Department of Oral & MAXILLOFACIAL

Pathology & Microbiology

OSTEOMYELITIS
Lecture 3 on PULP & PERIAPICAL LESIONS

Dr. Amit Gupta

Reader
Department of Oral Pathology
CONTENTS

• Introduction
• Definition
• History
• Classification
• Pathogenesis
• Experimental studies
• Acute suppurative osteomyelitis
• Infantile osteomyelitis
• Chronic suppurative osteomyelitis
• Chronic focal Sclerosing Osteomyelitis
• Chronic Diffuse Sclerosing Osteomyelitis
2
CONTENTS

• SAPHO syndrome
• Chemical osteomyelitis
• Osteoradionecrosis
• Dry socket
• Differential diagnosis
• Treatment
• Conclusion

3
 INTRODUCTION
• Osteomyelitis of jaw is a challenging disease for the
clinicians and patients despite many advances in
diagnosis and treatment .

• Different terminologies & classification systems are

used based on a variety of features:
– Clinical course
A mixture of these classification
– Pathological-anatomical
systems has occurred throughout
– Radiological the literature leading to the
features,
– confusion & thereby hindering
Etiopathogenesis
comparative treatment.
4
 DEFINITION

• The word “osteomyelitis” originates from the ancient

Greek word –
– “Osteon’’ bone
– “muelinos’’ marrow
– “itis’’ inflammation

“Inflammatory condition of bone that begins as an

inflammation of medullary cavity & haversian
systems & extend to involve the periosteum of
affected area.”
5
 HISTORY
• The prevalence, clinical course and
management of osteomyelitis of
jawbones have changed profoundly
over the past 50 years.

“The Introduction Of Antibiotic

Therapy, Specifically Penicillin”

In the Preantibiotic Era:

-Classical Presentation:
After the introduction of antibiotics: Florey ME, Florey HW. General and
- Axhausen 1934,1973,
(Becker Wassmund
Bunger1935
1984)
local administration of penicillin.
Lancet 1943;1:387.

6
Overview Of Currently Used
Classification Systems &
Terminology

7
 CLASSIFICATION SYSTEMS

- The heterogeneity of classification system was borne by the

fact that several modalities were used to define and describe
maxillofacial osteomyelitis.

- 1970…Waldvogel & Medoff

– I. Hematogenous osteomyelitis
– II. Osteomyelitis secondary to a contiguous focus of infection
– III. Osteomyelitis due to vascular insufficiency
(Classification based on etiology and pathogenesis)

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Dual classification based on pathological
anatomy and pathophysiology
(Cierny et al.1985)
Classification by (Marx 1991; Mercuri1991; Koorbusch1992)

The two major groups: Acute and

Chronic Osteomyelitis
Classification based on Pathogenesis.
(Vibhagool 1993)

-1970…Waldvogel & Medoff

I. Hematogenous osteomyelitis
II. Osteomyelitis secondary to a contiguous focus of infection
III. Osteomyelitis due to vascular insufficiency
Classification based on clinical picture,
radiology, and etiology
(Topazian RG 1994)
PATHOGENESIS
of
OSTEOMYELITI
S
 The compromise of local
blood supply is a critical
factor and finds a common
pathway in the establishment
of acute and chronic
osteomyelitis
(Wann fors & Gazelius 1991)

15
https://www.youtube.com/wa
tch?v=Afp0QGb7GoU TRAUMA / INFECTION

Inflammation
Liberation of proteolytic enzyme
& destruction of bacteria
Tissue necrosis

Vascular thrombosis
Necrotic tissue + dead bacteria
with WBC’s
Pus accumalation
In intramedullary pressure

Vascular collapse
Venous stasis & Ischemia Pus travel through haversian &
nutrient canals
Topazian 2002 Subperiosteal abscess
 Elevation of Periosteum
Further in vascular supply
compression of neurovascular
bundle
Mandibular anesthesia
Penetration of periosteum

Mucosal & cutaneous, Abscess & fistulae

host defense + AB therapy

Formation of SEQUESTRA

INVOLUCRUM

CLOACAE
PUS
Topazian 2002
 PATHOGENESIS

Source of Infection
Osteomyelitis can be caused by:

HEMATOGENOUS SPREAD
In jaw-less common
 Involves the metaphysis of long bones in children (because of its
anatomy) or the vertebral bodies in adults.
Bass 1928, Engel 1939, Heslop, Rowe 1956, Nade 1983

DIRECT INOCULATION OF MICROORGANISMS INTO BONE

Penetrating injuries and surgical contamination.

