DENTAL CARIES Epidemiology Clinical Types Enamel Caries Dentin Caries PULPITIS Reversible Pulpitis Irreversible Pulpitis Pulpal Necrosis Common Diagnostic Techniques History and Nature of Pain Reaction to Thermal Changes Reaction to Electrical Stimulation Reaction to Tooth Percussion Radiographic Examination Visual Clinical Examination Palpation of Surrounding Area Histopathology of Pulpal Disease Acute Pulpitis Chronic Pulpitis Chronic Hyperplastic Pulpitis PERIAPICAL LESIONS Chronic Apical Periodontitis Periapical Granuloma Periapical Cyst ACUTE PERIAPICAL CONDITION Periapical Abscess OSTEOMYELITIS Acute Osteomyelitis Cellulitis Chronic Osteomyelitis Garré Osteomyelitis

1. Infections of Teeth and Bone
Sana Rasheed
Akhtar Saeed Medical and Dental College, Lahore, Pakistan.

2. Dental Caries
Definition
Dental caries is a multifaceted disease involving interplay
among the teeth, the oral host factors of saliva and
microflora, and the external factor of diet.
Bacteria accumulate on the enamel surface, where they
elaborate acidic and proteolytic products that demineralize
the surface and digest its organic matrix.
Although dental
caries is restricted to the hard tissue of the
enamel, dentin, and cementum,
if left untreated, the process will
ultimately penetrate through the pulpal
canal beyond the tooth into the adjacent
soft tissue, where it will initiate
a painful and destructive inflammatory
reaction.
In this location it may spread into the
marrow spaces of the bone and possibly
the soft tissues and muscles of
the face and neck.

3. • Streptococci are essential
for development of caries,
particularly of smooth
(interstitial) surfaces.
• These are viridans
streptococci which are a
heterogeneous group
including
• Streptococcus mutans,
• S. sobrinus,
• S. salivarius,
• S. mitior
• S. sanguis

8. EPIDEMIOLOGY
• The caries activity in a particular society or
geographic area is closely correlated with the
amount of sugar consumed per capita.
• In the more industrialized countries, where
diets have traditionally had a high content of
refined carbohydrates, the caries rate has
been considerably higher than in less-
developed countries.
• In the very young, when diets are high in
sucrose and without adequate preventative
practices, the pits and fissures of the first
molars commonly become involved with
caries within the first 3 years after eruption.
• The second molars have the next highest
susceptibility, followed by the second
premolars.
• First the interproximal surfaces become
involved, followed by the buccal and lingual
surfaces.
1st molars 2nd molars
2nd
premolars
Interproximal
surfaces
Buccal and
lingual
surfaces
Smooth
surfaces of
Anterior teeth

9. CLINICAL TYPES

11. Pit and fissure caries
• most common type
• appear at an early age
• occlusal and buccal
surfaces of the molars of
the primary and
secondary dentition
This form of caries is the most destructive, because it
quickly goes deeply into the dentin, remains hidden
as it undermines the enamel, and becomes clinically
evident as
pain caused by pulpal involvement or as a large cavity
when a substantial portion of the tooth crumbles.

12. Smooth-surface caries

13. • less common
• occurs on the interproximal
(contact) areas of the teeth,
cervical regions of the buccal
and lingual surfaces of the
teeth
• In adults, smooth-surface
cervical caries is usually the
result of a major alteration in
the quantity or quality of the
saliva.
• Reasons: radiation therapy,
medications, autoimmune
diseases
Baby bottle caries : When caries is present on the labial surfaces of the
primary teeth of infants, it is nearly always caused by a habit of leaving the
feeding bottle containing milk or juice in the infant’s mouth when sleeping

