Inflammatory Lesions of the Jaws










Atlas of Oral and Maxillofacial Radiology, First Edition. Bernard Koong.
© 2017 John Wiley & Sons Ltd. Published 2017 by John Wiley & Sons Ltd.
64
5.1 Periapical inflammatory lesions
(Figures5.1–5.17)
Synonyms: apical periodontitis, periapical rarefying osteitis, peri-
apical condensing or sclerosing osteitis, periapical granuloma.
Periradicular inflammatory lesions related to pulpal pathology
are mostly seen at the apical aspect of the tooth root(s), centred at
the apical foramen, i.e. periapical inflammatory lesion. However,
these lesions are sometimes centred upon the root surface away
from the apical foramen, most of which are related to lateral
canals and foramina (normal variant) or root fractures. The term
osteomyelitis is reserved for more extensive infection of bone.
Clinical presentation varies substantially, from an asympto-
matic low‐grade chronic picture to severe infections with
substantial local and systemic manifestations.
Osteomyelitis (see section5.4), the radicular cyst (see Chapter8)
and involvement of the soft tissues including cellulitis and abscess
collections (see section5.5) are possible sequelae.
Radiological features
Cone beam computed tomography (CBCT) and multidetector
computed tomography (MDCT) are more sensitive for periapi-
cal lesions than 2D intraoral and panoramic radiography
although 2D radiography is usually the first modality of choice.
Where indicated, soft tissue involvement is best examined with
MDCT, often with intravenous contrast.
Magnetic resonance imaging (MRI) may be useful:
For identification of early lesions.
Where 2D radiography, MDCT and CBCT are equivocal
and there remains clinical suspicion for periapical inflam-
matory disease.
Where there are unusual symptoms.
It should be noted that, even when the clinical presentation is
that of an acute periapical inflammatory lesion, it often
reflects an acute phase of a chronic lesion (acute‐on‐chronic)
and the bony changes seen radiologically reflect the chronic
features. The acute features are often only demonstrated with
multislice CT or MRI.
Early or lower grade lesions often present as widened apical
periodontal ligament space with preservation of the lamina
dura.
Very early or acute lesions may not demonstrate bony
changes detectable with 2D radiography, CBCT or MDCT.
MRI may demonstrate periapical inflammatory marrow
oedema.
With some progression, it usually presents as a lucency or
hypodense focus centred at the apex of a root with effacement
of the lamina dura.
Sometimes, these lesions are centred elsewhere on the root
surface, related to accessory lateral pulp canals and foramina
(normal variant) or root fractures. Lateral canals and root
fractures may not be radiologically detectable.
Margins can be ill defined or relatively well defined.
Many of these lesions identified radiologically are longstand-
ing and are either acute‐on‐chronic or solely chronic in nature.
Therefore, the margins are often relatively well defined.
More acute lesions tend to demonstrate less or poorly
defined margins.
Adjacent reactive sclerosis is a common feature since many
lesions demonstrated radiologically are chronic in nature.
The degree of sclerosis is variable. It can be focal and mild
or dense, extensive and diffused, related to the degree of
chronicity.
Occasionally, the sclerosis can be extremely focal and dense
where the widened apical periodontal ligament space or
small apical lucency is not apparent. Some refer to these as
periapical condensing/sclerosing osteitis. However, MDCT
and CBCT almost always demonstrate subtle widening of
the periodontal space or a small periapical hypodense or
lucent focus, which may not be appreciated on panoramic
or periapical radiography.
Apical root resorption may be seen with chronic lesions.
The pulp chamber and root canals of the involved tooth may
appear larger/wider than the contralateral tooth, related to
arrested deposition of dentin.
Larger lesions may efface the jaw cortices.
CHAPTER 5
Inflammatory Lesions oftheJaws
Inflammatory Lesions oftheJaws 65
There may be periosteal response (periosteal new bone
formation).
Lesions approximating the maxillary antral bases:
Commonly stimulate variable reactive mucosal thickening
at the antral floor.
Focal reactive periosteal response (focal periostitis) is also
quite commonly seen, appearing as a dome‐shaped opaque
lamina.
There may be focal effacement of the antral cortical floor,
often not appreciated with 2D radiography.
Occasionally, there is variable inflammatory disease affecting
the ipsilateral paranasal sinuses, secondary to the periapical
inflammatory lesion. This is usually limited to the maxillary
sinus.
These features are better appreciated with MDCT or CBCT.
Differential diagnosis
Key radiological differences
Periapical
osseous
dysplasia
Presence of internal opaque deposits or
homogeneous ‘ground‐glass’ appearance. Early
lesions without internal opacities can appear
similar to chronic periapical inflammatory
lesions. Theperiapical osseous dysplasia is
usually multiple. CBCT or MDCT is more
sensitive in demonstrating subtle internal
increased densities.
Radicular
cyst
It can be difficult to differentiate from chronic
periapical inflammatory lesions. The radicular
cyst tends to demonstrate corticated borders
although this may not be evident in early
cystic change. Expansion and displacement of
structures (e.g. mandibular canal) are cystic
features. As a rule of thumb, lesions larger
than 10 mm have been considered to be more
likely to be radicular cysts but other features
must be taken into account. CBCT/MDCT can
better differentiate these lesions.
Bone island May resemble the adjacent chronic reactive
sclerosis but bone islands are usually well
defined and homogeneous internally, isodense
with cortical bone. In addition, there is almost
always a periapical lucent/hypodense appear-
ance or widening of the apical periodontal
ligament space with apical inflammatory lesions.
Fibrous
healing
Postendodontic therapy fibrous healing can
appear similar and differentiation is often
difficult. Fibrous healing tends to demonstrate a
well‐defined thick cortex, which may be slightly
irregular. CBCT and MDCT may better
demonstrate these features and may also be
used to evaluate the integrity of the endodontic
treatment.
Malignant
lesions
Demonstrate aggressive borders. Metastatic
and infiltrative malignant lesions often
demonstrate other and/or adjacent lesions,
e.g. periradicular lucencies elsewhere on the
same or adjacent teeth, with absence of
lamina dura.
Osteomyelitis A periapical inflammatory lesion rarely
progresses to osteomyelitis. Osteomyelitis
involves a much larger region of bone and
may not be centred upon the root apex.
Sequestra and periosteal new bone formation
are features of osteomyelitis.
Post‐treatment appearances ofperiapical lesions
(Figures5.15–5.17)
After successful endodontic therapy or extraction, apical
appearances include re‐establishment of normal periapical
structures, variant trabecular architecture, fibrous healing and
periapical osseous prominence at the maxillary sinus base, as
follows.
Re‐establishment ofnormal periapical structures
Radiological features
New bone formation begins at the periphery of the periapical
lucency. This new bone is usually relatively homogeneous in
appearance initially and eventually remodels.
Re‐establishment of the lamina dura and periodontal ligament
space, if the tooth has not been extracted (i.e. endodontically
treated).
Variant trabecular architecture (Figure5.16)
Bony healing and remodelling following successful treatment
may result in a trabecular appearance that is different from
the trabecular bone typical of that region of the jaws.