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CONTIGUOUS FOCUS OF INFECTION ( most common in jaw)
occurs in patients with:
- Severe vascular disease
- Odontogenic infection ( Staph. Aureus), pulpal or PDL tissue
- Trauma-2nd leading cause
- Pericoronitis ( 3rd Molars)

- Surgical intervention
– Various transplants & implants
– Additional trauma to pre-existing chronic local infection.
– Foreign bodies.

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MICRORGANISMS INVOLVED

Nonspecific oseomyelitis:
Staphylococcus aureus
Staphylococcus albus
Streptococcus viridans
Bacterioids, Porphyromonas or Prevotella

Specific osteomyelitis may be caused by

Mycobacterium tuberculosis
Actinomyces organisms
Treponema palidium
 Microbiology

• S. aureus, S. epidermidis, Actinomyces were considered

as the major pathogens for Osteomyelitis.

• Recent studies favor the concept of Polymicrobic

infection.

• This shift in the doctrine is explained mainly by the

modern sophisticated culture methods, especially
involving anaerobic media.

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 Microbiology

• Staphylococci have a large variety of adhesive proteins

and glycoproteins that mediate binding with bone
components

Pathogenesis

• The formation of a glycocalyx surrounding the infecting

organisms.

• Protects the organisms from the action of phagocytes &

prevents access by most antimicrobials.
 Interrelationship of periapical infections
PULPITIS
acute chronic

Periodontitis
acute chronic

Periapical abscess Periapical Granuloma

acute chronic Periodontal cyst

Osteomyelitis
acute chronic

Periostitis

Cellulitis Abscess Shafer-6th ed.

Why incidence of osteomyelitis is much
higher in the mandible ??

– It is much less common in the Maxilla due to:

• the excellent blood supply from multiple nutrient
feeder vessels.
• is composed almost entirely of spongy bone with a
very thin cortex.
• Infectious process of this bone can either remain
localized or spread into the soft tissues and result in a
cellulitis, fistula or sinusitis.

– In Case Of Mandible: dense poorly vascularized thick

cortical plates and the blood supply primarily from the
inferior alveolar neurovascular bundle(single source).
 TYPES OF
OSTEOMYELITI
S
Acute Suppurative Osteomyelitis

• It is a sequela of periapical infection resulting in the

diffuse spread of infection throughout the medullary
spaces, with subsequent necrosis of a variable amount of
bone.

• Most frequent cause:- dental infection.

• Polymicrobial infection:-
– Staph aureus, Staph albus, streptococci, Bacteroides,
Prevotella, Porphyromonas species.

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Acute Suppurative Osteomyelitis

Clinical features:-
- SITE:- Maxilla & Mandible
Mandible- body> symphysis> angle> ascending ramus> condyle

Signs and symptoms

• Deep intense pain
• Trismus
• Elevated temperature
• Regional lymphadenopathy
• Teeth in affected area are loose & sore making eating difficult
• Parasthesia or anesthesia of lips due to involvement of mandibular
nerve. 27
Acute Suppurative Osteomyelitis

• Pus discharge from gingival margin

• When periostitis develop, swelling and redness of skin develops
• Pathological fractures may occur because of weakening of jaw by
destructive process.
• Increased white cell count

Acute odontogenic osteomyelitis with massive suppuration. Pus in the

sulci of the incisors and canines on both sides, extending distally to the
28
right molars with multiple fistula formation
Acute Suppurative Osteomyelitis
Radiographic features:-
- Evident after 3 (1-2) weeks of progression of disease.
- Early stage

- Later stage: mottled/ moth eaten appearance.

29
Acute Suppurative Osteomyelitis
Histologic features:-

Bony trabeculae are devoid of cells Sequestrum is separated from surrounding

in lacunae bone & exfoliates through the sinus
30
Osteomyelitis of maxilla in infants/
Infantile osteomyelitis
Rees in 1847

Etiopathogenesis

Failure to have adequate drainage of mucus from airway

immediately after birth
Haematogenous route
Infected feeding bottles
Infection at time of birth (small abrasion suffered at the time of
delivery)
Prominent bulge in maxillary alveolar ridge may cause injury
Staphlococcus aureus

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 Clinical features

• Acute inflammation of bone with spreading thrombosis of its

nutrient vessels.
• Swelling followed by sinus discharging pus.
• Chronic stage- sequestra & extrusion of affected tooth buds.
• May lead to permanent deformity of maxilla, loss of teeth, scars
beneath lower eyelid.