14. Cemental (root) caries
• found in the older population, due to gingival recession

15. • Recurrent caries
• caries that arises around an
existing restoration
• results in marginal “ditching” or
or leakage
• Progress at variable rates,
depending on the extent of
sclerosis of the adjacent dentin
and the patient’s diet and oral
hygiene habits
Acute (rampant) caries and chronic caries
• Young patients are most susceptible to acute or
rampant caries, because they have teeth with large
pulpal chambers and wide and short dentinal tubules
containing little or no sclerosis.
• this is often combined with a diet high in refined
carbohydrates and less-than-adequate oral hygiene
They are capable of simultaneously developing multiple
rapidly advancing carious lesions that quickly destroy
tooth structure, penetrate into the pulp, and elicit severe
pain.
Chronic caries is most common in older
patients whose teeth have smaller pulpal chambers,
usually with additional deposits of a denser and less tubular dentin on the pulpal walls, referred to as tertiary
or secondary dentin. Additionally they have dentinal
tubules that have undergone significant degrees of sclerosis,
which offers some degree of resistance to the progression
of the carious process

16. ENAMEL CARIES

17. • This process of enamel caries is a
dynamic one and, initially at least,
consists of alternating phases of
demineralisation and remineralisation,
rather than a continuous process of
dissolution.
• Alteration occurs in the loss and
redeposition of mineralizing salts that is
caused by fluctuations in the pH in that
particular location.
In some situations
if the pH can be stabilized in its normal
range, the whole process may stop or
even reverse, which is referred
to as arrested caries.
Arrested caries may also occur
when
• an adjacent tooth is extracted or
• when an undermined cusp fractures
off, making the carious area self-
cleansing
• Improved oral hygiene

18. • Four zones can be identified
• (1) translucent zone, the
advancing front of initial
demineralization;
• (2) dark zone, where the
previously liberated salts are
redeposited;
• (3) body of lesion, containing
the region of maximal
demineralization; and
• (4) surface zone, remaining
relatively unaffected until it is
sufficiently undermined to
collapse, resulting in
cavitation.

19. The early lesion
• The earliest visible changes are seen as a white opaque spot that
forms just adjacent to a contact point.
• The enamel is hard and smooth to the probe.
• The initial lesion is conical in shape with its apex towards the dentine,
and a series of four zones of differing translucency can be seen.

22. There is no more than a pinhole lesion in an occlusal pit, but cutting away
the surrounding enamel shows it to be widely undermined?
• Once bacteria have penetrated the enamel they reach the amelodentinal junction
and spread laterally to undermine the enamel.
• This has three major effects.
• 1. The enamel loses the support of the dentine and is therefore greatly
weakened.
• 2. It is attacked from beneath.
• 3. Spread of bacteria along the amelodentinal junction allows them to attack the
dentine over a wide area.

23. DENTIN CARIES

24. • The lesion is therefore conical with its apex towards the pulp.
• Dentin caries progresses at a much faster rate than enamel caries.
• It is more porous, because it contains dentinal tubules and is less
densely mineralized.
• For caries to progress in dentin, bacterial strains capable of producing
large amounts of proteolytic and hydrolytic enzymes are needed,
rather than the acid-producing types of enamel caries. Lactobacilli
may be important in dentine caries.

25. • Collections of bacteria in adjacent tubules coalesce to form irregular
liquefaction foci. These in turn coalesce to form progressively more
widespread tissue destruction.
• In some areas bacteria also spread laterally, and, occasionally, large
bacteria-filled clefts form at right angles to the general direction of
the tubules.

26. Why does dentin caries has a rapid course
and more pain in young patients?
• In the teeth of younger patients the dentinal
tubules are less densely mineralized,
• shorter in length, and
• wider in diameter, allowing for ease of penetration
and progression of the invading microorganisms.
• In older patients, deposits of calcifying salts
usually narrow the dentinal tubules, making the
teeth less porous. In addition,
• the dentin will be thicker because of the
production of additional normal and abnormal
secondary dentin on the pulpal walls.
Dentinal caries in younger patients
often quickly involves the pulpal
tissue, which produces an acute
inflammatory reaction and intense
pain.
in older patients it
has a slower course with intermittent
mild pain

