osteomyelitis.pptx

• The word “osteomyelitis” originates from the
ancient Greek words osteon (bone), muelinos
(marrow) and itis(inflammation) hence means
inflammation of medullary portion of the bone.
• Osteomyelitis may be considered an inflammatory
condition of bone that usually begins as an infection
of the medullary cavity, rapidly involves the haversian
systems, and quickly extends to the periosteum of
the area.
2

Predisposing factors
Conditions that alter
host defences
Conditions that alter
vascularity of bone
Virulence of
organisms
3

Etiology
• Osteomylitis of the jaws is caused by :
• Odontogenic infections – originating from pulpal or
periodontal tissues, pericoronitis, infected cyst or
socket.
• Trauma- compound fracture, surgery.
• Infections of oro-facial region caused by lymph
nodes infected from furuncles, lacerations and
peritonsillar abscess.
• Infections caused by hematogenous route- wound
on the skin, middle ear infection, systemic
tuberculosis.
4

Acute Inflammation
(edema, pus formation)
Increased
intramedullary pressure
Vascular collapse
Compromised local blood
supply
Pus extension
Haversian system /
nutrient canal
involvement
Elevation
of periosteum
Disrupted blood
supply
Avascular bone
Sequester formation
6

• Small sections of necrotic bone may be
completely lysed, whereas larger ones may be
isolated by a bed of granulation encased in a
sheath of new bone ie. involucrum.
• The involucrum may be penetrated by
channels called cloace through which pus
escapes to an epithelial surface.
7

• Osteomylitis of maxilla is much less frequent than
that of the mandible because the maxillary blood
supply is collateral, thin cortical plates and a relative
paucity of medullary tissues prevents the
confinement of infections within bone and permits
the dissipation of edema and pus into the soft
tissues and paranasal sinuses.
8

• In the mandible, the regions affected in
decreasing frequency are the body, symphysis,
angle, ramus and condyle.
9

Topazian and Goldberg:
Suppurative osteomyelitis
1. Acute suppurative
osteomyelitis
2. Chronic suppurative
osteomyelitis
• – Primary chronic
suppurative osteomyelitis
• – Secondary chronic
suppurative osteomyelitis
3.Infantile osteomyelitis
Nonsuppurative osteomyelitis
1. Chronic sclerosing
osteomyelitis
• – Focal sclerosing
osteomyelitis
• – Diffuse sclerosing
osteomyelitis
2. Garre's sclerosing
osteomyelitis
3. Osteoradionecrosis
11

 It may spread by hematogenous route or contiguous
sites of infection.
 The organisms enter the bloodstream through a minor
wound in the skin, or infection of upper respiratory
tract, middle ear.
 Contiguous sites of infection include periapical,
periodontal disease, pericoronitis, contaminated
fractures.
13

 The clinical presentation varies depending on whether
the infection is confined to the medullary cavity or has
spread to accumulate subperiosteally.
 Infection confined to medullary cavity leads to altered
sensation in the distribution of mental nerve on
affected side.
 There is an indurated swelling over the affected area
and teeth are tender to percussion.
 Tender regional lymphadenopathy is present.
14

 As the infection spreads to involve the cortex and
periosteum, there is deep boring pain with a fluctuant
intra and extra oral swelling over the affected area.
 Patient develops a high intermittent fever, malaise.
 The periosteum can be elevated upto the TMJ, where a
septic arthritis can occur.
 Laboratory findings show mild leucocytosis and raised
ESR.
15

 Inadequately treated acute osteomylitis progresses to
subacute or chronic form.
 Primary chronic osteomylitis 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.
 Secondary chronic osteomylitis occurs after acute
OML, when the treatment did not succeed in
eliminating the disease.
17

 The patient may present
with draining fistulae,
pathologic fracture or only
localized pain and swelling.
 Enlargement of mandible
due to deposition of
subperiosteal new bone.
 Teeth may become loose.
 Pathologic fracture may
occur.
18