Radiological features
A variety of altered trabecular bone pattern is seen.
There is usually re‐establishment of normal periodontal
ligament space and lamina dura.
Fibrous healing (Figure5.17)
Radiological features
The classical periapical fibrous healing presents as a lucency
with a well‐defined relatively thick corticated border which is
sometimes irregular.
This may also present as a widened apical periodontal liga-
ment space. Classically, the lamina is thicker than is usually
seen and may be slightly irregular.
It is often difficult to definitively differentiate between peria-
pical fibrous healing and an inflammatory lesion and clinical
correlation is required.

66 Atlas of Oral and Maxillofacial Radiology
Periapical osseous prominence at themaxillary sinus
base (Figure5.15)
Occasionally, following extraction or endodontic manage-
ment, healing of a maxillary posterior periapical inflamma-
tory lesion or radicular cyst can result in the appearance of a
bony prominence at the sinus floor. This is related to osseous
infill of the previously elevated mucoperiosteal lining by the
inflammatory lesion (focal periostitis) or radicular cyst prior
to ‘collapse’ of this elevated mucoperiosteum.
Radiological features
When other opaque prominences at the maxillary sinus base
cannot be excluded with 2D radiography, MDCT or CBCT is
recommended.
Appearance of a bony prominence at the maxillary floor
centred at the apex of an endodontically treated root apex or
at an edentulous site corresponding with the previous site of
the apex of the extracted tooth.
This bony prominence is of variable size, morphology and
density.
Differential diagnosis
Key radiological differences
Any opaque
prominence at the
maxillary sinus base
may resemble
periapical osseous
healing
Examples include osteoma,
exostoses, septae at the sinus floor,
calcifications related to chronic
inflammatory sinus disease and
root remnants. Post‐treatment
periapical healing is usually centred
at an apical region (even if the
tooth has been extracted) and
internally demonstrates the
appearances of variable stages of
bone formation and remodelling.
These features are better demon-
strated with MDCT or CBCT.
Apical lucency with
effaced lamina dura
and surrounding
reactive sclerosis
Caries at the margins of
the restoration, which
probably involves the
pulp
Figure5.1 Periapical chronic inflammatory lesion: cropped panoramic radiograph.

Furcation hypodense inflammatory
lesion, probably centred bucally or
lingually (note the trabecular bone
projected over the lesion). This is
probably related to a lateral canal
at the furcation
Periapical hypodense inflammatory
lesion with effacement of the lamina
dura. This lesion is not completely lucent
in appearance, related to preservation of
trabecular bone buccal and/or lingual to
the lesion and also the mandibular cortices
Inflammatory widening
of the apical periodontal
ligament space, with early
effacement of the lamina dura
Reactive sclerosis
related to chronicity
Dressing and temporary
restoration related to
endodontic management
Figure5.2 Periapical and furcation inflammatory lesions: periapical radiograph. (Courtesy of Koong B. Diagnostic imaging of the periodontal and implant
patient. In: Lindhe J, Lang NP, editors. Clinical Periodontology and Implant Dentistry. 6th ed. Wiley Blackwell; 2015. Reproduced with permission from Wiley.)
Inflammatory lucency
centred at the apex of
a root with effacement
of the lamina dura.
Well-defined appearance
is related to chronicity
Inflammatory widened
apical periodontal ligament
spaces with preservation
of the lamina dura
Increased density
appearances adjacent to
the apical lesions reflect
reactive sclerosis, related
to chronicity
Essentially absent
crowns related to
large carious lesions
Figure5.3 Periapical inflammatory lesions of 35 and 36: corrected sagittal CBCT image.

68 Atlas of Oral and Maxillofacial Radiology
Lucent furcation
inflammatory lesion
Lucent periapical
inflammatory
lesions with
effacement of
the lamina dura
Substantial reactive sclerosis
involving most of the posterior
body of the mandible extending
to the inferior cortex, reflecting
the chronic nature of
the inflammatory lesions
Essentially absent
crowns of 47 and 48,
related to caries
Figure5.4 Chronic periapical and furcation inflammatory lesions of 48 and 47: cropped panoramic radiograph.
Inflammatory widened
apical periodontal
spaces of both roots,
with focal effacement
of the buccal cortex
over the lesion of
the buccal root
Figure5.5 Periapical inflammatory lesion (apical periodontitis) of 14: axial MDCT image.

Reactive
mucosal
thickening
Focal
periostitis
Periapical
inflammatory
lesion
Large lucent
carious
lesion
Figure5.7 Periapical inflammatory lesion of carious 27 with reactive changes at the maxillary antral base: cropped panoramic radiograph.
Inflammatory
widened apical
periodontal space
with adjacent
reactive sclerosis
Figure5.6 Periapical inflammatory lesion (apical periodontitis) of 13: corrected coronal CBCT image.
Apical lucent inflammatory
lesion. Associated focal
periostitis and effacement of
the sinus cortical floor with
reactive mucosal thickening
Apical root resorption
related to chronicity
Figure5.8 Periapical inflammatory lesion of 25: corrected sagittal CBCT image.

70 Atlas of Oral and Maxillofacial Radiology
Absence of the labial cortex
over the entire root, including
the root apex. Note that this is
essentially not appreciated on
the periapical radiographs
Hypodense focus identified in
(b) is non-specific in appearance,
although it reflects a part of
the bony lesion. Note that this
is not appreciated on
the periapical radiograph (a)
(a) (b) (c) (d)
11 21
11
Figure5.10
Labial perioendo lesion of 11: periapical radiographs (a,b) and surface‐rendered (c) and corrected sagittal (d) MDCT images.
Apical lucent inflammatory lesion of the distobuccal root,
with effacement of the lamina dura and also focal effacement of the
cortical floor of the right maxillary sinus. Note is made of the reactive
mucosal thickening. These findings are not appreciated on the
panoramic radiograph, related to projection of the inferior
cortex of the zygomatic process of the maxilla
(a)
(b)
Figure5.9 Periapical inflammatory lesion of 16: cropped panoramic radiograph (a) and coronal CBCT image (b).

Inflammatory widened
16 palatal root apical
periodontal ligament
space with associated
focal effacement of
the maxillary sinus
cortical floor
Almost fully opacified right
maxillary sinus with mucosal
thickening and air–fluid
meniscus
Opacified right
ethmoidal air cells
(a) (b)
(c)
Figure5.11 Palatal root apical inflammatory lesion of 16 with secondary right‐sided paranasal sinus inflammatory disease: coronal MDCT images (a–c).
Focal inflammatory lucent lesion centred
on the distal root surface with effacement
of the lamina dura, related to a lateral
canal. There is adjacent reactive sclerosis
related to chronicity
Lateral canal. Note that this is often
subresolution on CBCT and MDCT and
almost never demonstrated on plain 2D
radiography
Figure5.12 Inflammatory lesion of 35 related to a lateral canal: corrected sagittal CBCT image.