27. HISTOPATHOLOGY
• Five microscopic zones that reveal the stages of dentinal caries that
eventuates in a cavity:
Zone 1, fatty degeneration :
The deepest zone, reflects the earliest changes of caries
infection where bacterial enzymes have advanced ahead
of the bacteria in the dentinal tubules, causing a
breakdown of the cell membranes of the organic
component of the dentin-liberating lipid.
Zone 2, translucent zone :
is a band of hypermineralized dentin in which the
dentinal tubules are sclerotic because of the
redeposition of calcifying salts released from the
demineralized zone.
Zone 3,
demineralization:
is composed of dentin
that is softer than
normal because of the
initial action of the
bacterial enzymes
Zone 4, brown
discoloration :
is due to a reduction in the
mineral content and the presence
of distended dentinal tubules
packed with bacteria. This zone is
usually soft enough to be
removed with a hand instrument.
Zone 5, cavitation :
Differs from the previous zone, because no
mineralization is present and the organic component
is partially dissolved by the bacteria. This zone is the
clinically observed base of a large cavity. It also has a
brown coloration and easily peels away in layers
along the incremental lines of growth.

29. • In Zone 5 the tubules
will contain focal, dense
accumulations of
bacteria that form
liquefaction foci,
referred to as beading
(Figure 3-12, A). These
foci fuse horizontally,
producing transverse
clefts.
a large area of liquefaction of dentin caused by the
horizontal fusion of the focal accumulations
of bacteria within individual tubules (“transverse clefts”)

30. PULPITIS
An inflammation of the pulpal tissue that
may be acute or chronic, with or without symptoms, and
reversible or irreversible.

31. Acute pulpitis
• In the early stages the tooth is hypersensitive.
Very cold or hot food causes a stab of pain
which stops as soon as the irritant is removed.
As inflammation progresses, pain becomes
more persistent and there may be prolonged
attacks of toothache.
• The pain may start spontaneously, often when
the patient is trying to get to sleep.
• The pain is partly due to the pressure on the
irritated nerve endings by inflammatory
infiltrate within the rigid pulp chamber and
partly due to release of pain-producing
substances from the damaged tissue. The pain
at its worst is excruciatingly severe, sharp and
stabbing in character. It is little affected by
simple analgesics.
Acute pulpitis may be confined to one horn of the
coronal pulp (focal acute pulpitis) or involve the whole
pulp (total acute pulpitis).
 most commonly found in the teeth of children and
adolescents.
 The exudate remains within the enclosed chamber,
builds pressure, and quickly extends to all parts of
the healthy pulp.
 An acute pulpitis can arise when the pulp becomes
suddenly overheated to the extent that the blood
vessels rupture, causing focal areas of hemorrhage.
 This may occur during crown preparation, when
inadequate cooling does not accompany the high-
speed removal of the tooth structure.

33. Acute closed pulpitis
• There is initial hyperaemia limited to the area immediately beneath
the irritant.
• Infiltration by inflammatory cells and destruction of odontoblasts and
adjacent mesenchyme follow.
• A limited areas of necrosis may result in formation of a minute
abscess, localised by granulation tissue.
• Inflammation spreads until the pulp is obliterated by dilated blood
vessels and acute inflammatory cells.
• Necrosis follows.

34. Pulpal abscess
• The core is composed of a purulent exudate consisting of polymorphonuclear leukocytes
against a background of fibrin, necrotic tissue debris, and extravasated red blood cells.
• A zone of granulation tissue consisting of newly formed capillary blood vessels, plump
fibroblasts, plasma cells, and lymphocytes surrounds this core.
The liberated autolytic
enzymes that result
from tissue destruction
and the exotoxins of the
invading bacteria quickly
spread to all parts of the
remaining healthy pulp
and eventually through
the apical foramen into
the adjacent periodontal
membrane.
Because of the
intenseness of the irritant
in the
form of virulent bacteria
and the lack of drainage
Purulent exudate
penetrates the cortical
bone surrounding
the apical periodontal
membrane and invades
the marrow
spaces of the medullary
bone
At this point the condition
represents a form of focal
acute suppurative
osteomyelitis.

