OSTEOMYELITIS

Introduction :

Osseous in Latin means bony and Osteon in Greek means bone. Myelos is marrow. Itis in Greek means inflammation.

Osteomyelitis means inflammation of medullary portion of the bone or bone marrow or cancellous bone.

Osteomyelitis was common earlier but at present the incidence of jaws was less because of worldwide availability of

  • Antibiotics.
  • Better awareness in medical and dental conditions.
  • Dental health care is increased day by day and even spread to layman.

Few cases even occur

  • Due to resistant organisms to antibiotics.
  • Medially handicapped individuals.

DEFINITION :

“An inflammatory condition of soft bone, that begins as an infection of medullary cavity and haversian systems of cortex and extends to involve the periosteum of the affected area”.

PREDISPOSING FACTORS :

Conditions that alters host defences and due to chronic debilitating systemic diseases:

  • Diabetes mellitus
  • Agranulocytosis
  • Leukaemia
  • Severe anaemia
  • Malnutrition
  • Drug abuse
  • Chronic alcoholism
  • Sickle cell disease
  • Typhoid (febrile illness)

Conditions that alter vascularity of bone :

  • Irradiation osteoporosis
  • Paget’s diseas
  • Fibrous dysplasia
  • Bone malignancy
  • Metallic bone necrosis (Hg, Bi, Ar)

Virulence of organisms:

Certain organisms precipitate thrombi formation by virtue of their destructive lysosomal enzymes.

ETIOLOGY:

Odontogenic infection from pulpal:

osteomyelitis

  • Periodontal tissues
  • Pericoronitis
  • Infected socket
  • Tumor
  • Cyst

Trauma:

post-traumatic-osteomyelitis

  • Second leading cause
  • Especially from compound fracture

Infection of orofacial regions:

  • Periostitis following gingival ulceration
  • Lymph nodes infected from faruncles
  • Laceration
  • Peritonsillar abscess

Infection derived by haematogenous route:

furuncle-of-face

  • Furuncle on face
  • Wound on skin
  • Upper respiratory tract infection
  • Middle ear infection
  • Mastoiditis
  • Systemic TB

CLASSIFICATION:

According to Topazian classification was done based on absence or presence of suppuration: 

  1. Suppurative
    • Acute suppurative osteomyelitis
    • Chronic suppurative osteomyelitis

i) Primary

ii) Secondary

  • Infantile osteolmyelitis
  • Non-suppurative osteomyelitis
  • Chronic sclerosing osteomyelitis

i) Focal

ii) Diffuse

  • Garre’s sclerosing osteomyelitis
  • Actinomycotic ostemyelitis
  • Radiation osteomyelitis
  • Specific infective osteomyelitis

i) TB

ii) Syphilis

 

  • Based on clinical course:

According to JOMS 1993: 51; 1994 by Hudson et al

 

  • Acute forms of osteomyelitis (suppurative and non-suppurative)
  • Contigous focus

i) Trauma

ii) Surgery

iii) Odontogenic infection

  • Progressive

i) Burns

ii) Sinusitis

iii) Vascular insufficiency

  • Hematogenous (metastatic)

i) Developing skeleton (children)

ii) Developing dentition (children)

  • Chronic forms of osteomyelitis
  • Recurrent multifocal

i) Developing skeleton (child)

ii) Escalated osteogenic activity (< age 25yrs)

  • Garre’s osteomyelitis

i) Unique proliferative subperiosteal reaction

ii) Developing skeleton

  • Suppurative or non-suppurative

i) Inadequately treated forms

ii) Systemically compromised forms

iii) Refractory forms

  • Sclerosing
    • Diffuse

i) Fastidious microorganisms

ii) Compromised host and pathogen interface

  • Focal

i) Predominantly odontogenic

ii) Chronic localized injury

 

  • Based on pathogenesis of altered, vascular perfusion (Vibhagool et al, 1993)

3 types:

i) Haematogenous osteomyelitis

ii) Osteomyelitis secondary to a contiguous focus infection

iii) Osteomyelitis with or without peripheral vascular disease.

 

  • Classification and staging system for osteomyelitis (Cierny et al, & Vibhagool)

 

  • Anatomic type:

i) Stage I: medullary osteomyelitis – involved medullary without cortical,           Haematogenous

ii) Stage II: superficial osteomyelitis – less than 2 cm bony defect without cancellous bone.

iii) Stage III: localized osteomyelitis – < 2 cm bony defect on radiograph, does not appear to involve both cortices.

iv) Stage IV: diffuse osteomyelitis – > 2 cm pathologic feature, infection, non-union.