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Atlas of Oral and Maxillofacial Radiology, First Edition. Bernard Koong. © 2017 John Wiley & Sons Ltd. Published 2017 by John Wiley & Sons Ltd.645.1 Periapical inflammatory lesions (Figures5.1–5.17)• Synonyms: apical periodontitis, periapical rarefying osteitis, peri-apical condensing or sclerosing osteitis, periapical granuloma.• Periradicular inflammatory lesions related to pulpal pathology are mostly seen at the apical aspect of the tooth root(s), centred at the apical foramen, i.e. periapical inflammatory lesion. However, these lesions are sometimes centred upon the root surface away from the apical foramen, most of which are related to lateral canals and foramina (normal variant) or root fractures. The term osteomyelitis is reserved for more extensive infection of bone.• Clinical presentation varies substantially, from an asympto-matic low‐grade chronic picture to severe infections with substantial local and systemic manifestations.• Osteomyelitis (see section5.4), the radicular cyst (see Chapter8) and involvement of the soft tissues including cellulitis and abscess collections (see section5.5) are possible sequelae.Radiological features• Cone beam computed tomography (CBCT) and multidetector computed tomography (MDCT) are more sensitive for periapi-cal lesions than 2D intraoral and panoramic radiography although 2D radiography is usually the first modality of choice. Where indicated, soft tissue involvement is best examined with MDCT, often with intravenous contrast.• Magnetic resonance imaging (MRI) may be useful: ◦For identification of early lesions. ◦Where 2D radiography, MDCT and CBCT are equivocal and there remains clinical suspicion for periapical inflam-matory disease. ◦Where there are unusual symptoms.• It should be noted that, even when the clinical presentation is that of an acute periapical inflammatory lesion, it often reflects an acute phase of a chronic lesion (acute‐on‐chronic) and the bony changes seen radiologically reflect the chronic features. The acute features are often only demonstrated with multislice CT or MRI.• Early or lower grade lesions often present as widened apical periodontal ligament space with preservation of the lamina dura.• Very early or acute lesions may not demonstrate bony changes detectable with 2D radiography, CBCT or MDCT. MRI may demonstrate periapical inflammatory marrow oedema.• With some progression, it usually presents as a lucency or hypodense focus centred at the apex of a root with effacement of the lamina dura.• Sometimes, these lesions are centred elsewhere on the root surface, related to accessory lateral pulp canals and foramina (normal variant) or root fractures. Lateral canals and root fractures may not be radiologically detectable.• Margins can be ill defined or relatively well defined. ◦Many of these lesions identified radiologically are longstand-ing and are either acute‐on‐chronic or solely chronic in nature. Therefore, the margins are often relatively well defined. ◦More acute lesions tend to demonstrate less or poorly defined margins.• Adjacent reactive sclerosis is a common feature since many lesions demonstrated radiologically are chronic in nature. ◦The degree of sclerosis is variable. It can be focal and mild or dense, extensive and diffused, related to the degree of chronicity. ◦Occasionally, the sclerosis can be extremely focal and dense where the widened apical periodontal ligament space or small apical lucency is not apparent. Some refer to these as periapical condensing/sclerosing osteitis. However, MDCT and CBCT almost always demonstrate subtle widening of the periodontal space or a small periapical hypodense or lucent focus, which may not be appreciated on panoramic or periapical radiography.• Apical root resorption may be seen with chronic lesions.• The pulp chamber and root canals of the involved tooth may appear larger/wider than the contralateral tooth, related to arrested deposition of dentin.• Larger lesions may efface the jaw cortices.CHAPTER 5Inflammatory Lesions oftheJaws Inflammatory Lesions oftheJaws 65• There may be periosteal response (periosteal new bone formation).• Lesions approximating the maxillary antral bases: ◦Commonly stimulate variable reactive mucosal thickening at the antral floor. ◦Focal reactive periosteal response (focal periostitis) is also quite commonly seen, appearing as a dome‐shaped opaque lamina. ◦There may be focal effacement of the antral cortical floor, often not appreciated with 2D radiography. ◦Occasionally, there is variable inflammatory disease affecting the ipsilateral paranasal sinuses, secondary to the periapical inflammatory lesion. This is usually limited to the maxillary sinus. ◦These features are better appreciated with MDCT or CBCT. Differential diagnosisKey radiological differencesPeriapical osseous dysplasiaPresence of internal opaque deposits or homogeneous ‘ground‐glass’ appearance. Early lesions without internal opacities can appear similar to chronic periapical inflammatory lesions. Theperiapical osseous dysplasia is usually multiple. CBCT or MDCT is more sensitive in demonstrating subtle internal increased densities.Radicular cystIt can be difficult to differentiate from chronic periapical inflammatory lesions. The radicular cyst tends to demonstrate corticated borders although this may not be evident in early cystic change. Expansion and displacement of structures (e.g. mandibular canal) are cystic features. As a rule of thumb, lesions larger than 10 mm have been considered to be more likely to be radicular cysts but other features must be taken into account. CBCT/MDCT can better differentiate these lesions.Bone island May resemble the adjacent chronic reactive sclerosis but bone islands are usually well defined and homogeneous internally, isodense with cortical bone. In addition, there is almost always a periapical lucent/hypodense appear-ance or widening of the apical periodontal ligament space with apical inflammatory lesions.Fibrous healingPostendodontic therapy fibrous healing can appear similar and differentiation is often difficult. Fibrous healing tends to demonstrate a well‐defined thick cortex, which may be slightly irregular. CBCT and MDCT may better demonstrate these features and may also be used to evaluate the integrity of the endodontic treatment.Malignant lesionsDemonstrate aggressive borders. Metastatic and infiltrative malignant lesions often demonstrate other and/or adjacent lesions, e.g. periradicular lucencies elsewhere on the same or adjacent teeth, with absence of lamina dura.Osteomyelitis A periapical inflammatory lesion rarely progresses to osteomyelitis. Osteomyelitis involves a much larger region of bone and may not be centred upon the root apex. Sequestra and periosteal new bone formation are features of osteomyelitis.Post‐treatment appearances ofperiapical lesions (Figures5.15–5.17)After successful endodontic therapy or extraction, apical appearances include re‐establishment of normal periapical structures, variant trabecular architecture, fibrous healing and periapical osseous prominence at the maxillary sinus base, as follows.Re‐establishment ofnormal periapical structuresRadiological features• New bone formation begins at the periphery of the periapical lucency. This new bone is usually relatively homogeneous in appearance initially and eventually remodels.• Re‐establishment of the lamina dura and periodontal ligament space, if the tooth has not been extracted (i.e. endodontically treated).Variant trabecular architecture (Figure5.16)• Bony healing and remodelling following successful treatment may result in a trabecular appearance that is different from the trabecular bone typical of that region of the jaws.Radiological features• A variety of altered trabecular bone pattern is seen.