35. Chronic pulpitis
• The pulps of individual teeth are not
precisely represented on the sensory
cortex.
• The pulp pain is therefore poorly
localized and may be felt in any of the
teeth of the upper or lower jaw of
the affected side. Rarely, pain may be
referred to a more distant site such
as the ear.
• Pulp pain is not provoked by pressure
on the tooth.
• Many pulps under large carious
cavities die painlessly.
• In other cases there are bouts of dull
pain, brought on by hot or cold
stimuli or coming on spontaneously.
There are often prolonged
remissions.
 Chronic pulpitis occurs when there is little or no penetration into the
pulp by large numbers of the virulent types of bacteria.
 Occurs often in older teeth, because they have restorations done or
sclerosis or reparative dentin.
 On microscope: (Pulp fibrosis) presence of loose, delicate
connective tissue with bundles of dense collagen and a severe
reduction in both the size and number of the vascular structures and
peripheral nerves. A diffuse infiltrate of lymphocytes and plasma
cells exists throughout the pulp.
Pulp fibrosis pulp stones (spherical calcifications) or dystrophic
calcifications (linear calcifications) pulpal necrosis periapical
granuloma.
Periapical granuloma : indolent and asymptomatic, and it is composed
of a circumscribed nodule of fibrous tissue with a
mild infiltrate of lymphocytes and plasma cells.

37. Chronic closed pulpitis
• Mononuclear cell infiltrate.
• A small area of pulpal necrosis and pus formation may be localised by
a well-defined wall of granulation tissue, and a minute abscess may
form.
• The remainder of the pulp may then appear normal.
• Partial calcific barrier forms beneath the lesion.
• Or reactionary dentine continue to form round the opening.
• This may allow preservation of the remainder of the pulp.
• Pulp death is the end result.

40. Open pulpitis
• The pulp survives but is chronically inflamed, beneath a wide
exposure, despite the heavy infection.
• Associated with open apices which allow an adequate blood supply.

41. Chronic Hyperplastic Pulpitis

42. • Chronic hyperplastic pulpitis
• a rare condition that is primarily confined
to the molars of children. result of
rampant acute caries in young teeth.
• The combination of an open chronic
pulpitis, an ample blood supply, and the
increased regenerative capacity of young
pulpal tissue appear, in some instances, to
stimulate the pulpal tissue to proliferate or
to produce granulation tissue.
• a surface layer of stratified squamous
epithelium.
• pulpal tissue may undergo excessive
overgrowth (hyperplasia) and project out
of the crown of the tooth.
Because this lesion clinically
projects from the pulpal chamber, it is
commonly referred to as a pulp polyp.
 Clinically, a pulp polyp appears as a
dusky red or pinkish soft nodule
protruding into the cavity. It is
painless but may be tender and bleed
on probing
 These lesions produce no symptoms
because they are said to be deficient
in nerve fibers.
The usual treatment of a tooth with a
pulp polyp is extraction.

44. REVERSIBLE PULPITIS
The diagnosis of reversible pulpitis implies that the pulp is
capable of a full recovery if the irritating factors subside or are
removed.
Vasodilation, some transudation, a slight infiltrate of
lymphocytes, and disruption of the odontoblastic layer.
The pain of reversible pulpitis is sharp and intense and
responds to a sudden change in temperature.
 The pain generally remains for 5 to 10 minutes and seldom lasts
longer than 20 minutes.
 Changes in the position of the body, such as lying down, do not
generally affect the nature or the duration of the pain.
 Treatment: prevention from further thermal stimulation, and
placing sedative dressings in the base of carious defect.

46. IRREVERSIBLE PULPITIS
Pulp will most likely not recover
The pulpal tissue will exhibit a wide spectrum of acute
and chronic inflammatory changes.
The remaining pulp must be removed or the tooth
must be extracted.
Pain is less intense.
Pain is spontaneously initiated, not the result of a
sudden temperature changes.
It lasts for a prolonged period, usually longer than 20
minutes.
The pain may be initiated or accentuated when the
patient reclines.
The pain from an irreversible pulpitis may be referred
to another nearby location

48. PULPAL NECROSIS
• In pulpal necrosis the pulpal tissue may be infected with bacteria.
Infected pulpal necrosis is usually the result of dental decay, in which
case the infection can quickly extend into the apical areas of the tooth
and the surrounding bone. These occurrences produce a great deal of
pain and other systemic reactions.
• Noninfected (aseptic) pulpal necrosis usually occurs after a traumatic
incident and may not produce symptoms for many months. The first
sign of noninfected pulpal necrosis may be a change in the coloration
of the tooth.

