osteomyelitis of jaw bones / dental implant courses by Indian dental academy

Osteomyelitis Of Jaw Bones
Seminar on-
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiandentalacademy.com

Learning Objectives
At the end of the session the learners should be able
to-
 Classify osteomyelitis
 Enumerate predisposing factors.
 Discuss pathogenesis of osteomyelitis
 Describe the radiographic features of
osteomyelitis.
 Discuss differential diagnosis of osteomyelitis

Contents
 Definition
 Classification
 Predisposing factors
 Etiology & Pathogenesis
 Clinical findings
 Radiographic features
 Treatment

Introduction
 The word “osteomyelitis” originates from the ancient
Greek words osteon (bone) and muelinos (marrow)
and means infection of medullary portion of the bone.
 Osteomyelitis is infection of bone that involves all the
three components of bone: periosteum, cortex and
marrow.

Classification of Osteomyelitis of the Jaws
Suppurative
Osteomyelitis
• Acute Suppurative
Osteomyelitis
• Chronic Suppurative
Osteomyelitis
Primary- no acute
phase preceding
Secondary- follows
acute phase
• Infantile osteomyelitis
Non Suppurative
Osteomyelitis
• Diffuse scelerosing
osteomyelitis
• Focal scelerosing
osteomyelitis
• Proliferative
periostitis(periostitis
ossificans, Garre’s
osteomyelits)
• Osteoradionecrosis

Predisposing factors
 Frequency and severity of odontogenic infections and
intimate relationship of the root ends of the teeth to the
medullary cavity, the relative infrequency of
osteomyelitis of the jaws is remarkable.
 Its low incidence is largely a result of host resistance. In
addition to the virulence of microorganisms, conditions
affecting host resistance and alteration of jaw
vascularity are important in the onset and severity of
osteomyelitis.

 Systemic disease with concomitant alterations in host
defenses may influence profoundly in the course of
osteomyelitis.
 An underlying alteration of host defenses probably occurs
in the majority of patients with osteomyelitis of the jaws
can be detected , given the current state of knowledge of
host defenses.
 Osteomyelitis has been associated with diabetes,
autoimmune disease, agranulocytosis, leukemia, severe
anemia, malnutrition, syphilis, cancer,
chemotherapy,steroid drug use, sickle cell disease,
acquired immunodeficency syndrome. Tobacco and
alcohol use frequently are associated with condition.www.indiandentalacademy.com

 The clinician should consider host compromise and
treat any compromising condition, When feasible,
concomitantly with the infection.
 Condition that alter the vascularity of bone predispose
patients to the onset of osteomyelitis and include
radiation, osteoporosis, osteopetrosis, Paget’s disease
of bone, fibrous dysplasia, bone malignancy, and bone
necrosis caused by mercury, bismuth and arsenic.

Etiology and Pathogenesis
 Hematogenous osteomyelitis of the jaws is infrequent;
the disease is caused primarily by contiguous spread of
odontogenic infections orignating from pulpal or
periodontal tissues.
 Trauma especially compound fractures are second
leading cause of jaw osteomyelitis
 Infections derived from periostitis after gingival
ulceration, lymph nodes infected by furuncles or
lacerations or hematogenous origin account for an
additional number of jaw infectionswww.indiandentalacademy.com

 Osteomyelitis of maxilla is much less frequent than that
of mandible because the maxillary blood supply is more
extensive.thin cortical plate and relative paucity of
medullary tissues in the maxilla preclude confinement of
infections within bone and permit the dissipation of
edema and pus into soft tissues and paranasal tissues.
 In mandible the regions affected, in decreasing
frequency, are the body, symphysis, angle, ramus and
condyle

 Compromise of the blood supply is a critical factor in the
establishment of osteomyelitis.
 Most periapical and periodontal infection are localized
by the production of a protective pyogenic membrane or
soft tissue abscess wall. If sufficiently virulent,
microorganism may destroy this barrier.
 Reduced host resistance during surgery or repeated
movement of unreduced fractures may contribute to
development of suppurative osteomyelitis.
 Mechanical trauma burnishes bone, causing ischaemia,
and introduces organisms deeply into underlying tissues

 The process leading to osteomyelitis is initiated by acute
inflammation: hypermia, increased cappilary permeability
and infiltration of grannulocytes.
 Tissue necrosis occurs as proteolytic enzymes are
released and as destruction of bacteria and vascular
thrombosis ensue.
 When pus, composed of necrotic tissue and dead bacteria
within white blood cells, accumulates, intramedullary
pressure increase resulting in vascular collapse, venous
stasis and ischemia.
 Pus travels through the haversian and nutrient canals and
accumalates beneath the periosteum, elevating it from
cortex and thereby further reducing the vascular supply.

