Osteomyelitis is an inflammatory condition of bone caused by infection that typically begins in the bone marrow and spreads. It can be acute or chronic. Acute osteomyelitis is characterized by constitutional symptoms like fever and pain in the affected area. Chronic osteomyelitis occurs after inadequate treatment of acute osteomyelitis and is marked by non-healing bone wounds. Staphylococcus aureus and Streptococcus pyogenes are common causes. Treatment involves antibiotics, removal of infected tissue, and sometimes surgery.

1. OSTEOMYELITIS OF BONES
DEFINITION
An inflammatory condition of bone that begins as an infection of medullary cavity &
Haversian systems of cortex & extends to involve periosteum of affected are.
Osteon = bony myelos= marrow itis= inflammation
Pathophysiology: Flow Chart
PREDISPOSING FACTORS
SYSTEMIC FACTORS COMPROMISING HOST IMMUNITY
Diabetes mellitus Malnutrition
Autoimmune disorders Chemotherapy
AIDS Corticosteroid and other immunosuppressive therapy
Agranulocytosis Alcohol and Tobacco
Anemia Drug abuse
Leukemia Prior major surgery
Syphills HEerpes simplex virus(Zoster) and Cytomegalovirus infection
Acute inflammation
[ edema, pus formation]
Pus, organism extension
Increased inflammatory
pressure
Haversian system / nutrient
canal involvement
Vascular collapse[ stasis,
thrombosis, ischemia of bone]
elevation of periosteum
disrupted blood supply
Compromised local blood supply
Avascular bone
Sequester formation

2. LOCAL AND SYSTEMIC FACTORS ALTERING BONE VASCULARITY
Smoking Osteoporosis
Diabetes mellitus bisphosphonate-induced osteochemonecrosis
Florid osseous dysplasia other forms of osteonecrosis[Hg, Bi Ar]
Fibrous dysplasia tobacco
Paget’s disease Radiation therapy and osteoradionecrosis
Osteopetrosis Bone malignancy
[Albers – Schonberg disease] [primary or metastatic ]
ETIOLOGY
 Odontogenic infection
 Traum Infection derived from periostitis following gingival ulceration,lumph nodes
infected from furuncles , laceration and peritonsillar abscess
 Infections derived by hematogenous route - furuncle on face , wound infection ,
middle ear infection ,mastoiditis , systemic tuberculosis.
HUDSON’ CLASSIFICATION
 ACUTE FORM OF OML [SUPPURATIVE & NON SUPPURATIVE INCLUDE
 CONTIGUOUS FOCUS
 TRAUMA
 SURGERY
 ODONTOGENIC INFECTIONS
 PROGRESSIVE
 BURNS
 SINUSITIS
 HEMATOGENOUS [METASTATIC ] - DEVELOPING SKELETON [CHILDREN]
CHONIC FORMS OF OML
 RECURRENT MULTIFOCAL-
1]- DEVELOPING SKELETON [CHILDREN]
2]- ESCALATED OSTEOGENIC ACTIVITY [AGE <25 YEARS]
 GARRE’S
1]- UNIQUE PROLIFERATIVE SUBPERIOSTEAL REACTION
2]-DEVELOPING SKELETON [CHILDREN TO YOUNG ADULTS]

3.  SUPPURATIVE OR NON SUPPURATIVE
1]- INADEQUATELY TREATED FORMS
2]- SYSTEMATICALLY COMPROMISED PATIENTS
3]-CHRONIC REFRACTORY OML
 DIFFUSE SCLEROSING
1]-FASTIDIOUS ORGANISM
2]-COMPROMISED HOST/PATHOGEN INERFACE
ACUTE SUPPURATIVE OSTEOMYELITIS
It may have appearance of a typical odontogenic infection . It can be localised & widespread ,
with extensive sequestration & possible pathological fracture.
MICROBIOLOGY
CAUSATIVE AGENT- pyogenic organism

