIDs areusually effectivein symptomatic relief, with responserates of
up to 80% (Iyer et al 2011).
Radiographically :
On plain radiographs and CT, It may shows areas of lytic destruction of
bone, or sclerotic areas, with or without subperiosteal reaction, however
no sequestra is found Fig 29
On MRI images active disease exhibits edematous marrow changes,
including T1 hypointensity and hyperintensity on both T2 and STIR
sequences, whereas at areas with sclerosis the MRI images will show
homogeneous T1 and T2 hypointensity. Surrounding soft-tissue edema may
or may not be present (Iyer et al 2011).
a b
Fig 30 (a) anteroposterior radiograph of right clavicle shows hyperostosis and lamellated
periosteal elevation (arrows). (b) Coronal reformatted CT image obtained in bone windows
illustrates marked clavicular sclerosis (arrow).
 Osteomylitis in SAPHO syndrome
It is a systemic disease, the appreviation SAPHO stands for Synovitis =
[inflammatory arthritis], Acne= [pustulosa], Pustulosis = [psoriasis,
palmoplantar pustulosis ] , Hyperostosis [ acquired ] , and Osteitis= [
osteomyelitis ]
Clinical features. Pain and swelling are seen, but suppuration is never
found in this condition.
The symptoms may start gradually or suddenly and persist for a long time,
with repeated exacerbations and remissions.

34. 34
The lesions are often extensive: Condylar process involvement is not rare
and the entire mandible may be involved
Radiographic features.
-The radiographic findings are complex and variable, and no consistent
relationship has been confirmed among the pictures seen on the
radiographs as osteolysis, osteosclerosis, and periosteal reaction.
-active bone remodeling can be seen resulting in deformation of the
condylar process or displacement of the mandibular canal.
-On plain radiographs, progressivebonesclerosis with scattered osteolyses
(mixed type) is a common finding (Fig31). However, bone resorption may
be prominent at the early stage or when symptoms flare up, whereas only
the sclerotic changes may be observed during the more quiescent chronic
stage (Suei et al 2005, Colina et al 2009).
-The lesions are usually associated with solid periosteal reaction. However
cortical bone resorption could also be seen, it even could be diffuse and
extensive, and may occur externally.
-Bone resorption on the external bone surface is a pathognomonic finding
and is usually confirmed on panoramic radiographs fromthe inferior border
of the mandibular body to the posterior border of the mandibular ramus. In
advanced cases, a remarkable reduction of mandibular bone volume is
observed (Fig31 b).
- On CT images, the density of the partially resorbed cortical bone may be
identical to that of the sclerotic cancellous bone and the periosteal
reaction. Low-density areas (osteolytic lesions) may be scattered within
these otherwiseuniformly dense regions (Fig32). In somecases, the original
cortex is almost or entirely disrupted and a cortex-like radiopaque zone,
newly formed by periosteal bone deposition, is observed external to the
site of the original cortex and the mandible appears enlarged (bone
enlargement) (Suei et al 2005, Colina et al 2009) (Fig33).

35. 35
Fig 31 A, Panoramic radiograph of left mandible with osteomyelitis in SAPHO syndrome.
Osteolyticareas(arrows) are observed inareaswithsevere scleroticchanges(mixedpattern). B,
More than 5 years afterthe radiographsin A were taken, the left mandibular bone volume has
been reduced by bone resorption on external bone surfaces and osteosclerotic changes are
prominent.
Fig32. An axial CT image of mandibular osteomyelitis in SAPHO syndrome. Osteolytic areas
(arrows) are scattered in the lesion. Solid periosteal reaction is seen
Fig33. An axial CT image of mandibular osteomyelitis in SAPHO syndrome at the level of
mandibular canals (long arrows) shows the enlargement of the left mandible (short arrows).