 Compression of the neurovascular bundle accelerates
thrombosis and ischemia and results in osteomyelitis-
mediated inferior alveolar nerve dysfunction.
 Extensive periosteal elevation occurs more frequently in
children, pre-sumbaly because the periosteum is bound
less firmly to bone than in adults.if pus continues to
accumulate, the periosteum is penetrated and mucosal and
cutaneous abscesses and fistuals may develop.
 As the effectiveness of host defenses and therapy
increases the osteolytic process may become chronic.
Inflammation regresses, grnnulation tissue forms, and new
blood vessels lyse bone, thus seperating fragments of
necrotic bone(sequestra) from vital bone.www.indiandentalacademy.com

 Small sections of bone may be lysed completely, whereas
larger ones may be isolated by a bed of grannulation
tissue encased in a sheath of new bone(involucrum).
 Sequestra may be revascularized, remain quiescent,
resorb, or be infected chronically and require surgical
removal before infection subsides completely.
 Occasionally the involucrum is penetrated by
channels(cloacae) through which pus escapes to an
epithelial surface.
 Bone surrounding a sequestrum sometimes appears
radiographic as less densely mineralized than the
sequestrum itself because increased vascularity of
adjacent vital bone creates a relative remineralization.

Pathogenesis of Osteomyelitis
Acute inflammation Pus,organism
(edema, pus formation) extension
Increased intramedullary Haversian system/nutrient
pressure canal involvement
Vascular collapse Elevation of
(stasis, ischaemia of bone) periosteum
Avascular bone Disrupted blood supply
Avascular infected bonewww.indiandentalacademy.com

Microbiology
Streptococci, bacteriodes, Peptostreptococci
and other opportnuistic infection.
As chronic state is reached
Actinomyces, Eiknella, Arachina,
Coccidioides, M.tuberculosis, Klebsiella
may play major role.

Clinical Findings
 Four types of osteomyelitis of the jaws are found
clinically
i. Acute suppurative
ii. Secondary chronic
iii. Primary chronic
iv. Nonsuppurative
 A subacute stage also exsists in which acute
symptoms such as elevated temperature and white
blood cell count are nearly normal but in which
production of pus and extension into adjacent bone
continues.

 Early acute suppurative osteomyelitis (acute
intramedullary osteomyelitis) of mandible usually is
charecterized:-
1) deep, intense pain
2) high intermittent fever
3) parasthesia or anesthesia of lower lip
4) a clearly identifiable cause, usually deep
caries in an involved tooth
 Conventional radiographs do not show any changes in
early disease process. In the initial phase of the acute
form of the disease, teeth are not loose, swelling is
minimal, and fistulas are not present.

 Immediate antibiotic therapy may prevent involvement of
periosteum(subperiosteal osteomyelitis).Identification
and correction of immunocompression conditions should
be attempted.
 If the disease is not contorlled within 10 to 14 days after
onset, subacute suppurative osteomyelitis is established.
 Pus extends through haversian canals to accumulate
under the periosteum and then may penetrate and
extend into soft tissues.

 Deep pain, malaise, fever, and anorexia are present teeth
begin to loose and become sensitive to percussion. Pus
exudes around gingival sulcus and through mucosal, and
possibly, cutaneous fistulas; a fetid odor is often present.
 Firm cellulitis of cheek, expansion of bone from increased
periosteal activity, abscess formation with localized
warmth, erythema, tenderness to palpation and mental
nerve parasthesia also may be noted.
 Trismus is not always present but regional
lymphadenopathy is constant finding. The patients
temperature may reach 101o to 102o F and is often
dehydrated.

 Inadequately treated acute osteomyelitis, the clinical
finding are the limited to fistulas, induration of soft
tissues, and a thickened or “wooden” character to the
affected area with pain and tenderness on palpation.
 Primary chronic osteomyelitis, the form not preceded by
an episode of acute symptoms, is insidious in onset with
slight pain, slow increase in jaw size, and gradual
development of sequestra, often without fistulas.