• There is usually re‐establishment of normal periodontal ligament space and lamina dura.Fibrous healing (Figure5.17)Radiological features• The classical periapical fibrous healing presents as a lucency with a well‐defined relatively thick corticated border which is sometimes irregular.• This may also present as a widened apical periodontal liga-ment space. Classically, the lamina is thicker than is usually seen and may be slightly irregular.• It is often difficult to definitively differentiate between peria-pical fibrous healing and an inflammatory lesion and clinical correlation is required. 66 Atlas of Oral and Maxillofacial RadiologyPeriapical osseous prominence at themaxillary sinus base (Figure5.15)• Occasionally, following extraction or endodontic manage-ment, healing of a maxillary posterior periapical inflamma-tory lesion or radicular cyst can result in the appearance of a bony prominence at the sinus floor. This is related to osseous infill of the previously elevated mucoperiosteal lining by the inflammatory lesion (focal periostitis) or radicular cyst prior to ‘collapse’ of this elevated mucoperiosteum.Radiological features• When other opaque prominences at the maxillary sinus base cannot be excluded with 2D radiography, MDCT or CBCT is recommended.• Appearance of a bony prominence at the maxillary floor centred at the apex of an endodontically treated root apex or at an edentulous site corresponding with the previous site of the apex of the extracted tooth.• This bony prominence is of variable size, morphology and density.Differential diagnosisKey radiological differencesAny opaque prominence at the maxillary sinus base may resemble periapical osseous healingExamples include osteoma, exostoses, septae at the sinus floor, calcifications related to chronic inflammatory sinus disease and root remnants. Post‐treatment periapical healing is usually centred at an apical region (even if the tooth has been extracted) and internally demonstrates the appearances of variable stages of bone formation and remodelling. These features are better demon-strated with MDCT or CBCT.Apical lucency with effaced lamina duraand surrounding reactive sclerosis Caries at the margins ofthe restoration, which probably involves the pulp Figure5.1 Periapical chronic inflammatory lesion: cropped panoramic radiograph. Furcation hypodense inflammatorylesion, probably centred bucally orlingually (note the trabecular boneprojected over the lesion). This isprobably related to a lateral canalat the furcationPeriapical hypodense inflammatorylesion with effacement of the laminadura. This lesion is not completely lucentin appearance, related to preservation oftrabecular bone buccal and/or lingual tothe lesion and also the mandibular corticesInflammatory wideningof the apical periodontalligament space, with earlyeffacement of the lamina duraReactive sclerosisrelated to chronicityDressing and temporaryrestoration related toendodontic managementFigure5.2 Periapical and furcation inflammatory lesions: periapical radiograph. (Courtesy of Koong B. Diagnostic imaging of the periodontal and implant patient. In: Lindhe J, Lang NP, editors. Clinical Periodontology and Implant Dentistry. 6th ed. Wiley Blackwell; 2015. Reproduced with permission from Wiley.)Inflammatory lucency centred at the apex ofa root with effacementof the lamina dura.Well-defined appearanceis related to chronicity Inflammatory widenedapical periodontal ligamentspaces with preservationof the lamina dura Increased densityappearances adjacent tothe apical lesions reflectreactive sclerosis, relatedto chronicity Essentially absentcrowns related to large carious lesions Figure5.3 Periapical inflammatory lesions of 35 and 36: corrected sagittal CBCT image. 68 Atlas of Oral and Maxillofacial RadiologyLucent furcationinflammatory lesionLucent periapical inflammatorylesions witheffacement ofthe lamina duraSubstantial reactive sclerosisinvolving most of the posteriorbody of the mandible extending to the inferior cortex, reflectingthe chronic nature ofthe inflammatory lesionsEssentially absentcrowns of 47 and 48,related to cariesFigure5.4 Chronic periapical and furcation inflammatory lesions of 48 and 47: cropped panoramic radiograph.Inflammatory widenedapical periodontalspaces of both roots,with focal effacement of the buccal cortexover the lesion ofthe buccal root Figure5.5 Periapical inflammatory lesion (apical periodontitis) of 14: axial MDCT image. ReactivemucosalthickeningFocalperiostitis PeriapicalinflammatorylesionLarge lucentcariouslesionFigure5.7 Periapical inflammatory lesion of carious 27 with reactive changes at the maxillary antral base: cropped panoramic radiograph.Inflammatorywidened apicalperiodontal spacewith adjacentreactive sclerosis Figure5.6 Periapical inflammatory lesion (apical periodontitis) of 13: corrected coronal CBCT image.Apical lucent inflammatory lesion. Associated focal periostitis and effacement of the sinus cortical floor with reactive mucosal thickening Apical root resorptionrelated to chronicity Figure5.8 Periapical inflammatory lesion of 25: corrected sagittal CBCT image. 70 Atlas of Oral and Maxillofacial RadiologyAbsence of the labial cortex over the entire root, including the root apex. Note that this is essentially not appreciated on the periapical radiographs Hypodense focus identified in (b) is non-specific in appearance,although it reflects a part ofthe bony lesion. Note that thisis not appreciated onthe periapical radiograph (a) (a) (b) (c) (d)11 2111Figure5.10 Labial perioendo lesion of 11: periapical radiographs (a,b) and surface‐rendered (c) and corrected sagittal (d) MDCT images.Apical lucent inflammatory lesion of the distobuccal root,with effacement of the lamina dura and also focal effacement of the cortical floor of the right maxillary sinus. Note is made of the reactivemucosal thickening. These findings are not appreciated on thepanoramic radiograph, related to projection of the inferiorcortex of the zygomatic process of the maxilla (a)(b)Figure5.9 Periapical inflammatory lesion of 16: cropped panoramic radiograph (a) and coronal CBCT image (b). Inflammatory widened16 palatal root apicalperiodontal ligament space with associatedfocal effacement ofthe maxillary sinus cortical floor Almost fully opacified rightmaxillary sinus with mucosalthickening and air–fluidmeniscusOpacified right ethmoidal air cells (a) (b) (c)Figure5.11 Palatal root apical inflammatory lesion of 16 with secondary right‐sided paranasal sinus inflammatory disease: coronal MDCT images (a–c).Focal inflammatory lucent lesion centred on the distal root surface with effacement of the lamina dura, related to a lateral canal. There is adjacent reactive sclerosis related to chronicity Lateral canal. Note that this is often subresolution on CBCT and MDCT and almost never demonstrated on plain 2D radiography Figure5.12 Inflammatory lesion of 35 related to a lateral canal: corrected sagittal CBCT image. 