36. 36
Osteoradionecrosis
-Osteoradionecrosis is one of the most serious oral complications of head
and neck cancer treatment. It is an inflammatory condition of bone
(Osteomyelitis) that occurs after the bone has been exposed to therapeutic
doses of radiation; it is characterized by the presence of exposed bone for a
period at least 3 months, occurring at any time after the delivery of the
radiation therapy. Dose above 50 Gy usually is required to cause this
irreversible damage (Baltensperger and Eyrich 2009)
-Osteoradionecrosis was once considered an infection initiated by bacteria,
which invaded the radiation-damaged bone; hence, the term “radiation-
induced osteomyelitis” or radio-osteomyelitis was commonly used.
-Marx (1983) conclusively identified this condition as a radiation-induced
avascular necrosis of bone. He was able to demonstrate that radiation
caused a hypoxic, hypocellular, and hypovascular tissue, leading to a
spontaneous or trauma-initiated tissue breakdown. The result is a chronic
non-healing wound, susceptible to super infection.
 Clinical Features
-The mandible is much more commonly affected than the maxilla due to its
lower blood supply compared with the maxilla. The compact bone structure
of the mandibular bone has also been suggested as a reason for ORN
susceptibility, The posterior mandible is affected more often than the
anterior portion because The posterior body of the mandible is more
frequently in the direct field of the radiation treatment because primary
tumors and metastatic lesions in lymph nodes being treated are commonly
adjacent to this part of the mandible.
-Loss of mucosal covering and exposure of bone is the hallmark of
osteoradionecrosis.
- Pathologic fracture also may occur.
-Pain may or may not be present. Intense pain may occur, with intermittent
swelling and drainage extraorally. However, many patients feel no pain
with bone exposure
-The lesion may be accompanied by symptoms of dysesthesia, fetor oris,
dysguesia, and food impaction in the area (White and pharaoh 2006,
Koga et al 2008)

37. 37
 Radiographic Features(conventional and CT or
CBCT):
The radiographic picture of osteoradionecrosis is nearly similar to that of
osteomylitis
-An early characteristic changes: is a well-defined area of bone resorption
within the outer cortical plate of the mandible
-Later changes: are quite variable and may be predominantly lytic or
sclerotic or mixture
-However, the presence of osteoradionecrosis cannot always be diagnosed
radiographically and often clinically obvious signs of exposed necrotic bone
may not be accompanied by significant radiologic changes specially when
using plain radiographs which underestimate the extent of radiation-
damaged bone, and do not correlate with the clinical status of patients.
-With mandibular osteoradionecrosis, CT may additionally show cortical
interruptions and loss of spongiosa trabeculation. In other sites CT may
show the presence of subtle fractures, alterations in bone architecture and
dystrophic soft-tissue calcification
-Comparing the information yield from CT and panoramic radiographs for
mandibular osteoradionecrosis showed that Bone changes, such as cortical
thinning, mono-cortical destruction, sclerosis, sequestration, central
necrosis, bi-cortical destruction, were better visualized by CT, whereas
Widening of the periodontal ligament spaces was seen only on panoramic
radiograph (Store and Larheim 1999) Fig 34, 35
1-location
The mandible, especially the posterior mandible is more commonly
affected than maxilla
2-Periphery:
-The periphery is ill defined (similar to that in Osteomyelitis)
3-Internal structure
A range of bone formation to bone destruction occurs, often with the
balance heavily toward more bone formation, and this gives the affected

38. 38
bone an overall sclerotic or radiopaque appearance, similar to chronic
osteomyelitis. (The bone pattern is granular).
-Scattered regions of radiolucency may be seen, with and without central
sequestra.
4-Effects on Surrounding Structures
-Inflammatory subperiosteal newboneformation is uncommon because of
the deleterious effects of radiation on potential osteoblasts in the
periosteum, however in very rare cases the periosteum appears to have
been stimulated to produce bone, resulting in new bone formation on the
outer cortex in an unusual shape.
-The most common effect on the surrounding bone is the stimulation of
sclerosis.
-In the alveolar process of the maxilla and mandible, there may be irregular
widening of the periodontal membrane space similar to that seen in
malignant neoplasia or it may simulate periapical rarefying osteitis. Also,
there may be bone resorption, very similar to periodontal disease
5-differential diagnosis
 sclerotic lesions of chronic osteomylitis
 malignant neoplasms
a b
Fig 34 (a) CT scan of a female patient(age 73),whoreceived combined radiotherapy (86 Gy) for
carcinoma of the right side of the tongue, showing sclerosis and a sequestrum in the anterior
mandible and a lingual defect also containing a sequestrum on the left side. (b) Panoramic
radiograph of the same patient, showing the defect in central area of the left mandible