32
 CHRONIC SUPPURATIVE
OSTEOMYELITIS

May develop in case of inadequate treatment of acute osteomyelitis

or as a sequelae of periapical infection without a preceding stage.
-PRIMARY
(no acute phase preceding)

-SECONDARY
(follows an acute phase)
 CHRONIC SUPPURATIVE
OSTEOMYELITIS
Clinical features:

• Mild pain, increase in temp.,

slight elevation of leukocyte
count.

• Teeth may be loose or sore, but

not to the extent of interfering
with food intake.

• Bone & overlying skin may be

perforated with pus discharge.

• Acute exacerbation can lead to acute suppurative osteomyelitis

Acute Form Transforming Into Secondary
Chronic Form Of Osteomyelitis
• As a sequel of acute osteomyelitis, the clinical presentation of
secondary chronic osteomyelitis of the jaws may also show a great
variety, depending on the:
Acute & secondary chronic
• Intensity of the disease

forms of osteomyelitis are the

• Magnitude of imbalance
• Time frame

“same disease at different

stages of their course”
Classical signs:
Sequestra & Fistula

36
 CHRONIC SUPPURATIVE
OSTEOMYELITIS

Radiographic features
• Trabeculae appear as thin or fuzzy
• Mottling
• Sequestra appear more dense
• New bone appear as grey shadow external to cortical
plate
istologic features:-

Chronically inflamed & reactive fibrous connective tissue filling

the intertrabecular spaces
Chronic focal sclerosing osteomyelitis /
Condensing Osteitis

An unusual reaction of bone to

infection,
the tissue reacts by proliferation
rather than destruction, since the
infection (low grade) acts as a
stimulus rather than an irritant.
 Chronic focal sclerosing osteomyelitis /
Condensing Osteitis
Clinical features:-
- Arises most commonly in children & young adults.

- Tooth most commonly involved is mand 1st molar,

which presents a large carious lesion.

- There may be no signs and symptoms other than

mild pain associated with infected pulp.

40
RADIOGRAPHIC FEATURES

Condensing osteitis
Histologic features

Chronic focal sclerosing osteomyelitis / Condensing Osteitis 42

 TREATMENT

Associated tooth should be extracted or endodontically

treated
Sclerotic bone need not be removed unless symptomatic
 Chronic Diffuse Sclerosing
Osteomyelitis
• It represents a proliferative reaction of the bone to a
low grade infection.

• Portal of entry of infection is through periodontal

disease.

• Condition is analogous to the focal form of the

disease.

44
Chronic Diffuse Sclerosing
Osteomyelitis

Clinical features
- May occur at any age, common in
3rd decade onwards, especially in
edentulous areas.
- Approx. 2/3rd of patients are
women.
- No racial predilection

- The bone often is mildly expanded & tender with episodes of

swelling and pain

- Acute exacerbation of dormant chronic infection is there,

resulting in vague pain, unpleasant taste, mild suppuration, formation
of fistula. 45
Chronic Diffuse Sclerosing Osteomyelitis
Radiographic features:-

- “cotton wool” appearance.

- sometimes bilateral.
- Border between the sclerosis & normal bone is often indistinct.
DIFFERENTIAL DIAGNOSIS

• Florid Cemento-osseous Dysplasia

• Benign cementoblastoma
• Fibrous dysplasia
• Osteoid osteoma
• Pagets disease of bone

47
 Florid Cemento-osseous Dysplasia vs
Chronic Diffuse Sclerosing Osteomyelitis
• Typically occurs in middle-aged black women.
• Clinically, these lesions are often asymptomatic and may present as
incidental radiological findings.
• Presumably, these lesions arise from the periodontal ligament and
therefore tend to be restricted to the tooth bearing area of the jaws.
• Radiologically, they consist of masses of varying degrees of
opacity with or without a radiolucent margin affecting more than
one quad.

Florid Cemento-osseous
Chronic Diffuse Sclerosing Osteomyelitis Dysplasia
Benign cementoblastoma vs
Chronic Focal Sclerosing
Osteomyelitis
Attached to root and complete root out line is
not seen
Surrounded by radiolucent border

Benign cementoblastoma Condensing osteitis

SAPHO syndrome/Chronic Recurrent
Multifocal Osteomyelitis (CRMO)
• In 1986 Chamot et al. described a syndrome associated:
– Synovitis S
– Acne A
– Pustulosis P
– Hyperostosis H
– Osteitis O

• In the past few studies, a possible relationship between diffuse

sclerosing osteomyelitis and chronic recurrent multifocal
osteomyelitis has been described
(Brandt et al. 1995; Kahn et al. 1994; Mann et al. 1996; Suei et al. 1996;
Schilling et al. 1999; Eyrich et al. 1999; Roldan et al. 2001; Fleuridas et al.
2002).
 SAPHO syndrome

• CRMO is characterized by periods of exacerbations and

remissions over many years.