72 Atlas of Oral and Maxillofacial RadiologyA palatally centred inflammatorylesion, with focal effacement of thelamina dura and adjacent reactivesclerosis. This is likely to berelated to a lateral canal,which is subresolutionFigure5.13 Endodontically treated 11 with ongoing chronic pain: corrected sagittal CBCT image.Hyperintense marrowoedema extending fromthe root apex to the inferioralveolar neurovascularbundle, which explainsthe lip numbnessRight and leftinferior alveolarneurovascularbundlesWidened apicalperiodontal ligamentspacesMandibularcanal(a) (b)Figure5.14 Apical inflammatory lesions (apical periodontitis) of 36. The patient presented with 36 pain and numbness of the lip: corrected sagittal and coronal MDCT images (a) and MRI coronal STIR image (b). Inflammatory Lesions oftheJaws 73Opaque bony prominence at the sinus floor related to postendodontic therapy healing of an apical inflammatory lesion Figure5.15 Postendodontic therapy healed apical lesion, 27: cropped panoramic radiograph.Postendodontic and apicectomy bony healing.Note the re-establishment of the periodontalligament space and lamina dura at the residualroot apex. The new bone demonstrates a variant architecture. This may resemble more ‘normal’trabecular bone after several years of remodellingbut may also remain different indefinitely Figure5.16 Postendodontic treatment and apicectomy: cropped periapical radiograph.Lucency with well-defined heavily corticatedborder which is irregular. Note that these featuresare not well identified on the panoramic radiograph (a) (b)Figure5.17 Postendodontic treatment apical fibrous healing: cropped panoramic radiograph (a) and axial CBCT image (b). 74 Atlas of Oral and Maxillofacial Radiology5.2 Periodontal inflammatory disease (Figures5.18–5.34)• Synonyms: periodontal disease, gum disease.• Bacterial dental plaque‐related inflammatory disease affecting the periodontium.• Much of the injury is a result of the host response to the bacteria. However, some bacteria can also directly cause injury to the periodontium, with the release of toxins.• Gingivitis refers to inflammation of the gingival tissues. Gingivitis precedes periodontitis but does not always progress to periodontitis.• Periodontitis generally refers to the condition where the plaque‐related inflammatory process affects the periodontal bone. The key clinical feature is periodontal pocket forma-tion, detected with a periodontal probe. Other features include bleeding, periodontal bone loss, tooth mobility and purulent exudates, depending on the severity of the disease.• There are several subtypes. More aggressive subtypes usually occur in younger patients (under 30 years).• Apart from the aggressive varieties, periodontal disease is mostly chronic in nature, with acute episodes. A cyclical pattern, with periods of quiescence and active inflamma-tion, is typical.• Increased incidence with age.• There are several factors which predispose or contribute to the progression of periodontal diseases. ◦Systemic factors including smoking, diabetes, some haema-tological diseases, some genetic/hereditary disorders and acquired immunodeficiency syndrome (AIDS). ◦Radiotherapy. ◦Xerostomia. ◦Local conditions which promote plaque formation. For example, overhangs, tooth crowding, dental calculus (calcified plaque), root fractures and dentures.Radiological features• General points: ◦Gingivitis is not radiologically detected. ◦Periodontal bone loss demonstrated at one radiological examination does not necessarily mean that there is ongoing active disease. That is, the bone loss may be related to previous disease activity where appropriate therapy has controlled the disease process. Clinical correlation is essential. ◦Imaging evidence of periodontal bone loss over a period of time probably reflects disease progression. ◦Following successful periodontal treatment and disease con-trol, there may be periodontal bone regeneration but this is usually not the case. Therefore, no evidence of periodontal bone changes in postperiodontal treatment imaging can be compatible with successful treatment. ◦MDCT and CBCT more accurately demonstrate the periodontal bone loss and morphology as well as the pres-ence of furcation and perioendo defects. 2D intraoral and panoramic radiography typically underestimates the severity of periodontal bone loss and may not demonstrate furcation and perioendo defects but may be sufficient. ◦The extent of periodontal bone loss including furcation and perioendo defects demonstrated radiologically may not correlate with the clinical findings (e.g. periodontal probing), related to: ■ Soft tissue attachment at the bony defects. ■ Difficult access to periodontal probing contributing to non‐detection of an existing defect.• Key radiological features ◦Lucent periodontal bone loss originates at the alveolar crest. The margins often appear relatively well defined as the peri-odontal bone loss is usually chronic in nature. Acute epi-sodes and more aggressive subtypes may demonstrate more ill‐defined margins. ◦Surrounding reactive sclerosis is usually a feature, related to the chronic nature of most cases. This sclerosis can be extensive, reflecting the degree of chronicity. This can persist, following successful treatment. ◦Can be focal, involving one or a few teeth, or generalised (widely distributed), involving most or all teeth. ◦Widened periodontal ligament spaces may reflect increased mobility of a tooth, related to loss of periodontal bone support. The widening can involve the entire root or be limited to the apical and cervical regions of the root. The lamina dura is some-times thickened. It should be noted that many other conditions, including increased occlusal loading, can contribute to this. ◦MRI may demonstrate marrow oedema.• Severity of periodontal bone loss. ◦More accurately demonstrated with MDCT and CBCT. ◦Normal: the periodontal alveolar crest is approximately 2–3 mm from the cementoenamel junction (CEJ). ◦Early bone loss includes: ■ Slight decrease in density and definition, blunting or loss of the alveolar crestal cortex. ■ Periodontal bone loss of up to 1 mm. ◦Moderate bone loss refers to periodontal bone loss of more than 1 mm, up to the midpoint of the root length. ◦Severe bone loss extends beyond the midroot or extends into a furcation.• Morphology of periodontal bone loss. ◦More accurately demonstrated with CBCT and MDCT than 2D intraoral and panoramic radiography. ◦Horizontal bone loss. ■ Bone loss between two teeth is parallel with the CEJ, usually involving multiple teeth. ◦Vertical (angular) defects. ■ Refers to a focal vertical or oblique defect centred upon one tooth more than the adjacent tooth (in Inflammatory Lesions oftheJaws 75 relation to the CEJs of these adjacent teeth). Multiple teeth may demonstrate angular defects. ■ Often not easily identified on 2D radiography when the buccal and/or lingual cortices remain preserved. Better demonstrated with CBCT/MDCT. ■ Clinical detection of narrow defects, especially interdental lesions, can be challenging. ■ Can be associated with a specific local contributing factor, such as a vertical root fracture or overhang. ◦Infrabony defect. Focal periodontal bone loss, classified by the number of preserved bony walls: ■ Three‐walled: usually, the buccal and lingual cortices and one proximal wall are preserved. ■ Two‐walled: usually, the buccal or lingual cortex is effaced. ■ Single‐walled: usually, both buccal and lingual cortices are effaced. Only the one proximal wall remains. ■ On 2D radiography, these appear as varying degrees of hypodense periodontal defects. Single‐walled defects usually appear more lucent and well defined. ◦Interdental crater defect. ■ Concaved crestal bone loss between two teeth with rela-tive preservation of the buccal and lingual cortices.