39. 39
a c
b
Figure35 (a) CT scan of male patient(age 79),who receivedexternal radiotheraphy (70 Gy) for a
carcinoma of the left parotid gland, showing a defect in the left mandible extending from the
midline to the ascending ramus and involving both cortices with multiple sequestration. (b)
Panoramicradiographof same patient,showing the defect in the left mandible extending into
the leftcoronoidprocess, partof whichis obscured. (c) MPR of the same patient, showing ORN
in left ramus and coronoid process
MRI imaging of osteoradionecrosis
On MRI, the ORN lesion appears as new heterogeneous signal within the
marrow of an irradiated area (intermediate or low T1 signal, intermediate
or high T2 signal), no contrast enhancement, all suggestive of nonviable
bone.

40. 40
Fig 36 CurvedMPR of the jaw. 62-year-oldfemalepatientwithosteoradionecrosis of the jaw. A
curvedMPR alongthe oral midline wascreatedtodisplaythe mandible and maxilla in one slice.
The large osteonecrosis of the right mandibular ramus (arrow) can be readily depicted in this
T1w syngo SPACE sequence.
The medical literature describes severaldrugs and substances that facilitate
or induce conditions similar to osteoradionecrosis of the jaws, it was
termed osteochemonecrosis , such as corticosteroids and other cancer and
anti-neoplastic drugs. Exposure to white phosphorous among workers in
the match-making industry in the nineteenth century has led to unusual
necroses of the jaws, which became known in the literature as phossy jaw
or phosphorous necrosis of the jaw, in the recent years a similar condition
was found to be associated with bisphosphonate therapy (Baltensperger
and Eyrich 2009)
Bisphosphonate-related osteonecrosis of
the jaws
-In the recent years bisphosphonate therapy has become a widely accepted
mainstay of therapy in various clinical settings such as multiple myeloma,
metastatic cancer therapy, and treatment of advanced osteoporosis,
paget’s disease.
-With the increased prescription of these drugs, the incidence and
prevalence of bisphosphonate-associated complications of the jaw

41. 41
continues to be elucidated. This trend seems to be even more the case in
patients receiving injectable bisphosphonates, such as pamidronate and
zoledronic acid; however cases of osteonecrosis of the jaw have also been
reported associated with chronic oral administered bisphosphonates
(Baltensperger and Eyrich 2009).
-The pathophysiological mechanisms leading to bisphosphonate-induced
osteochemonecrosis of the jaws are yet far from being fully understood;
however, it seems apparent that important differences to the pathogenesis
of osteoradionecrosis do occur (Hellenstein and Marek 2005). In
bisphosphonate-induced osteochemonecrosis of the jaws osteoclastic
action is reduced, but osteoblastic production continues, leading to an
osteopetrosis-like condition (Whyte et al. 2003). These alterations in bone
physiology with eventual increase of the medullary bone as the disease
progresses and the inability of osteoclasts to remove superinfected
“diseased” bone are regarded as causative factors.
- It deserves to be mentioned that the jaws are particularly susceptible due
to the high bone turnover. Supporting this theory is that there has been
only 1 case of bisphosphonate-associated osteonecrosis outside the oral
cavity
 Clinical Features
-Patients typically have an area of exposed bone after an invasive dental
surgical procedure however denture trauma and spontaneous cases have
been known to occur.
-Ulceration of palatal tori resulting in bone exposure is most likely the
result of trauma
-may be asymptomatic or present with pain and swelling
-The most common areas affected are:
 The posterior mandible (60%).
 The maxilla (40%).
 Both (9%).
-The incidence of bone exposureis difficult to determine, but recent studies
suggest that approximately 3% of patients receiving these drugs will have
exposed bone. It should be noted that because the skeletal half-life of