 Acute osteomyelitis is similar to an acute primary
abscess in that the onset and course may be so rapid
that bone resorption does not occur and, thus, a
radiolucency may not be present on a radiograph.
 For radiographic evaluation 30 to 60 percent of the
mineralized portion of bone must be destroyed. This
degree of bone alteration requires a minimum of 14
days after onset of acute osteomylitis.
19

 The density of trabeculae will be decreased with
blurring or fuzziness in about ten days after acute
infection.
 Subsequently large multiple areas of radiolucencies
develop, which are enlarged trabecular spaces caused
by foci of necrosis and bone destruction.
 Chronic osteomylitis- islands of normal bone are
separated by irregular areas of bone destruction,
showing a moth-eaten appearance. This occur due to
enlargement of medullary spaces and widening of
Volkmann’s canals due to destruction by lysis and
replacement with granulation tissue.
20

 Segments of necrotic bone or sequestra become
detached, and gets surrounded by new bone or
involucrum.
 The involucrum is separated from sequestra by a zone
of radiolucency.
 The sequestra appear more dense and are better
defined.
21

 Fistulous tracts may
appear on the
radiographs as
radiolucent bands
traversing the body of
the jaw and penetrating
the cortical plates.
23

 The roots of teeth may undergo external resorption
and the lamina dura becomes less distinct as it blends
with the surrounding sclerotic bone.
 Stippled or granular densification of bone caused by
subperiosteal deposition of new bone or deposition of
new bone on surfaces of existing trabeculae .
24

 Evaluation and correction of compromised host
defenses.
 Gram staining and culture
 Imaging to rule out tumours
 Imaging of the region to find the extent of lesion
 Administration of stain- guided antibiotics
 Removal of loose teeth and sequestra
 Administration of culture guided antibiotics
 Sequestrectomy, debridement, decortication, resection
or reconstruction.
26

For medically compromised /Hospitalized patients-
 Penicillin G- 2million IU every 4 hourly plus
metronidazole 500mg 6hourly.
 When improved then :
 Penicillin V 500mg 4hourly plus metronidazole 500mg
6 hourly.
 Ampicillin/Sulbactum- 1.5 to 3g I.V 6 hourly.
 Amoxicillin/Clavulanate- 875/ 125mg bid for 6 weeks.
27

Incase of allergy to penicillin:
 Clindamycin 300-600mg orally 6 hourly
 Cephalosporin 250-500mg orally 6 hourly
28

 Clindamycin is effective against penicillinase
producing staphylococci, streptococci and anerobic
bacteria.
 Cephalosporins are not recommended as first choice
of drug because they are moderately effective against
oral anaerobes and their broad spectrum coverage
increases antibiotic complications.
29

 Are used to deliver high concentrations of antibiotics
into the wound bed and in immediate proximity to the
infected bone.
 The antibiotic leaches out from the beads, producing a
high local concentration.
 Tobramycin or gentamycin is contained in a acrylic
resin bead, these beads are left for 10 to 14 days and
then removed through a small incision.
30

 In the early acute stage , surgery is limited to removal
of severely loose teeth and bone fragments and
incision and drainage of fluctuant areas.
 If drainage persists despite antibiotic therapy, then
appropiate surgical modalities should be considered.
31

 Sequestra are generally seen 2 weeks after onset of
infection. They are avasular and poorly penetrated by
antibiotics.
 They can be resorbed, spontaneously expelled
through the mucosa or skin or removed.
 It can be removed with a minimum of surgical trauma.
32

 It is the ‘unroofing’ of the bone to expose the
medullary cavity for thorough debridement.
 It permits the removal of formed and forming
sequestra.
 It is done intra-orally, provides direct access to bone
and prevents facial scarring.
33

 It refers to the removal of chronically infected cortex of
bone, thus an access is provided to medullary cavity.
 It helps to improve regional vascular supply of the
involved area and shortens the healing time.
34