• Furcation defects. ◦2D intraoral and panoramic radiography: ■ Classically a hypodense focus or lucency is seen at the furcation, with effacement of the lamina dura. The degree of decreased density appreciated is dependent upon theseverity, morphology, projection of the roots and the presence/absence of the adjacent buccal and lingual cortices. ■ The classical ‘J‐shaped’ lucency is sometimes seen. ■ Early furcation involvement usually presents as a widened furcation periodontal ligament space. ◦Bony furcation defects (especially maxillary molars) are often not appreciated with 2D radiography. MDCT and CBCT are much more accurate in identifying the presence, and in demonstrating the morphology, of thesedefects. In cases where the periodontal bone loss approaches the furca-tion regions, the presence of bony furcation defects cannot be fully excluded with 2D radiography. ◦May be related to pulpal pathology with accessory pulpal canals extending to the furcation. May also be related to iatrogenic perforation of the roots at the furcation.• Perioendo defect. ◦Lucent periodontal bone absence extending from the crestal bone to the apex of a tooth root. ◦Where there is severe periodontal bone loss, it is often difficult to identify the presence/absence of perioendo involvement on plain 2D imaging, related to the projection of the adjacent tooth and bony structures. ◦May reflect contiguity of periodontal and periapical inflammatory lesions, where both lesions essentially merge to form one larger lesion. These may be primarily related to periodontal inflammatory disease or pulpal pathology. ◦May be associated with a specific local contributing factor, for example a vertical root fracture.• Acute periodontal abscess. ◦These lesions are often an acute exacerbation of a chronic lesion. 2D radiography and CBCT usually onlydemon-strate the chronic bone defects. ◦Abscess or inflammatory infiltrate often drain via the peri-odontal defect into the oral cavity. However, these may occasionally extend into the adjacent soft tissues. In these cases, MDCT (with intravenous contrast) may demonstrate the cellulitis, collections and airway patency.• Severe inflammatory periodontal bone loss, including perioendo lesions, affecting the maxillary posterior teeth often induces a reactive mucosal thickening at the maxil-lary sinus bases (Figure 5.29; see also Figures 5.7–5.9). There may also be focal periosteal reaction (periostitis) at the sinus base, more often seen with perioendo lesions. Sometimes, there is associated focal effacement of the sinus floor. Not infrequently, there are variable degrees of ipsilateral paranasal sinus inflammatory disease secondary to severe periodontal defects, especially perioendo lesions (see also section5.1, Figure 5.11).• Related factors. There are many local factors which influence inflammatory periodontal disease that may be identified radiologically. ◦Dental calculus. ◦Dental restoration‐related factors including overhangs, mar-ginal deficiencies, incorrect contours and open contacts. ◦Caries at the cervical region of the tooth or involving the roots. ◦Root fractures. ◦Perforations related to endodontic therapy and post preparations.Differential diagnosisKey radiological differencesMalignant lesions Infiltrative and invasive margins.Langerhans cell histiocytosis Centred at the midroot.Benign tumours andcysts More well‐defined margins which may be corticated. Larger lesions may displace teeth and demonstrate expansion. 76 Atlas of Oral and Maxillofacial RadiologyOverhang of the amalgam restoration Moderate horizontalperiodontal bone loss Figure5.18 Moderate horizontal periodontal bone loss: periapical radiograph. (Courtesy of Koong B. Diagnostic imaging of the periodontal and implant patient. In: Lindhe J, Lang NP, editors. Clinical Periodontology and Implant Dentistry. 6th ed. Wiley Blackwell; 2015. Reproduced with permission from Wiley.)Widened periodontalligament space relatedto increased mobility Severe horizontalperiodontal bone loss Moderate horizontalperiodontal bone loss Figure5.19 Moderate to severe horizontal periodontal bone loss with increased mobility: periapical radiograph. (Courtesy of Koong B. Diagnostic imaging of the periodontal and implant patient. In: Lindhe J, Lang NP, editors. Clinical Periodontology and Implant Dentistry. 6th ed. Wiley Blackwell; 2015. Reproduced with permission from Wiley.)Absence of the crestalcortex suggests thatthe periodontal bone loss may be in anactive/progressivephase Figure5.20 Moderate horizontal periodontal bone loss: periapical radiograph. (Courtesy of Koong B. Diagnostic imaging of the periodontal and implant patient. In: Lindhe J, Lang NP, editors. Clinical Periodontology and Implant Dentistry. 6th ed. Wiley Blackwell; 2015. Reproduced with permission from Wiley.)Dental calculusdeposits Presence of the crestalcortex suggests thatthe periodontal bone loss may be in a stableor quiescent phase Figure5.21 Moderate horizontal periodontal bone loss and calculus deposits: periapical radiograph. (Courtesy of Koong B. Diagnostic imaging of the periodontal and implant patient. In: Lindhe J, Lang NP, editors. Clinical Periodontology and Implant Dentistry. 6th ed. Wiley Blackwell; 2015. Reproduced with permission from Wiley.) Inflammatory Lesions oftheJaws 77Severe mesialangular periodontal bone loss Furcation hypodenseappearances probably reflect bony furcationdefects Figure5.22 Moderate to severe periodontal bone loss with probable furcation defects: periapical radiograph.Focal narrow moderate angular periodontal defect. This would not be appreciated on an intraoral or panoramic radiograph (a) (b)Figure5.23 Focal moderate distal angular defect of 36, which is narrow buccolingually: axial (a) and corrected sagittal (b) MDCT images. (Courtesy of Koong B. Diagnostic imaging of the periodontal and implant patient. In: Lindhe J, Lang NP, editors. Clinical Periodontology and Implant Dentistry. 6th ed. Wiley Blackwell; 2015. Reproduced with permission from Wiley.) 78 Atlas of Oral and Maxillofacial RadiologyBitewing radiograph demonstrates a lucentfurcation defect which is not appreciatedon the periapical radiograph, related to thevariation in projection angle. This would beclearly demonstrated on CBCT or MDCTWell-defined horizontal bone loss between 36 and 37 seen in the bitewing appears as an ill-defined hypodense focus on the periapical view, raising the possibility of a crater defect,or that the bone loss is more severe buccallyor lingually, with absence of either cortex.This is related to the variation in the verticalprojection angle Distal overhang of the restoration of 35 is seenon the bitewing radiograph but is not appreciatedon the periapical radiograph, related to variation inthe projection angle(a)(b)Figure5.24 Severe periodontal bone loss of 36 with bony furcation defect. Horizontal bone loss elsewhere: bitewing (a) and periapical (b) radiographs. (Courtesy of Koong B. Diagnostic imaging of the periodontal and implant patient. In: Lindhe J, Lang NP, editors. Clinical Periodontology and Implant Dentistry. 6th ed. Wiley Blackwell; 2015. Reproduced with permission from Wiley.)‘J-shaped’ lucencysuggests a bony furcation defect Although less likely, a bonyfurcation defect cannot be fullyexcluded. CBCT or MDCT wouldclearly demonstrate the presenceor absence of a bonyfurcation defect Figure5.25 Appearances suggesting furcation defects: periapical radiograph. (Courtesy of Koong B. Diagnostic imaging of the periodontal and implant patient. In: Lindhe J, Lang NP, editors. Clinical Periodontology and Implant Dentistry. 6th ed. Wiley Blackwell; 2015. Reproduced with permission from Wiley.) Inflammatory Lesions oftheJaws 79The morphology and extent of this distal periodontal bony furcation defect is demonstrated J-shaped hypodense appearance raises the possibility of a bony furcationdefect, which is well demonstrated onthe MDCT image (a) (b)Figure5.26 Distal periodontal bony furcation involvement, 17: cropped panoramic radiograph (a) and axial MDCT image (b). (Courtesy of Koong B. Diagnostic imaging of the periodontal and implant patient. In: Lindhe J, Lang NP, editors. Clinical Periodontology and Implant Dentistry. 