  • Physiologic class:

i) Host – normal host

ii) Host – local compromise & systemic compromise

iii) Host – treatment is worse than disease

  • Systemic or local factors that affect immune surveillance, metabolism and local vascularity

i) Systemic – malnutrition, renal and hepatic failure, diabetes mellitus, chronic hypoxia, immune deficiency, malignancy, old ages, tobacco, alcohol abuse.

ii) Local      –        chronic lymphedema, venous stasis, major vessel disease, arthritis, extensive scarring, radiation fibrosis, small vessel disease, local loss of sensation.

PATHOGENESIS

Periapical and periodontal infections localised by protective pyogenic membrane

                                           ⇓   Sufficient virulent M.O

Destroy this barrier

Infection into the bone

Pus (necrotic tissue, dead cells) accumulates in canals (Yolkman Haversian)

⇓                                                                                  ⇓

Vascular collapse (thrombosis)                     compression of neurovascular bundle

⇓                                                                                    ⇓

Ischemia                                                         mandibular anesthesia

The island of dead bone formed becomes place for precipitate of ionized calcium mobilized form surrounding osteolytic process (so sequestrum appears more opaque).

If pus continues to accumulate the periosteum is penetrated and mucosal and cutaneous abscess and fistula develop.

Mechanical trauma burnishes the bone causing ischemia and introduces organism initiated by acute inflammation – hyperemia increase capillary permeability.

As natural host defences and therapy begins to be effective the process becomes chronic, inflammation regresses, granulation tissue is formed and new blood vessels causes lyses of bone thus separating fragment of necrotic bone from viable involucrum.

The process leading to the formation of osteomyelitis is initiated by acute inflammation, hyperemia increase capillary permeability, and infiltration of granulocytes.

Tissue necrosis occurs as proteolytic enzymes are liberated and as destruction of bacteria and vascular thrombosis continues, there is pus formation.

  • Radiographically: –

The bone surrounding sequestrum appears less densely mineralized than sequestrum. Ischemia causes increase in CO2 level, which attracts calcium due to change in patient. The Ca deposition leads to increase in mineralization of the sequestrum.

Osteomyelitis in mandible: –

Osteomyelitis in mandible is common in adults. In craniofacial skeleton only the mandible and the calvarium have myeloid compartments.

The important factor in establishment of osteomyelitis is the compromise in the blood supply and venous drainage of mandible.

  • Blood supply: – Primary supply is through inferior alveolar artery, except coronoid process supplied temporalis muscle vessels.

Secondary supply is periosteal supply through, which generally runs parallel to cortical surface of bone giving nutrient vessels those penetrate cortical bone and anastomoses with the branches of inferior alveolar artery.

  • Venous drainage: – There are two routes via inferior alveolar vein.

It runs upwards and joins pharyngeal plexus.

It runs downwards and joins external jugular veins.

                               Walden (1943) gave a description of vascular morphology of mandibular and associated structures to account for spread of osteomyelitis. He described mandibular vascular support as being provided through multiple arterial loops from major vessels, which renders a large portion of bone susceptible to necrosis with the occurrence of major vessel infectious thrombosis.

                               Walsel Vogel  (1970) describe,These tend to be segregation of terminal channels, which act like “end organs” due to lack of terminal collateral anastomoses, ultimately leading to vascular plugging by bacteria microthrombi or both. When afferent vessels anastomose with medullary channels there is a possibility of decrease in venous flow with associated areas of greater turbulence. These may be a reduction in host immune defence mechanism associated with these vascular channels in calcified tissue.

  • Osteomyelitis in maxilla: –

This is rare in adults due to

  • Extensive blood supply and significant collateral blood flow in mid face.
  • Porous nature of membranous bone.
  • Thin cortical plates.
  • Abundant medullary space.

These preclude confinement of infections with in bone and permit dissipation of oedema and pus into soft tissue and paranasal air sinuses.

  • MICROBIOLOGY: –

In past, the etiology of osteomyelitis was associated with skin surface bacteria, S. aureus and to lesser extent S. epidermidis, which was found that these organisms are found in bone not in skin.

However, aureus as primary offending pathogen does not hold true with regard to osteomyelitis.

Most of cases are caused by aerobic Streptococci (i.e., hemolytic streptococci, Streptococci viridans, anaerobic Streptococci, and Bacteroides)

Sometimes Klebsiella, Pseudomonas and Proteus are also found. Other organisms – M. tuberculosis, T. pallidium, Actinomyces, Coccidiodes, Tuberculosis bacilli, Treponema & Klebsei