 Resection and Reconstruction may be necessary to
resolve persistent, low grade chronic infection.
 Used in cases of pathological fracture, persistent
infection after decortication and marked disease of
both cortical plates.
35

 It is a rare type of osteomylitis in infants, few weeks
after birth and usually affects the maxilla. There is risk
of involvement of the eye, extension to dural sinuses
and the potential for facial deformities and loss of
teeth resulting from delayed or inappropriate
treatment.
 It occurs by the hematogenous route or from perinatal
trauma of the oral mucosa from the obstetrician’s
finger or the mucus suction bulb used to clear the
airway immediately after birth. Infection from
contaminated human nipple or artificial nipples have
also been implicated.
37

 Clinically the patient has facial cellulitis centered
about the orbit. There is high fever, anorexia and
dehydration.
 Pus is often present in the nostril on affected side.
Inner and outer canthal swelling, palpebral edema,
closure of eye, conjunctivitis and proptosis may result.
38

 The maxilla on the affected side is swollen both
bucally and palatally, especially in the molar region.
 Fluctuance is present and fistulas may exist in the
alveolar mucosa. During the early acute phase little
radiographic changes may be evident.
39

 Treatment should be prompt and aggressive to prevent
permanent optic damage, neurological complications,
loss of tooth buds or bone.
 It consists of intravenous antibiotics and drainage of
all abscesses.
 I.V penicillin and a penicillinase resistant penicillin ,
ampicillin or clindamycin should be given.
40

 It is an inflammatory, nonsuppurative painful disease
with a protracted course, occurring only in mandible
and affects both the basal bone and alveolar process
and is usually unilateral. In addition to the body, it
may also affect the angle, ramus and condyle.
 The cause of this condition is controversial. Some
believe that the condition is infectious whereas others
believe that some cases are non-infectious and result
from overuse of jaw, malocclusion and abnormal jaw
positioning habits.
42

 Reactive proliferation of bone is the primary response
in diffuse sclerosing osteomylitis producing a sclerotic
radiographic appearance.
 Episodes of recurrent swelling, pain, fever and
lymphadenopathy may occur.
 The jaw may enlarge slightly on the affected side from
the subperiosteal deposition of bone. It is mainly seen
in older persons and two thirds of the patients are
females.
43

 The early changes consist
of ill defined osteolytic and
osteosclerotic areas.
 As the lesion progresses,
they become more sclerotic
and there is an increase in
size of the involved part. It
involves a large portion of
mandible but does not
cross the midline.
44

 Paget’s disease
 Eosinophilic granuloma
45

 It is a non-suppurative inflammatory condition
leading to a localized area of bone sclerosis associated
with the apex of a carious tooth.
 It occurs due to when the resistance of the host is high
or the virulence of the micro-organisms is low,
involving roots of molar in young persons.
47

 There is a well circumscribed radiopaque mass in the
periapical region, the margins may be distinct or blend
with surrounding bone. The root outline is visible.
48

 Hypercementosis
 Periapical cemental dysplasia
 Osteosclerosis
49

 Endodontic therapy or extraction.
50

• It is also known as chronic nonsuppurative
sclerosing osteomylitis, chronic osteomylitis with
proliferative periosteitis, periosteitis ossificans.
• It was first described by Carl Garre in 1893.
• It is a non-suppurative inflammatory process where
there is subperiosteal bone deposition caused by
mild irritation and infection.
52

• Mandible is affected more commonly than
maxilla.
• It is characterized by a localized, hard, non
tender, unilateral bony swelling of the lateral
and inferior aspects of mandible. The skin
overlying the lesion is normal.
Lymphadenopathy, fever and leucocytosis do
not occur.
53

• This disease is rare in occurrence because it’s
occurrence depends upon the occurrence of
chronically integrated conditions like chronic
infection in a young individual, with a
periosteum capable of osteoblastic activity
and an equilibrium between the resistance of
the host and the virulence of infectious
agents.
54