42. 42
bisphosphonates is more than 10 years, it is possible that complications
may occur after cessation of therapy (Janovská 2012)
 Radiographic Features(conventional and CT or
CBCT):
-There are no specific radiographic findings with the clinically exposed
bone; in other cases the radiographic changes are not dissimilar to
osteoradionecrosis or chronic osteomyelitis with the presence of
sequestra Fig. 37,38,39
-Other reported findings include:
 An increase in bone sclerosis (Osteopetrosis-like image)
 widening of the periodontal membrane space,
 Thickening of the lamina dura
( Phal et al 2007)
Fig 37 Radiographic findings in bisphosphonate-associated osteonecrosis of the jaws.
A, Normal appearance
B, osseous sclerosis most commonly involved in the alveolar margin and lamina dura. The
sclerotic changes often diffuse rather than localized to the area of clinical involvement.
C, Inthe patientswithsequential imaging,the scleroticchangeswere oftenprogressiveandmay
encroachon the mandibularcanal.The sclerosisof the medullarycavity may be attenuated and
reminiscent of osteopetrosis.

43. 43
Fig 38 A 67-year-old woman presented with a nonhealing extraction socket. A, The
orthopantomogram demonstrates the nonhealing extraction socket in the right posterior
mandible (*) with sclerosis in the adjacent body and ramus of the mandible (arrow) and
generalizedthickeningof the lamina dura in the mandible (arrowhead) and maxilla. B, Axial CT
demonstrates the osseous sclerosis, as well as narrowing the mandibular canal (*), thin
periosteal new bone anteriorly (arrow) and generalized thickening of the lamina dura in the
mandible (arrowhead).
Fig 39. A 60-year-old woman presented with a nonhealing extraction site in the left posterior
mandible. A, Orthopantomogram demonstrates the nonhealing extraction site in the left
posteriormandible(*) andsclerosisof the leftramusandangle of the mandible (arrowhead). B,
Orthopantomogram, 23 months later with intervening curettage, demonstrates disorganized
bone formationinthe extractionsocketof the lowerleftthirdmolar,progressive sclerosisof the
leftramus,andangle of the mandible (arrow) withfurtherencroachmentonthe leftmandibular
canal (arrowhead).

44. 44
MRI imaging of bisphosphonates-induced osteonecrosis
-MRI considered an accurate imaging modality for assessment of bony
changes in the jaws following bisphosphonates therapy, as depending on
the studies utilized MRI in monitoring of this condition, all the clinically
detected focal lesions were visible in the MRI study, but not all those
detected by MRI were visible in the clinical examination, even after the
dental surgeon knew where to look, it could be used as a technique for
early detection in patients susceptible to this disease.
-MRI used for examination of the lesions involving cortical bone, marrow
spaces, and the extension to the soft tissues adjacent to the cortical bone,
and extension to the maxillary sinus or nasal fossa In the upper maxilla
could be also assessed (García-Ferrer et al 2008)
-In MRI, the bisphosphonates-induced osteonecrosis appears:
On T1-weighted images it is hypointense
On STIR and after the administration of gadolinium (contrast enhanced).
The lesions are showing very little brightness and had little or no contrast
enhancement, all suggestive of nonviable bone Fig. 40,41,42,43
Fig40, T1-weightedimage showshypointense areainrightmandible (whitearrow) that
correspondstofocal lesionof osteonecrosisandassociatedadenopathy(blackarrow).

45. 45
Fig 41 Oblique sagittal T1-weightedimageshowsfocal lesionof osteonecrosis (arrow) affecting
mandibular branch and involving mandibular canal
Fig 42 MRI of osteoradionecrosisinmaxilla,T1weightedimage showinghypoSI indicating bone
sequestrum in the right maxilla
Fig 43 Oblique sagittal T1-weighted image shows occupation of right maxillary sinus caused by
hypointenselesioninupperrightmaxilla(whitearrow),causing lysis of floor of maxillary sinus.
Associated submaxillary adenopathy (black arrow) is seen