49. • Change in tooth color due to pulpal necrosis:
• This is the result of the decomposing tissue debris and breakdown
products of the red blood cells entering the open ends of the empty
dentinal tubules and becoming distributed throughout the dentin.
This process alters the translucency of the tooth. After the tooth has
become nonvital, it loses its ability to rehydrate the dentin, making it
more brittle and subject to cracks and fractures.

50. • Pain due to inflammatory
response in the apical periodontal
membrane.
• Tooth may extrude from the
socket causing premature contact
with opposing teeth.
A diagnostic tool used to
determine if a tooth has
undergone pulpal necrosis
consists of gently tapping on
several teeth in the area with
a blunt instrument.
A tooth that has undergone
pulpal necrosis will be
identified, because the
pressure from the tapping will
produce intense pain. This is
referred to as the percussion
test.

51. COMMON DIAGNOSTIC TECHNIQUES
• The diagnostic procedures that are commonly used to assess the
status of a symptomatic tooth and pulp are as follows:
• 1. History and nature of pain
• 2. Reaction to thermal changes
• 3. Reaction to mild electric stimulation
• 4. Reaction to tooth percussion
• 5. Radiographic examination
• 6. Visual clinical examination
• 7. Palpation of surrounding area

52. PERIAPICAL LESIONS

53. The four major factors follow:
• 1. Presence of an open or
closed pulpitis
• 2. Virulence of the involved
microorganisms
• 3. Extent of sclerosis of the
dentinal tubules
• 4. Competency of the host
immune response

54. CHRONIC APICAL PERIODONTITIS
Extension of the inflammatory process from the pulpal chamber into
the adjacent periodontal membrane around the apical foramen.
A positive reaction to a percussion test.
A transitory phase between pulpitis and the more distinct forms of
periapical lesions.

55. PERIAPICAL GRANULOMA
a pulpitis progresses into a
periapical lesion, pulpal
necrosis
drainage of the exudate is
inhibited, a
periapical granuloma can
be transformed into an
acute
periapical abscess
transformation into a
periapical cyst

56. RADIOGRAPHIC
FEATURES
• An oval or rounded
radiolucency with a
welldemarcated outline located
at the apex of the tooth.
• Possible findings:
hypercementosis of the apical
third of the root and
• resorption resulting in blunting
of the root tip.

57. HISTOPATHOLOGY
• an outer capsule of dense
fibrous tissue and a central
zone of granulation tissue.
• The central zone will often
contain macrophages with a
foamy cytoplasm caused by
phagocytized cholesterol.
• Some cholesterol crystals
may be present, surrounded
by multinucleated giant cells.
• Throughout, the soft tissue
will be a diffuse infiltrate of
lymphocytes and plasma
cells.

58. PERIAPICAL CYST
• Develops from untreated granuloma.
• The cyst’s epithelial lining is derived from the rests of Malassez.
• The rests are stimulated to proliferate by the low-grade inflammation
of the preceding periapical granuloma.
• The cyst may become inflamed and symptomatic.
• It can result in the destruction of a large portion of the maxilla or
mandible.

59. RADIOGRAPHIC FEATURES
• The periapical cyst is well circumscribed, often with a
distinct thin line of cortication separating it from the
surrounding bone.
• It may be associated with resorption of the apices of the
teeth, displacement of the roots, or both.
• It is distinctly rounded and unilocular and may become
very large, resulting in erosion of the inferior border and
bulging of the buccal and lingual cortical plates.

61. HISTOPATHOLOGY
• Outer dense fibrous connective tissue capsule that
surrounds a central lumen containing a thick,
proteinaceous fluid and cellular debris.
• The lumen is lined by a nonkeratinized, stratified
squamous epithelium containing rete pegs that are
generally elongated and branched.
• Collections of cholesterol-laden macrophages are
commonly present.
• A diffuse infiltration of plasma cells and lymphocytes in
capsule and epithelial lining.
• Cholesterol crystals surrounded by foreign-body giant
cells.
• The presence of eosinophilic refractile hyaline bodies,

64. ACUTE PERIAPICAL CONDITIONS

65. • The factors leading to the development of acute lesions at the apex
of a tooth:
• 1. Young tooth with open tubules
• 2. Rampant caries
• 3. Closed acute pulpitis
• 4. Presence of highly virulent microorganisms
• 5. Weakened host defense system