Radiographic findings
• Intra-oral radiograph will
reveal a carious tooth
opposite the bony mass.
• Occlusal radiograph will
show a focal area of well
calcified bone is which is
smooth and has a laminated
or onion skin appearance.
• No trabecular pattern is
seen between shell of new
bone and cortex.
55

Differential diagnosis
• Caffey’s disease
• Fibrous dysplasia
• Ewing’s sarcoma
57

Management
• Removal of infected tooth and curettage of
socket.
• Surgical recountouring may be done.
• Endodontic treatment if possible.
• Antibiotics – if signs of infection present.
58

• Actinomycotic OML of jaws is a chronic infection
manifestating both granulomatous and suppurative features
and usually involves soft tissues and occasionally bone of
cervicofacial, abdominal and thoracic region.
• It forms external sinuses that discharge distinctive sulphur
granules and spreads unimpeded by anatomical barriers when
endogenous oral commensals invade the tissues of
cervicofacial, thoracic and abdominal regions.
60

• Organisms gain entry into soft tissues directly or by extension
from bone through periapical or periodontal lesions, fractures
or extraction sites.
• Firm soft tissue masses are present on the skin, purplish dark
red areas with zones of fluctuance. Spontaneous drainage of
serous fluid containing granular material, which represent
colonies of bacteria. Regional lymph nodes are enlarged. The
patient usually has no fever and does not feel ill.
• These infections produce dense bone and scarring of soft
tissue and have been described as ‘lumpy jaw’.
61

• Radiolucent areas of varying sizes and delay in
healing of extraction sites. Periostitis, diffuse
mandibular radiolucencies and marked
sclerosis is seen.
• Sequestra may sometimes be seen.
62

Diagnosis
• It is based on culture or biopsy of the lesion. In
actinomycosis the smear reveals gram positive
organisms of various morphological types, diptheroid
and filamentous forms.
• Specific immunoflorescence staining to distinguish
between various forms is available.
• Biopsy of the wall of an abscess or fistula is useful in
making the diagnosis when material is not available
for smear and culture.
63

Management
• Many therapeutic regimes have been used like iodide,
radiation, incision and drainage, excision of soft tissue and
bone and use of antibiotics. Abscesses should be surgically
disrupted with a haemostat and all loculations penetrated.
• Penicillin is the drug of choice; the dose depends upon
severity of the disease. The suggested regime is 10 to 20
million units per day intravenously for 4 to 6 weeks, followed
by 5 to 10 million units for 3 to 4 months. In patients allergic
to penicillin, Tetracycline 250mg 4 times daily for 8 to 16
weeks may be prescribed. Erythromycin 500mg 4times daily
for 6 months.
• Sequestrectomy and saucerisation may be necessary.
64

• Tuberculous Osteomyelitis of maxilla and mandible
was earlier considered a rare disease.
• The supposed rarity of the disease in the jaws
arouses clinical suspicion, when a positive history of
systemic infection is absent.
• The diagnosis is established only after a biopsy and
microbiological study.
66

Pathogenesis
• The tuberculous microorganism belongs to the
mycobacterium genus. There are 3 possible methods of
inoculation of the bacteria into the bone:
• Direct inoculation of the bacilli into the oral mucosa through
an ulcer or break in the continuiuty of the mucosa.
• Spread to the bone via an extraction socket or an infected
fracture line.
• Hematogenous or lymphatic spread from a primary focus
elsewhere in the body.
67

• The disease progresses slowly with the formation of a
tubercle in the bone marrow. There is an increased vascularity
of the periosteum with initial subperiosteal resorption of the
bone, followed by laying down of a new layer of reactive
bone.
• As the disease progresses, there is caeseation necrosis in the
central portion of bone. The pus extends peripherally and a
subperiosteal abscess is formed, later the tuberculosis debris
is expelled into the soft tissues, from where they follow path
of least resistance.
• The abscess reddens but is not warm and is therefore called
as ‘cold abscess’.
68