46. 46
References
 Ariji Y, Izumi M, Gotoh M, Naitoh M, Katoh M, Kuroiwa Y, Obayashi N, Kurita
K, Shimozato K, Ariji E. MRI features of mandibular osteomyelitis: practical
criteria based on an association with conventional radiography features and
clinical classification. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2008
;105(4):503-11
 Baltensperger M and Eyrich G.K. Osteomylitis of the jaws. Eds 2009, ch1, p 5-
37
 Bernier S, Clermont S, Maranda G, Turcotte JY. Osteomyelitis of the jaws. J
Can Dent Assoc 1995 May;61(5):441-2,445-8
 Colina M, Govoni M, Orzincolo C, Trotta F. Clinical and radiologic evolution of
synovitis, acne, pustulosis, hyperostosis, and osteitis syndrome: a single center
study of a cohort of 71 subjects. Arthritis Rheum. 2009 Jun 15;61(6):813-21.
 Estrela C, Bueno MR, Leles CR, Azevedo B, Azevedo JR. Accuracy of cone
beam computed tomography and panoramic and periapical radiography for
detection of apical periodontitis. J Endod. 2008 Mar;34(3):273-9
 Heggie AA, Shand JM, Aldred MJ, Talacko AA. Juvenile mandibular chronic
osteomyelitis: a distinct clinical entity. Int J Oral Maxillofac Surg. 2003;
32(5):459-68.
 Hellstein JW, Marek CL. Bisphosphonate osteochemonecrosis (bis-phossy
jaw): is this phossy jaw of the 21st century. J Oral Maxillofac Surg. 2005
;63(5):682-9
 Hudson JW. Osteomyelitis of the jaws: a 50-year perspective.J Oral Maxillofac
Surg 1993 Dec;51(12):1294-30
 Iyer RS, Thapa MM, Chew FS. Chronic Recurrent Multifocal Osteomyelitis:
Review. AJR Am J Roentgenol. 2011 Jun;196(6 Suppl):S87-91
 Janovská Z. Bisphosphonate-related osteonecrosis of the jaws. A severe side
effect of bisphosphonate therapy. Acta Medica (Hradec Kralove).
2012;55(3):111-5
 Koga DH, Salvajoli JV, Alves FA. Dental extractions and radiotherapy in head
and neck oncology: review of the literature. Oral Dis 2008 ;14:40-44
 Marx RE. Osteoradionecrosis: a new concept of its pathophysiology. J Oral
Maxillofac Surg 1983,41:283-288

47. 47
 Phal PM, Myall R.W.T, Assael L.A, Weissman J.L. Imaging Findings of
Bisphosphonate-Associated Osteonecrosis of the Jaws. AJNR Am J Neuroradiol
2007; 28:1139–45
 Scheinfeld MH, Avery L, Dym H. Teeth: What Radiologists Should Know 1.
RadioGraphics 2012;32:1927-1944
 Store G and Larheim TA, Mandibular osteoradionecrosis: a comparison of
computed tomography with panoramic radiography Dentomaxillofacial
Radiology (1999) 28, 295 - 300
 Suei Y, Taguchi A, Tanimoto K. classification of mandibular osteomylitis. Oral
Surg Oral Med Oral Pathol Oral Radiol Endod. 2005; 100(2):207-14.
 Tanaka R and Hayashi T. Computed tomography findings of chronic
osteomyelitis involving the mandible: correlation to histopathological findings.
Dentomaxillofacial Radiology (2008) 37, 94–103
 Topazian RG. Osteomyelitis of the Jaws. In Topizan RG, Goldberg MH (eds):
Oral and Maxillofacial Infections. Philadelphia, WB Saunders 1994, Chapter 7,
pp 251-88
 Tutton LM and Goddard PR. Pictorial review: MRI of the teeth. The
British Journal of Radiology, 75 (2002), 552–562.
 White SC and Pharoah MJ. Oral radiology principales and interpretation, sixth
edition.2006. ch 20, p 325-342.
 Whyte MP, Wenkert D, Clements KL, McAlister WH, Mumm S.
Bisphosphonate-induced osteopetrosis. N Engl J Med. 2003; 349:457-63.
 Yamaoka M, Ono Y, Takahashi M, Ishizuka M, Uchihashi T, Yasuda K,
Uematsu T, Furusawa K. Acute inflammation in horizontal incompletely
impacted third molar with radiolucency in the elderly. Clin Interv Aging.
2009;4:337-42
 García-Ferrer L, Bagán JV, Martínez-Sanjuan V, Hernandez-Bazan S, García R,
Jiménez-Soriano Y, Hervas V. MRI of mandibular osteonecrosis secondary to
bisphosphonatesAJR Am J Roentgenol. 2008;190(4):949-55