• This rare disease is noted predominantly in children.

 Chronic Osteomyelitis with Proliferative
Periostitis (Garre’s chronic nonsuppurative
sclerosing osteitis, Periostitis ossificans)
Reactive periostitis (Etiopathogenesis) due to:
Carl Garre in 1893
-Dental infection with associated periapical inflammation
Mild
It isinflammation actofaschronic
a distinct type a stimulant & affected
osteomyelitis periosteumby
characterized forms
several rows of reactive vital bone that are parallel to each other &
focal gross thickening of periosteum with peripheral reactive
cause expansion of surface
bone formation, presenting with typical onion skin like
-reduplication
Overlying softoftissue
cortical plates,orresulting
infection cellulitisfrom
thatmild infection
involves or
the deeper
irritation. secondary to periodontitis, fracture, non odontogenic
periosteum
infections

-Periosteal osteosclerosis analogous to the endosteal sclerosis of

chronic focal and diffuse sclerosing osteomyelitis
 CLINICAL FEATURES

• Age – young below 25 years

• Commonly affecting long bones (tibia).

• Jaw bone: common in mandible, in premolar- molar region.
Maxilla is rarely affected

• Present with tooth ache or pain in the jaw or bony hard

swelling on outer surface of jaw of several week duration.

• Unifocal or multiple quadrant involvement

RADIOGRAPHIC FEATURES
D/D – lesions with periostel new bone formation or
neoperiostosis
– Infantile cortical hyperostosis( Caffe’s disease)
– Hypervitaminosis A
– Syphilis, leukemia, Ewing’s sarcoma, metastatic
neuroblastoma
– Fracture callus
Histopathologic Features

Garre’s Osteomyelitis
 TREATMENT

Eliminate source of infection

Lesions resolve within 6-12 months
 CHEMICAL
OSTEOMYELITIS

 Necrosis of jaws occur due to contact with caustic

chemicals & protoplasmic poisons

1)The extent of
Necrosis bone damage
following varies according
occupational exposure to the:
• - Phosphorus
Quantity & nature of the chemical responsible.
necrosis
- Superimposed pyogenic infection further complicate
the condition.
2) Necrosis following therapy
• Mercury
• Bismuth
• Arsenic
58
 PHOSPHORUS
NECROSIS
Necrosis of the jaw “phossy jaw” –Thoma

 Sequestra grey pumice whitish area

59
 Necrosis Following Therapy

Arsenic (Arsenic trioxide)

• To devitalize inflamed pulp tissue before root canal
treatment.

• Prolonged application or leakage leads to toxic effects

beyond the pulp tissue & necrosis of periodontal
ligament region & alveolar bone.

60
RADIATION (OSTEORADIONECROSIS
or OSTITIS)

• Osteoradionecrosis: complication of irradiation of bone

• Osteonecrosis- Frandsen 1962
• Radiation dysplasia – Pappas 1969, Vaughan

The changes in bone depend upon:

• Age of bone
• Dose of radiation
• Presence or absence of infection

61
• Radiotherapy- major role in the treatment of head and neck
malignancies.

• Aside from its effect on the tumor cells, radiation also has serious
side effects on the soft and hard tissues:
– Mucositis, atrophic mucosa,
– xerostomia, and radiation caries

• Because of its mineral composition, bone tissue absorbs 3-4 times

more energy than soft tissues and is therefore more susceptible to
secondary radiation.
Factors leading to
OSTEORADIONECROSIS ??
• Irradiation of an area of previous surgery before adequate
healing.

• Irradiation of lesion in close proximity to bone.

• High dose of irradiation

• Poor oral hygiene & continuous use of irritant.

• Surgery/Trauma in irradiated areas

63
Osteoradionecrosis may lead to:

• Marked pain
• possible loss of bone leading to functional and aesthetic
impairment.
• Chronic nonhealing wound, susceptible to superinfection.
• Obliterative endarteritis

• Fetor-oris with discharge of pus through sinuses

 Dry socket, Alveolitis sicca dolorosa,
Postoperative osteitis,
Localized acute alveolar osteomyelitis,
Alveolar osteitis

It is a post-operative complication that interferes with the

healing process that takes place after a tooth extraction.

Meyer (1971):
osteitis circumscripta superficialis,
osteitis circumscripta media and
osteitis circumscripta profunda.

The term latter considered as a localized form of osteomyelitis.