Clinical Features
• The sites involved are ramus and body of
mandible.
• The age group involved is 15 to 40 years
69

• Closed lesion or lumpy jaw- The lesion is
located centrally in the jaw. The patient will
present only with a swelling and no draining
sinuses. There is absence of any oral septic
focus.
• Open lesion- There is presence of multiple
extraoral and intraoral sinuses with
mucopurulent discharge. Oral septic focus
may or may not be present
70

Diagnosis
• In cases of closed lesions, in the absence of an oral
septic focus, aspiration is a must to differentiate
between a cystic lesion, neoplasm and cold abscess.
• The smear is tested for acid fast bacilli. Culture is
done on Lowenstein Jensen medium.
• Mantoux test- an intradermal injection of 5
tuberculin units in a 0.1ml solution of purified
protein derivative is given. A positive reaction may be
seen clinically after 48 hours as erythema and
induration measuring more than 5 to 10mm. A
negative mantoux test does not exclude tuberculosis.
71

• Chest radiographs are a must to rule out pulmonary
involvement.
• Closed lesions of the jaws are seen as a small well
defined radiolucency, usually in the ascending ramus
with destruction of the buccal or medial cortical
plate.
• A full body scan with technetium 99 diphosphonate
is done to rule out systemic involvement.
72

• Computed tomography- is a useful imaging system,
the extent of disease can be accurately determined.
• Diagnosis of subperiosteal abscess, muscle
involvement and lymph node is facilitated.
• Biopsy – An incisional biopsy is done for open
lesions. Aspiration is done for closed lesions.
Histopathological evaluation is to evaluate for
tuberculoma, early caesation, Langhan’s giant cells
and lymphoid activity.
74

Management
• Depending on the severity of disease and the
patient’s body weight, the physician starts a
suitable Antikoch therapy.
• Usually a six month regimen with four drugs is
advised: isoniazide, rifampicin, ethambutol,
pyrizinamide. For the next four months:
isoniazide and rifampicin is advised.
75

• Radiotherapy is considered a major column 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
adjacent to the neoplasm.
• Because of its mineral composition, bone tissue
absorbs more energy than soft tissues and is
therefore more susceptible to secondary radiation. In
cases where the bone is irradiated exceeding a
certain local dose, osteoradionecrosis may develop,
leading to marked pain in the patient .
77

 It was once considered an infection initiated by bacteria,
which invaded the radiation damaged bone; hence, the term
“radiation-induced osteomyelitis” or radioosteomyelitis was
commonly used.
 Marx 1983 identified this condition as a radiation-induced
avascular necrosis of bone. He was able to demonstrate that
radiation caused a hypoxic, hypocellular, and hypovascular
tissue, leading to a spontaneous or trauma-initiated tissue
breakdown. The result is a chronic nonhealing wound,
susceptible to superinfection.
78

• Dose rates in excess of 60Gy have been found to
increase the risk.
• A total dose of approximately 6500 to 7000 Gy or
greater particularly to floor of mouth and mandible
showed increased incidence of ORN.
79

• It can be spontaneous, but it most commonly results
from tissue injury like denture related injury, tooth
extraction, ulcers.
• The absence of reserve reparative capacity is a result
of the prior radiation injury. The irradiated mandible,
periosteum, and overlying soft tissue undergo
hyperemia, inflammation, and endarteritis.
• These conditions ultimately lead to thrombosis,
cellular death, progressive hypovascularity, and
fibrosis. The radiated bed is hypocellular and devoid
of fibroblasts, osteoblasts, and undifferentiated
osteocompetent cells.
80

Classification
• Grade I ORN is the most common presentation.
Exposed alveolar bone is observed.
• Grade II designates ORN that does not respond to
hyperbaric oxygen (HBO) therapy and requires
sequestrectomy/saucerization.
• Grade III is demonstrated by full-thickness
involvement and/or pathologic fracture.
81

Clinical symptoms include the following:
• Pain
• Swelling
• Trismus
• Exposed bone
• Pathologic fracture
• Malocclusion
• Oral/ cutaneous fistula formation
82