Fig. 2.1a–c Elder case of advanced secondary chronic osteomyelitis of
the left mandible. The massive affection of the left mandible
demonstrates extraoral fistula and scar formation (a). Intraoral view of
the same patient with large exposure of infected bone and sequestra
(b). Large sequester collected from surgery (c)

Radiographic Features( Worth)
Moth eaten appearance
Islands of sequestra seperated by band of
radiolucency
Stippled/granular densification

Imaging modalities
 Conventional Radiography
 CT
 MRI
 Radionuclide bone scanning

Bone scanning
Radionuclide Imaging or Skeletal Scintigraphy
Radiopharmaceuticals are absorbed at areas of reactive
bone formation.
Done by injecting 99m Tc Methylene diphosphonate
i.v.
Radioisotope concentrates in areas of increased blood
flow and osteoblastic activity

Method:
Rectilinear scintillation camera (Sodium iodide) obtains
images of isotope containing areas
Resulting image shows distribution at areas of
increased bone activity

Computed Tomography
Detects early bone changes
Features
Increased attenuation of medullary cavity
Destruction of cortical bone
Appearance of sequestra
New bone formation
Advantages of CT
Reveals
Extent of lesion
Extent of cortical erosion
Identification of sequestrawww.indiandentalacademy.com

Magnetic Resonance Imaging
When all other tests are negative MRI and CT are helpful

Radiographic features
 Periapical radiolucency
 Solitary radiolucency with ragged and poorly
defined borders.
 Mixed radiolucent radiopaque lesion not
contacting the teeth. (salt and pepper
appearance)
 Solitary radiopacities not necessarily contacting
the teeth.

Chronic osteomyelitis
 Rounded periapical radiolucency may resemble
periapical abscess, cyst, grannuloma
 Borders are poorly defined and ragged because of
irregular extension of inflammation and infection
through marrow spaces and channels.
 The bony course of draining tract transversing jaw
bone seen as radiolucency through cortical plate
which is deeper or longer unlike in chronic alveolar
abscess which is restricted to alveolar bone.
Sequestrum is seen as radiopacity within
radiolucency.

Differential diagnosis for periapical
radiolucency
 Chronic alveolar abscess
 Infected malignant tumor
 Pagets disease
 Eosinophilic grannuloma

Differential diagnosis for solitary radiolucency
with ragged and poorly defined borders
 Chronic osteitis
 Fibrous dysplasia
 Metastatic jaw tumors
 Chondrosarcoma
 Ewing sarcoma

Differential diagnosis for mixed radiolucent-
radiopaque lesion not contacting the tooth
 Fibrosseous lesions of periodontal origin
 Mottled type of fibrous dysplasia
 Rarefying and condensing osteitis
 Paget’s disease
 Malignant tumor

Focal sclerosing osteomyelitis
It represents low grade infection
Features-
 Borders of the radiopaque lesion may be ragged or
smooth and well defined or vague.
 Identification depends on the presence of symptoms
of chronic infection such as tenderness, pain or local
swelling.
 Regional lymphadenitis is frequent complaint and a
drainig sinus may accompany.

Histopathological features
 Dense sclerotic, nonvital bone.
 Acute inflammation in some areas and ocassionally
focal collection of pus.

Differential diagnosis
Lesions included in differential diagnosis for solitary
intrabony area of scelrosis are-
 Osteoblastic or scelrosing malignancy
 Condensing ostetis
 Focal cementosseous dysplasia

Diffuse sclerosing osteomyelitis
 Uncommon disease that affects the broad area of
the body of the mandible, mostly molar, angle and
lower ramus region.

Theories about etiology
1) Chronic infection by bacteria of low virulence from skin,
oral cavity or blood bacterias such as
propionobacterium acnes, actinomyces species,
eikenella corrodens.
2) DSO may be related to SAPHO syndrome in which
pustular lesions are associated with similar skin lesions
3) DSO is expression of chronic recurrent multifocal
osteomyelitis.
4) Genetics
5) DSO is linked to tendoperiostitis
6) Hyperactive immune response

Clinical features
 Recurrent pain
 Swelling of inferior aspect of cheek and trismus.
 Average age of occurrence is years.
 Equal gender predilection
 Cyclic episodes over month and year.
 During exaceberation subfebrile temperature and
elevation of sledom entation rate.
 Submandibular lymph nodes are affected.

 Charecteristically limited to half of the mandible
 Mostly involves mandibular molar angle and ramus
region.
 Changes occur slowly
 Osteolytic areas predominate first and symptoms are at
their worst.
 As episodes become less frequent and less severe
dense diffuse bony scelrosis predominate and
radiolucent component diminishes.