4. Most commonly found organisms are Staphylococcus aureus & Streptococcus pyrogens.
ETIOLOGY
1]-ODONTOGENIC INFECTION
2]-LOCAL TRAUMATIC INJURIES
3]-PERITONSILLAR ABSCESS
4]-INFECTED COMPOUNDED ODONTOMA
5]-COMPOUND FRACTURES OF JAWS
6]-FURUNCULOSIS
7 ]-HEMATOGENOUS INFECTIONS
CLINICAL FEATURES
OCCURRENCE; In adults more common in mandible & involves alveolar
process angle of mandible , posterior part of ramus & coronoid process
A]-Early cases are characterised by
1]- Generalized constitutional symptoms- high intermittent fever , malaise , nausea,
vomiting, anorexia
2]-Deep seated boring , continuous intense pain in affected area
3]-Intermittent parasthesia or anesthesia of lower lip which help differentiation with alveolar
abscess
B]- Established cases have-
1]- Deep pain,malaise, fever, dehydration anorexia
2]-Teeth ininvolved area begins to loosen & become sensitive to percussion.
3]-Purulent discharge through sinus-
a]-intraorally
-around gingival sulcus or
-through buccal vestibule
b] extraorally on face, through cutaneou s fistulae
4]-fatid odor ,trismus, dehydration ,acidosis & toxaemia
5]- Regional lymphadenopathy present
Lab studies show -1]-Moderate leukocytosis[PMNL] 3]- Anemia

5. 2]-Slightly elevated ESR 4]-Albuminuria
CHRONIC OML
It can be 1]-Primary- resulting from organisms which are less virulent
2]- Secondary- occurring after acute oml, when treatment did not succeed in
eliminating infection.
CLINICAL FEATURES
-Pain & tenderness ; pain is minimal
-Non healing bony & overlying soft tissues wounds with induration of soft tissues
-intra oral or extra oral draining fistulae
-Thickend or ‘’ wooden ‘’’character of bone
-Enlargement of mandible, because of deposition of sub periosteal new bone
-Pathological fractures may occur
-sterile abscess [Brodie’s abscess] common in long bones , rare in jaws
-teeth in area tend to become loose & sensitive to palpation & percussion.
RADIOGRAPHIC FEATURES
WORTH’S CRITERIA 1969
 ‘MOTH –EATEN’ appearance [ enlagement of medullary spaces & widening of
VoKmann’s canals]
 Islands i. e. ‘seqeustrum’ [ avascular necrotic bone , which harbors
microorganisms] with evidence of trabeculae pattern & marrow spaces
 The CT Scans are informative in oml . It gives accurate indication of;
 Bone destruction
 Periosteal reaction
 Medullary destruction
 Cortical involvement
 MRI Scan is more accurate compared to CT Scans which informed about-
 Bone marrow & soft tissues changes
 Positron Emission Tomography [PET] is resently introduced –
 To confirms diagnosis of OML very early
 TREATMENT
 Clinical evaluation & correction of host defense deficiencies
 Administration of empirical antibiotics
 Imaging to rule out bone tumours
 Removal of septic foci such as loose teeth & sequestra

6.  Administration of culture guided antibiotics; repeated cultures
 Possible placement of irrigating drains / poly methyl methacrilate –antibiotic
beads
 Surgical management by sequestrectomy, decortications, debridement,
resection,& reconstruction
 Hyperbaric oxygen therapy;
 PATHOGENESIS
 OML is intsiated by----a contiguous focus of infection
 Or by hematogenous spread
 The imp factor in establishment of OML is compromise in blood supply.
 1]----a]primary supply—mandible is supplied by ----
 Inferior alveolar artery except coronoid process which is supplied by
temporalis muscle vessels
b]—Secondary supply-----It is periosteal supply which runs ||to cortical
surface of bone giving off nutrient vessels those penetrate cortical bone &
anastomose with branches of Inferior Alveolar artery
2]---VENOUS DRAINAGE OF MANDIBLE There are 2 routes
a]—VIA INF ALV VEIN--------It runs upwards & joins pharyngeal plexus
b]---It runs downwards & joins EXT JUG VEINS.
OTHER TYPES OF OML----
INFANTILE OML-------
1st
described by---REES In 1847
Occur within 1st
9 months of life & as early as 1 week after birth.
 ETIOLOGY----
 Hematogenous infection
 Infection
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