Osteoradionecrosis of
left mandible has
resulted in a
pathologic fracture
83

• The incidence of involvement of mandible is 2-
3%. ORN of maxilla is rare.
• The second most common bone is temporal.
The time period between radiotherapy and
ORN has been reported as a mean of 7.5 to 20
years.
84

• Fractionated delivery of irradiation doses reduce the
risk of radiotherapy.
• Localized modes of delivery by brachytherapy limits
damage to surrounding tissues.
• 3D conformational radiation therapy and intensity
modulated therapy are able to maximise delivery to
treatment areas and minimize dose to surrouding
normal tissues.
• Radioprotectors can also be administered eg.
Amifostine (ethyol) is administered to reduce the
incidence of xerostomia. 86

PRE IRRADIATION DENTAL CARE
• Preventive dental measures are effective in reducing
the risk of osteoradionecrosis.
• The radiotherapist must seek dental consultation
early before initiation of radiation therapy to allow
achievement of optimal oral health. Failure to do so
may result in bone necrosis months or years after
completion of radiation therapy.
87

• All non restorable teeth in the direct beam of
radiation and teeth with significant periodontal
disease should be extracted 10 to 14 days before
radiation therapy begins. In patients with poor oral
health, extraction of all teeth is recommended.
• Complete instructions to practice oral hygiene should
be given. Custom trays should be provided to permit
application of 0.4% stannous fluoride gel or 1%
sodium fluoride gel.
88

POST RADIATION DENTAL CARE
• Dentures should not be used in the irradiated arch
for one year after radiotherapy.
• A saliva substitute may be used to lubricate the
mouth to replace diminished flow from irradiated
mucus and salivary glands.
• If post radiation pulpitis develops and the involved
tooth is restorable, endodontic therapy should be
undertaken. Caution should be undertaken not to
introduce organisms beyond the apex by
instrumentation.
89

• Removal of the teeth should be performed as
atraumatically as possible, with trimming of sharp
bony margins.
• Initial treatment is directed at controlling frank
infection, if present.
• If discrete abscesses or cutaneous fistulas are
present, aerobic and anaerobic cultures should be
obtained for sensitivity testing. Penicillin plus
metronidazole or clindamycin alone is
recommended.
90

• Ultrasound Therapy- It is used with local
debridement and is non-invasive and
promotes neovascularity and neocellularity of
ischaemic tissues and has been used
successfully.
• Pateints who are medically compromised may
achieve pain relief by resection of the
segment of involved bone.
91

Hyperbaric Oxygen Therapy
• This therapy consists of breathing 100% oxygen through a face
mask or hood in a large chamber at 2.4 absolute atmospheres
pressure for 90 minutes sessions or dives for as many as 5
days a week totalling 30 or more sessions, often followed by
another 10 or more sessions.
• HBO treatment causes an increase in arterial and venous
oxygen tension, which enhances healing by a direct
bacteriostatic effect on microorganisms that renders them
susceptible to lower antibiotic concentrations and by
enhancing phagocytic killing.
92

 It also helps in neoangiogenesis, fibroblastic
proliferation and collagen synthesis occur.
 HBO FACILITIES currently are limited, expensive
and complications exist ie oxygen toxicity, seizures,
high pressure nervous syndrome, decompression
sickness, pneumothorax, visual changes and
gastric distress.
 Optic neuritis and immunosuppressive disorders
are absolute contraindications.
93

 Treatment with pentoxifylline–tocopherol (PTX–Vit.E)
and clodronate in a patient with progressive severe
ORN has been reported.
 Pentoxifylline 800mg per day, Vit E 1000 IU per day
and Clodronate 1600mg per day for 3 years.
 PTX–Vit.E treatment has recently been shown to
significantly reduce the radiation-induced fibrotic
process. Clodronate is a well known biphosphonate
that inhibits osteoclastic bone destruction.
94

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