 Dry socket
Clinical presentation
• Focal osteomyelitis in which blood clot is lost with production
of foul odor & severe pain but no suppuration
• Associated with traumatic extractions
• Extremely painful condition
• Exposed bone is necrotic & sequestration of fragments is
common
• Healing is slow & painful
 Experimental &
Laboratory Studies
Experimental Studies
• Prostaglandin-E production has been shown to be five to thirty
fold higher in infected bone than in normal bone.

• In studies of an animal model of osteomyelitis, the production

of large amounts of prostaglandin was postulated to be
responsible for bone resorption and sequestrum formation.

• Effective phagocytosis has been shown to be an important

factor in host defense in patients with osteomyelitis.

• Lower intramedullary oxygen tension in infected bone impairs

phagocytic function.
Prostaglandins Med. 1979 Jun;2(6):403-12
Laboratory Studies

• Increased levels of proinflammatory cytokines such as IL-1,

IL-6 and TNF-ά

• Directly involved in the bone resorption and osteoclast activity

regulation that occur in OM and may therefore play a role in
its pathogenesis.

• IL-6 is implicated in OM pathogenesis as it influences

osteoclast function and stimulates bone resorption

Infection and Immunity, Aug. 1997; 65(8):3438–43

69
 Laboratory Studies

• The leukocyte count Elevated in cases of acute osteomyelitis, but

it is often normal in chronic cases.

• ESR usually elevated in both acute & chronic osteomyelitis.

Rises immediately after operative débridement, returns to normal
during the course of therapy is a favorable prognostic sign.

• The C-reactive protein level is another inflammatory index that

rises in acute and chronic osteomyelitis and decreases faster than
the ESR in successfully treated patients.

70
Investigations

• Culture & sensitivity

• Imaging
Radiographs
CT Scan
Scintigraphy
 Treatment of Osteomyelitis
ESSENTIAL MEASURES: ADJUNCTIVE TREATMENT:
Bacterial sampling & culture. Sequestrectomy & saucerization
Vigorous(emphirical) antibiotic Decortication, if necessary
treatment. Hyperbaric oxygen (useful in
Drainage. t/t-osteoradionecrosis,
Specific antibiotics based on anaerobic infection)
culture and sensitivity. Resection and reconstruction
Give analgesics for extensive bone destruction.
Debridement.
Remove source of infection, if
possible.

72
 CONCLUSION
• Osteomyelitis of the jaw is a disease with significant morbidity
unless it is recognized promptly and treated vigorously

• In recent years understanding of its microbiology has changed,

along with that of other oral infections.

Despite all advances, however proper management of

osteomyelitis continues to depend on careful clinical & imaging
examination, proper assessment of findings, an understanding of
the nature of the disease, & a repeated review of the effectiveness
of therapy in individual patient

73
 REFERENCES
• Donohue, Abelardo. Osteomyelitis of jaw C.M.A. journal Oct
1970; 103:748-50.
• Florey ME, Florey HW. General and local administration of
penicillin. Lancet 1943;1:387.
• Osteomyelitis of the Jaws Marc M. Baltensperger, Gerold K.
Eyrich.
• Yoshikazu Suei et al. Diagnosis and classification of mandibular
osteomyelitis. OOOE. 2005;100(2):207-14.
• Eversole LR. et al. Fibrous dysplasia: A nosologic problem in the
diagnosis of fibro-osseous lesions of the jaws. J. oral Path.
1972;1:189-220.
• Topazian 4th edition
• Cawson Oral Diseases Clinical and Pathological corelation 3rd
edition Mosby 2001
 REFERENCES

• Prasad KC et al. Osteomyelitis in the head and neck. Acta Oto-

Laryngologica, 2007; 127: 194-205.
• Nezafati S, Ghavimi MA, Yavari AS. Localized Osteomyelitis of
the Mandible Secondary to Dental Treatment: Report of a Case.
JODDD 2009; 3(2):67-9.
• Reggizi Oral Pathology Clinical and Pathological Corelations 3rd
edition 1989
• Rajendran Shaffers Textbook of Oral Pathology 6th edition 2009
• Corbett M, Dekel S, Puddle B, Dickson RA, Francis MJ. The
production of prostaglandins in response to experimentally
induced osteomyelitis in rabbits. Prostaglandins Med. 1979
Jun;2(6):403-12.
 REFERENCES

• Evans aj et al. Local expression of tumor necrosis factor alpha in

an experimental model of acute osteomyelitis in rats. infection
and immunity, aug. 1997; 65(8):3438–43.
• Pynn BR. Benign Cementoblastoma: A Case Report. J Can Dent
Assoc 2001; 67:260-2.
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THANK
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