66. Inflammatory events happen quickly and
cause a great deal of pain
If unchecked, infection and
purulent exudate rapidly
spread throughout the
affected jaw into the
adjacent structures and
the systemic circulation
Emboli of the infection
could lodge in the small
capillaries of a number of
distant organs or anatomic
locations

67. PERIAPICAL ABSCESS
• It is a progression of an
acute pulpitis in which
exudate extends into the
adjacent soft and hard
tissues.
• Internal pressure causes
extrusion of the tooth from
the socket and rapid
extension of the exudate
throughout the underlying
medullary bone.
CLINICAL FEATURES
 Pain, Temperature elevation and malaise are common.
 The tooth associated with the abscess will extrude from
the socket.
 Swelling and redness of the area
 Although the tooth is relatively insensitive or
unresponsive to hot, cold, and electrical stimulation,
gently tapping on it produces intense pain.
 Percussion test for diagnosis.

68. RADIOGRAPHIC FEATURES
• A slight widening of the apical periodontal space, with a gradual loss
of the distinctness of the adjacent alveolar bone (lamina dura).
• bone loss by exhibiting a faintness of the trabecular pattern and an
increased radiolucency.

69. HISTOPATHOLOGY
• An outer thin capsule of fibrous tissue is infiltrated with lymphocytes
and plasma cells.
• A wide zone of granulation tissue,
• containing a mixture of neutrophils, lymphocytes, plasma cells, and
macrophages,
• surrounds a
• central core of tissue that has undergone disintegration and
liquefaction and is composed of purulent exudate.

70. OSTEOMYELITIS
• An inflammatory
process within
medullary (trabecular)
bone that involves the
marrow spaces.
ACUTE OSTEOMYELITIS: A rapidly
destructive inflammatory
process within bone that consists of
granulation tissue,
purulent exudate, and islands of
nonvital bone (sequestra).

71. ACUTE OSTEOMYELITIS
• Acute osteomyelitis is a destructive lesion of the trabecular bone and
bone marrow of an acute inflammatory origin and usually contains
virulent strains of bacteria.
• Causes:
an untreated periapical abscess
osteoradionecrosis

72. CLINICAL FEATURES
intense pain and physical
illness.
a lack of drainage of
purulent exudate produces
a rapid increase in pain
with accompanying pyrexia
and malaise.
an alteration in the
conductivity of the inferior
alveolar nerve.
paresthesia of the lower lip
of the affected side.

73. RADIOGRAPHIC FEATURES
Initially the area is faintly visible and
eventually appears diffusely blotchy or
mottled with indistinct margins.
Islands of apparently intact bone are
often visible in central locations.
In reality, these fragments are dead,
nonresorbed bone surrounded by
wide zones of purulent exudate. An
island of dead bone is referred to as a
sequestrum.

74. CELLULITIS: A painful swelling of the
soft tissue of the mouth and face
resulting from a diffuse spreading of
purulent exudate along the fascial
planes that separate the muscle
bundles.
SINUS TRACT: A drainage pathway
from a deep focus
of acute infection through tissue,
bone, or both to an
opening on the surface.
PARULIS: A sessile nodule
on the gingiva at the site
where a draining sinus
tract reaches the surface.
FISTULA: A drainage
pathway or abnormal
communication between
two epithelium-lined
surfaces because of
destruction of the
intervening tissue.

77. • LUDWIG ANGINA: Cellulitis involving fascial spaces
• between muscles and other structures of the posterior floor
• of the mouth that can compromise the airway.

78. CELLULITIS
• Cellulitis is an acute condition in which purulent exudate, usually
accompanied by virulent forms of bacteria, involves the fascial planes
between the bundles of facial and perioral muscles.
• most commonly the result of extension of a periapical abscess into the soft
tissue.
exudate erodes through
the cortical plate of the
mandible or the maxilla
The erosion pathway
reaches the gingival
surface, it results in a
small nodule that
enlarges until it
ruptures.
The site of the opening
(stoma) of a sinus tract
on the gingiva is
commonly termed a
parulis

79. • Occasionally the exudate tracks onto the palate, producing a large
tumorlike mass.