6th ed. Wiley Blackwell; 2015. Reproduced with permission from Wiley.)Appearance of the mesial angulardefect suggests a three-walled defectAppearance of this distalangular defect suggests a largelytwo-walled defect where theremay be a focal region superiorly(completely lucent), where itis single-walled. There is likely tobe a three-walled defect at theapical third of this root(hypodense defect) There is appearance of bone projectedover the apex but a perioendo defectcannot be fully excluded. Allthe defects seen in this view are betterdemonstrated on CBCT and MDCT Figure5.27 Angular periodontal bone loss with suspected perioendo defect of 33: periapical radiograph. (Courtesy of Koong B. Diagnostic imaging of the periodontal and implant patient. In: Lindhe J, Lang NP, editors. Clinical Periodontology and Implant Dentistry. 6th ed. Wiley Blackwell; 2015. Reproduced with permission from Wiley.) 80 Atlas of Oral and Maxillofacial RadiologyPerioendo defect is well demonstrated.A periapical or panoramic radiographwould probably project the residualcortical bone, especially the lingualcortex, over the apical third of theroot, which may be misinterpretedfor presence of periapical boneFigure5.28 Perioendo defect of 31: corrected sagittal (cross‐sectional) MDCT image.A lucent perioendo defectcentred palatally. This wouldnot be appreciated onpanoramic and intraoralradiography Reactive mucosalthickening Figure5.29 Perioendo lesion of 27: coronal CBCT image. Inflammatory Lesions oftheJaws 81Grade III bony furcation defect of 16 is well demonstratedHyperintense marrow oedema between 16 and 17 and at the furcation defect of16, related to inflammationLow to intermediate signalbetween 16 and 17 and at the furcation of 16 Bright normal fattymarrow interdentallyelsewhere(a) (b) (c)Figure5.30 Grade III bony furcation defect of 16: axial MDCT image (a), axial MRI STIR (b) and T1 (c) images. (Courtesy of Koong B. Diagnostic imaging of the periodontal and implant patient. In: Lindhe J, Lang NP, editors. Clinical Periodontology and Implant Dentistry. 6th ed. Wiley Blackwell; 2015. Reproduced with permission from Wiley.)Inflammatory vertical periodontaldefect associated with root fracture Narrow lucency reflectsroot fracture (a)(b)Figure5.31 Periodontal defect associated with root fracture of 25: corrected coronal (a) and sagittal (b) CBCT images. 82 Atlas of Oral and Maxillofacial RadiologyFocal buccal and distopalatal periodontal defects, highly likely to be associated with vertical root fracture which is subresolution. Note the substantial beam hardening artefact associated with the non-metallic obturation of this premolar, quite commonly seen with CBCT Figure5.33 Focal periodontal defects related to root fracture of endodontically treated 35: axial CBCT image. (Courtesy of Koong B. Diagnostic imaging of the periodontal and implant patient. In: Lindhe J, Lang NP, editors. Clinical Periodontology and Implant Dentistry. 6th ed. Wiley Blackwell; 2015. Reproduced with permission from Wiley.)Severe focal vertical periodontaldefect centred palatally. This ishighly suspicious for a verticalroot fracture which issubresolution. This would notbe appreciated on panoramicand intraoral radiographyFigure5.34 Focal vertical periodontal defect of endodontically treated 25: coronal CBCT image. (Courtesy of Koong B. Diagnostic imaging of the periodontal and implant patient. In: Lindhe J, Lang NP, editors. Clinical Periodontology and Implant Dentistry. 6th ed. Wiley Blackwell; 2015. Reproduced with permission from Wiley.)Focal buccal and lingual verticalperiodontal defects, typically seen inrelation to vertical root fractures Linear lucency reflectsthe root fracture (a)(b)Figure5.32 Endodontically treated 46 distal root fracture with periodontal bony defects: corrected coronal (a) and axial (b) CBCT image. Inflammatory Lesions oftheJaws 835.3 Pericoronitis (Figures5.35–5.39)• Inflammatory lesion involving the tissues adjacent to the crown of a partially erupted tooth.• Related to food debris and/or bacterial accumulations below the gingival/mucosal margins around the partially erupted tooth. This is often related to the patient’s inability to access and clean these regions.• Most commonly associated with the mandibular third molars.• Clinical presentation varies from the low‐grade subclinical chronic pericoronitis to severe pain and/or swelling, some-times with cellulitis. Symptomatic presentations are often acute‐on‐chronic in nature, although solely acute pericoroni-tis is sometimes seen.Radiological features• The radiological changes seen are often related to chronic pericoronitis.• Pericoronal reactive sclerosis is the most commonly seen radiological feature, which can be extensive depending on the degree of chronicity.• There may be slight widening of the pericoronal space. Themargins are often relatively well defined with adjacent reactive sclerosis, related to the chronic nature of most cases. More acute cases may demonstrate ill‐defined margins.• Periosteal new bone formation is seen in more severe cases.• Severe cases may result in cellulitis and abscess collections, which usually require further evaluation with MDCT (usually with intravenous contrast).Differential diagnosisKey radiological differencesAny condition causing an increase in pericoronal densityappearanceThese may resemble the reactive sclerosis associated with chronic pericoronitis.Dentigerous cyst Corticated border. Larger lesions are expansile.Pericoronalreactive sclerosisReactivesclerosisPericoronalhypodenseappearanceFigure5.35 Chronic pericoronitis related to 38 and 48: panoramic radiograph. 84 Atlas of Oral and Maxillofacial RadiologyWell-defined slightly widenedfollicular space with surroundingreactive sclerosis (a) (b)Figure5.37 Chronic pericoronitis related to 38: axial (a) and corrected sagittal (b) MDCT image.ReactivesclerosisSlightly widenedfollicular space Figure5.36 Chronic pericoronitis related to 38: axial CBCT image. Well-defined slightly widenedresidual distal follicular spacewith surrounding reactive sclerosis Reactivesclerosis(a) (b)Figure5.38 Chronic pericoronitis related to 38: cropped panoramic radiograph (a) and axial MDCT image (b).Reactivesclerosis Hypercementosis, notclearly demonstratedon the panoramicradiograph Focal distal root resorption of 47is not definitively demonstratedon the panoramic radiograph.Impacted third molar crowns areoften projected over the adjacentsecond molar on a panoramicradiograph withoutroot resorptionSevere distalangular periodontalbone loss of 47Caries (a)(b) (c) Figure5.39 Chronic pericoronitis related to 48 with periodontal bone loss and resorption of 47: cropped panoramic radiograph (a) and two corrected sagittal CBCT images (b,c). 86 Atlas of Oral and Maxillofacial Radiology5.4 Osteomyelitis ofthejaws (Figures5.40–5.42)• Infection and inflammation of the jaws with associated bone destruction.• There are various classifications. From a radiological perspec-tive, two broad groups can be considered: ◦Acute (suppurative, rarefying). ◦Chronic (non‐suppurative, sclerosing). Often demonstrates acute phases. Osteomyelitis present for more than 4 weeks is usually considered to be chronic.• More commonly seen in the mandible, especially posteriorly.• Symptoms vary: can be very severe in some acute cases and mild or even essentially asymptomatic in some chronic cases. Chronic cases usually exhibit acute phases.• Odontogenic and traumatic compound fracture microbial infections are the most common causes.