 Subperiosteal and external cortical bone resorbtion are
observed.
 Scintigraphy is positive in DSO.
Histological features-
Dense remodelling of cortical and subcortical resulting in
increase bony volume.

Following conditions can cause a large diffuse radiopaque
involvement of bone.
 Florid cementosseous dysplasia
 Pagets disease
 Osteopetrosis

Proliferative Periostitis
 Synonyms- periostitis ossificans, Garre’s osteomyelitis
 It is charecterized by formation of new bone on the
periphery of the cortex over an infected area of
spongiosa.
 The formation of new bone is a response of inner
surface of periosteum to stimulation by a low grade
infection that has spread through bone and penetrated
the cortex.
 Microorganism involved staphylococci and streptococci
strains.
 Periapical odontogenic infection is frequent cause and
ocassionally pericoronotis.

Proliferative periostitis is uncommon dental complication
For this lesion to develop following peculiar combination
must coexist-
1. Periosteum must posses a high potential for
osteoblastic activity.
2. A chronic infection must be present.
3. A fine balance between resistance of host and the
number and virulence of present organisms so that
infection can continue at low, chronic stage, invasive
enough to stimulate the new periosteal bone
formation but not severe enough to induce bone
resorbtion.

Clinical features
 Mean age- 12 to 13.3 yr
 Etiology- infected mandibular first molar.
 Facial asymmetry is present due to swelling.
 Swelling is bony hard and usually non tender and
overlying skin or mucosa appears normal.
 Fever and leukocytosis are present.
 If chronic infection is estabilished beneath periosteum
and not treated, the swelling becomes hard as new
bone is laid down after elimination of infection, hard
elevation is usually eliminated as bone is recontoured
by functional forces.www.indiandentalacademy.com

 Smoothly contoured, moderately convex bony shadow
can be seen extending from preserved cortex of the
jaw.
 The space between this new thin shell of bone and
cortex may be radiolucent without images of trabaculae.
 Later alternating light and dark laminated appearance
may be seen when whole lesion mineralizes, the lesion
may be completely radiopaque.
 In most cases jaw bone appear normal on the
radiograph but sometime there may be accompanying
radiolucent or osteosclerotic osteomyelitis like changes
and small sequetra can often be seen.

Histopathological features-
 dense new bone with minimal vascular spaces.
 Periosteum is thickened and overactive osteoblastic
layer.

 Ewing sarcoma
 Osteogenic sarcoma
 Infantile cortical hyperostosis
 Ossifying haematoma
 Callus
 Tori
 Exotosis
 Peripheral osteoma

Treatment
 Osteomyelitis of the jaws usually require medical
and surgical treatment, although occasionally
antibiotic therapy alone is successful.

Principles of treatment of Osteomyelitis-
1. Evaluation and correction of host defense defencies
2. Gram stainnig, culture and sensetivity
3. Imaging to rule out bone tumors
4. Administration of culture-guided antibiotics, repeated culture
5. Removal of loose teeth and sequestra
6. Administration of culture-guided antibiotics, repeated culture
7. Possible placement of irrigation drains/polymethylacrylate-
antibiotic beads
8. Sequestrectomy, debribement, decortication, resection,
reconstruction.

HYPERBARIC OXYGEN THERAPY IN OSTEOMYELITIS
 HBO therapy consist of breathing 100% oxygen through
face mask in a chamber at 2.4 absolute atmosphere
pressure for 90-minute session or dives for as many as
5 days a week totaling 30 or more sessions often
followed by another 10 or more sessions.
 HBO treatment causes increase in arterial and venous
oxygen tension, the increased oxygen tension
enhances healing by direct bacteriostatic effect on
microorganisms that renders them to lower antibiotic
concentrations and by enhancing phagocytic killing.
 Osteomyelitis and osteoradionecrosis in certain patient
is refractory to usual medical and surgical treatment,
these patients may be candidates for HBO treatment in
conjunction with surgical and antibiotic care.