80. Oroantral fistula
• When a periapical abscess erodes into the
maxillary sinus, destroying the intervening bone and
lining, and the offending tooth is extracted, a
communication between the floor of the sinus and the
oral cavity may result.

81. • When purulent exudate emanating from a periapical abscess
penetrates the alveolar bone and enters the muscle layers, the lytic
enzymes from the microorganisms and the acute inflammatory
process break down the fascia that normally surrounds and binds the
muscle bundles.
• This breakdown of the fascia allows the exudate to spread throughout
the immediate region, greatly increasing the magnitude of the
infection.
• These patients exhibit extensive swelling of the affected facial region,
have considerable discomfort or pain, and develop signs and
symptoms of systemic involvement such as elevated temperature,
malaise, lethargy, and lymphadenopathy.

82. Involvement of the soft tissue and
muscle overlying the maxilla usually
results in periocular swelling and
temporary loss of sight on the
affected side.
When the muscle layers overlying the body of
the mandible are involved, patients experience a
puffy, pendulous swelling on the left side of the
face, closely resembling mumps.
Exudate may extend lingually into the muscle
spaces of the posterior floor of the mouth. Such
a posterior progression can result in the swelling
of the structures in and around the epiglottis.
Tissue swelling in this area is life
threatening, because it can
restrict the airway and result in
suffocation if emergency
measures
are not undertaken immediately.
The presence of cellulitis
in these locations has historically
been referred
to as Ludwig angina.

83. Another serious complication of cellulitis is the
extension
of the exudate into the maxillary cavernous sinus
area, resulting in thrombophlebitis.
From this location
fatal forms of brain abscess or acute meningitis are
possible unless rapid intervention is undertaken.

84. CHRONIC OSTEOMYELITIS
• It occurs in response to a low-grade inflammatory process
rather than the intense and destructive inflammation caused by
virulent bacteria.
• Induces bone to form and become denser.
• little or no pain is felt.
• a reduction of the marrow spaces.
• The area will radiographically appear mottled and more
radiopaque than normal. This process is histologically referred
to as osteosclerosis.

85. • Location It may be confined
to an area around the root of
a tooth or be present where a
tooth previously existed.
• These localized changes in the
bone are referred to as focal
chronic sclerosing
osteomyelitis.
• In other instances the
osteosclerosis may involve
larger areas of bone or
edentulous areas in one or
more quadrants. These
conditions are referred to as
diffuse chronic sclerosing

87. GARRÉ OSTEOMYELITIS

88. • Garré osteomyelitis is an unusual hyperplastic reaction of the
periosteum to a chronic osteomyelitis of the posterior mandible that is
unique to young patients.
• Also known as chronic osteomyelitis with proliferative periostitis.

89. • Associated with advanced acute caries in young patients that has
progressed to pulpitis and a periapical lesion.
• Periosteum is stimulated to thicken and lay down excess layers of
new bone.
• Cause: food impaction of the deepened gingival sulcus; a constant
lowgrade infection persists that stimulates the periosteum.
• Patients are in the age group that occurs shortly before the mixed
dentition stage or immediately afterward.
• The other common cause of this unique process is a molar that is
unable to fully erupt.

90. Upon palpation the area will be as hard as the normal surrounding bone,
and the patient will not exhibit pain when the area is slightly palpated.
The area is usually asymptomatic.

91. • RADIOGRAPHIC FEATURES
• The characteristic multiple thin layers of new bone, referred to as an
“onion skin” appearance.
• The trabecular bone will also exhibit the characteristic diffuse mottling of
mottling of a chronic osteomyelitis.
• HISTOPATHOLOGY
• The microscopic features of the reactive bone that forms in response
to the stimulated periosteum is less dense than normal cortical bone
and deposited in a layered pattern.
• The trabecular spaces are wide and occupied with a cellular
connective tissue.

93. TREATMENT
The condition slowly reverts to normal after the source of infection is
identified and resolved.
Sometimes extraction of the offending tooth.
Surgical recontouring of the tissue in the molar area is necessary.

94. References
• Contemporary Oral and Maxillofacial Pathology - 2nd Edition
• Cawson's Essentials of Oral Pathology and Oral Medicine