• Some cases are presumed to be seeded from distant infection (haematogenous spread).• Occasionally, no infectious agent is identified and culture results are negative, especially in the chronic cases, where some may be related to chronic recurrent multifocal osteomy-elitis (CRMO).• Occasionally chronic osteomyelitis is related to SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis and osteomyelitis).Radiological features• MDCT usually demonstrates more features although CBCT may be sufficient in some cases. MDCT is the imaging modality of choice if there is clinically evident or suspected soft tissue involvement, and intravenous contrast should be considered. Insufficiently examined with 2D radiography. ◦Can be focal or extensive, involving large segments of thejaw. ◦Lucent destruction of bone, with ill‐defined borders in the acute cases and more well‐defined borders in chronic cases. The number of lucent foci can be few, even one, or extensive and scattered. ◦Early cases may demonstrate a hypodense appearance of the trabeculae. ◦Adjacent sclerosis is seen in time. Can be extensive, related to the degree of chronicity. Chronic cases often demon-strate a segment of sclerotic bone with varying degrees of multifocal lucent bony destruction. ◦Sequestra formation is a key feature. ◦Focal destruction of cortices is often seen. ◦Periosteal response (periosteal new bone formation) is also a common feature. Can be exuberant, especially in the younger patient.• MRI may be useful. May demonstrate the presence of active inflammation not identified on MDCT: ◦Decreased T1 signal and increased T2 and short T1 inver-sion recovery (STIR) signal related to marrow oedema. Gadolinium contrast enhancement of the marrow and often the adjacent soft tissues. ◦Sequestra demonstrate low T1, T2 and STIR signal.• Nuclear medicine studies are occasionally employed.Differential diagnosisKey radiological differencesFibrous dysplasia Can resemble chronic osteomyelitis although sequestra and periosteal response are not seen in this condition.Malignant lesions Differentiation can sometimes be difficult. Bony destruction by some malignant tumours may leave residual bone that resembles sequestra. Some malignancies stimulate sclerosis in the adjacent bone and others stimulate periosteal response. Secondary infection of a malignant lesion should also be considered. Malignant lesions usually demonstrate more aggressive bone destruction. Aggressive destruc-tion of periosteal new bone formation is a malignant feature.Paget disease Usually involves the entire mandible. Sequestra and periosteal response are not seen. SequestrumPeriosteal response (a) (b)Inflammatory soft tissue thickening (c) Figure5.40 Right mandibular body osteomyelitis: MDCT axial and corrected coronal bone (a,b) and axial soft tissue (c) MDCT images.Laminated periosteal response Multiple lucent foci in a sclerotic background,not as well appreciated on the panoramic radiograph (a) (b)Figure5.41 Left mandibular body chronic osteomyelitis with a few acute episodes: axial MDCT image (a) and cropped panoramic radiograph (b). 88 Atlas of Oral and Maxillofacial Radiology5.5 Dentoalveolar andjaw infections involving theadjacent soft tissues (Figures5.43–5.46)• The extent of soft tissue involvement from dentoalveolar and jaw infections varies substantially. This can range from: ◦A small soft tissue inflammatory focus over the effaced cortex, where it may or may not be draining through the mucosa into the oral cavity.to: ◦Cellulitis and abscess collection, which may be life threat-ening. This may be superficial and may drain at the skin surface. It may involve various spaces, including the submandibular, sublingual, masticator, parapharyngeal and parotid spaces. Potential complications include airway compromise, cavernous sinus thrombosis, cerebral abscess, orbital infections and mediastinitis.• For the acutely infected sick patient, the imaging should be performed as efficiently as possible and the findings reported to the appropriate clinician immediately.• Abscess collections usually require surgical drainage.• Obviously, paragnathic soft tissue infections may be unrelated to the teeth and jaws, for example dermal and salivary gland infections.Radiological features• This section is limited to describing the soft tissue involve-ment (from dentoalveolar infections and osteomyelitis) in the region adjacent to the jaws.• Where there is more than minor soft tissue involvement or if there is suspicion for cellulitis or abscess collection related to a dentoalveolar infection or osteomyelitis, MDCT with intravenous contrast is the first modality of choice. CBCT is insufficient. While MRI may be useful in some cases, it is less sensitive in demonstrating the dentoalveolar and jaw changes.• Postintravenous contrast MDCT features include: ◦Thickening of the skin and subcutaneous fat stranding or streaking (linear densities). ◦Fat planes often demonstrate increased density ‘dirty’ appearances representing the inflammatory infiltrate. ◦Involved muscles are swollen and enhanced. ◦Abscess collection presents as a spherical or lobulated fluid density focus with rim enhancement. ◦Naturally, if this originates from the teeth and jaws, it should also be radiologically demonstrated (refer to sections 5.1–5.4).Generalised sclerosis of the right hemimandibleand much of the left bodyof the mandible withmultiple lucent fociPeriostealresponse Figure5.42 Chronic osteomyelitis right mandible: axial MDCT image. Inflammatory focal effacement of the lingualcortex over the apical third of the 37 distal root.The periodontal ligament space is otherwise essentially normal as the inflammatoryinfiltrate extends into the submandibular space Inflammatory infiltrate extends from the 37 distal root lesion into the submandibular space (a) (b) Figure5.43 Submandibular space cellulitis related to an inflammatory lesion of 37 distal root: axial bone (a) and soft tissue (b) MDCT images.Inflammatory soft tissuethickening over the 46mesial root withenhancement(d)Vertical buccal periodontal/corticaldefect over the 46mesial root. This is most likely related to a root fracture, which issubresolution (a)(b)Inflammatory infiltratewithin the submandibularspace (c)Figure5.44 Buccal inflammatory lesion of endodontically treated 46 mesial root with soft tissue involvement: postintravenous contrast corrected coronal and axial bone (a,b) and coronal and axial soft tissue (c,d) MDCT images. 90 Atlas of Oral and Maxillofacial RadiologyFocal buccal cortical fenestration over the 14 buccal root apex. The periapical appearances are otherwise within normal limits Inflammatory fatstrandingInflammatory soft tissue thickeningcentred over 14 identifies the offendingtooth. This is not appreciated on the boneMDCT image nor on the panoramicradiograph. This would probably not bedemonstrated on CBCT(a)(b) (c) Figure5.45 Facial cellulitis related to endodontically treated 14 buccal root. The offending tooth could not be clinically identified: cropped panoramic radiograph (a) and axial bone (b) and soft tissue (c) MDCT images. Inflammatory Lesions oftheJaws 91Fluid-attenuating abscess collection with rim enhancement. Note the effacement of the adjacentfat planes This acute pericoronitis with substantial soft tissue involvement is not appreciated on thebone MDCT image. This would also not beappreciated on a CBCT scan nor on 2Dradiography (a) (b)(c)Figure5.46 Left masticator space cellulitis with collection arising from acute pericoronitis related to impacted 38: postintravenous contrast coronal and axial soft tissue (a,b) and axial bone (c) MDCT images.

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