Infantile osteomyelitis
 Occurs few weeks after birth
 Occurs by trauma to oral mucosa when obstetrician’s
finger or mucous suction bulb used
 c/f : facial cellulitis involving orbit
 Irritability, malaise, hyperpyrexia,anorexia.
 Convulsions
 Inner and outer canthal swelling
 Palpebral edema
 Conjunctivitis, proptosis
 I/O maxilla swollen in molar region

Treatment
 Prompt and aggressive to prevent optic damage ,
neurological complications, loss of tooth buds and
bone
 Iv antibiotics and drainage of abscess
 Antipyretics, fluids, proper diet
 Oral antibiotics for 2 to 4 weeks
 Conservative sequestromy

Osteomyelitis associated with fracture
 Failure to use the effective methods of reduction,
fixation and immobilization may lead to osteomyelitis as
debris and microorganism gain acess to surgical site.
 Overzealous use of intraosseous wiring, bone plates or
screws that devascularize bone segments predisposes
patient to osteomyelitis.

Actinomycotic osteomyelitis
 Actinomycosis is chronic, slowly progressive infection
with grannulomatous and suppurative features, it
usually affects soft tissue and, occasionally bone.
 Infection with the organism occur in areas of tissue
damage or inflammation in concert with other oral
organism. The organism gain access to soft tissue
directly or by extension from bone through periapical or
periodontal lesions, fractures or extraction sites.
 Firm, soft tissue masses are present on the skin they
have purplish, dark red, oily areas with occasional small
zones of fluctuance.

 Radiolucencies of varying size and delay in healing of
extraction sites are common. Periostitis, diffuse
mandibular lucencies or marked bone sclerosis also
may be apparent on radiographs.

Osteoradionecrosis
 Cancer of maxillofacial region is usually treated by
radiation, surgery or combination therapy.
 Bone absorb more energy than soft tissue because of
its mineral composition.
 It’s a chronic, non-healing wound caused by
hypoxia, hypo-cellularity and hypo-vascularity of
irradiated tissue.

Clinical features
 Mandible is more commonly involved than
maxilla.
 Trismus
 Halitosis
 Elevated temperature
 Exposed bone ( fistula formation)
 Pathological fractures
 Indurated surrounding tissues

Pathophysiology
 In 1970 meyer presented the triad of radiation,
trauma and infection.
 In 1983 marx – osn is not a primary infection of
bone, rather a complex metabolic and tissue
homeostatic deficiency seen in hypo-cellular, hypo-
vascular and hypoxic tissue ( 3-h principle)

 Similar to than of osteomyelitis
 Cannot always be diagnosed on the radiographically
and often clinical obvious signs of exposed necrotic
bone may not be accompanied by significant radiologic
changes.
 Location- mandibular posterior region
 Periphery- ill defined
 Internal structure- sclerotic or radiopaque appearance,
scattered regions of radiolucency may be seen with or
without central sequestra.
 Effect on surrounding structure- stimulation of sclerosis

PREVENTION
PREIRRADIATION DENTAL CARE
 All nonrestorable and peridontally involved teeth
– extracted – 10 to 14 days before RT.
 Oral hygiene maintainance.
 Restoration of carious teeth.
 Fluoride application (1% NaF gel) – 15 min twice
a day for 2 weeks followed by once daily
thereafter.

POSTIRRADIATION DENTAL CARE
 No denture for 1 yr.
 Oral hygiene & fluoride application continued.
 Salivary substitute.
 Post-irradiation pulpitis – restoration.
 Necessary extraction – 1 or 2 teeth per
appointment, atraumatic & prophylactic antibiotic
regimen.

TREATMENT
CONSERVATIVE APPROACH
 Initial treatment is directed at controlling
infection.
 Antibiotics + irrigation.
 Ultrasound + irrigation.

Conclusion
 Osteomyelitis of jaw is a disease with significant
morbidity unless it is recognised promptly and
treated vigorously.
 Early recognition of osteomyelitis followed by
appropriate antibiotic treatment can prevent
extensive loss of bone and teeth.
 Nevertheless, surgery usually is necessary to drain
abscess and encourage sequestration and removal
of non vital bone.

References
 Oral and maxillofacial infection.Topazian
 Differential diagnosis of Oral and Maxillofacial
lesions, Wood & Goaz, fifth edition
 White & Pharon, Textbook of Oral Radiology, fifth
edition
 Chronic Suppurative Osteomyelitis of the mandible:
Case report, SC Yeoh, S MacMahon, M Schifter
Australian Dental Journal 2005;50:(3):200-203
 Diagnosis and classification of mandibular
osteomyelitis. OOOOE Vol. 100 No. 2 August 2005,
Yoshikazu Suei, Akira Taguchi, and Keiji Tanimoto,

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