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Osteomyelitis

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Osteomyelitis
SpecialtyRheumatology, podiatry Edit this on Wikidata

Osteomyelitis (osteo- derived from the Greek word osteon, meaning bone, myelo- meaning marrow, and -itis meaning inflammation) simply means an infection of the bone or bone marrow.[1] It can be usefully subclassified on the basis of the causative organism (pyogenic bacteria or mycobacteria), the route, duration and anatomic location of the infection.

Pathogenesis

In general, microorganisms may infect bone through one or more of three basic methods: via the bloodstream, contiguously from local areas of infection (as in cellulitis), or penetrating trauma, including iatrogenic causes such as joint replacements or internal fixation of fractures or root-filled teeth.[1] Once the bone is infected, leukocytes enter the infected area, and, in their attempt to engulf the infectious organisms, release enzymes that lyse the bone. Pus spreads into the bone's blood vessels, impairing their flow, and areas of devitalized infected bone, known as sequestra, form the basis of a chronic infection.[1] Often, the body will try to create new bone around the area of necrosis. The resulting new bone is often called an involucrum.[1] On histologic examination, these areas of necrotic bone are the basis for distinguishing between acute osteomyelitis and chronic osteomyelitis. Osteomyelitis is an infective process that encompasses all of the bone (osseous) components, including the bone marrow. When it is chronic, it can lead to bone sclerosis and deformity.

Chronic osteomyelitis may be due to the presence of intracellular bacteria (inside bone cells).[2] Also, once intracellular, the bacteria are able to escape and invade other bone cells.[3] In addition, once intracellular, the bacteria becomes resistant to some antibiotics.[4] These combined facts may explain the chronicity and difficult eradication of this disease. This results in significant costs and disability and may even lead to amputation. Intracellular existence of bacteria in osteomyelitis is likely an unrecognized contributing factor to its chronic form.

In infants, the infection can spread to the joint and cause arthritis. In children, large subperiosteal abscesses can form because the periosteum is loosely attached to the surface of the bone.[1]

Because of the particulars of their blood supply, the tibia, femur, humerus, vertebra, the maxilla, and the mandibular bodies are especially susceptible to osteomyelitis.[5] Abscesses of any bone, however, may be precipitated by trauma to the affected area. Many infections are caused by Staphylococcus aureus, a member of the normal flora found on the skin and mucous membranes. In patients with sickle cell disease, the most common causative agent remains Salmonella, but Staphylococcus aureus species become proportionally more common pathogens than in healthy hosts.

Cause

Age group Most common organisms
Newborns (younger than 4 mo) S. aureus, Enterobacter species, and group A and B Streptococcus species
Children (aged 4 mo to 4 y) S. aureus, group A Streptococcus species, Haemophilus influenzae, and Enterobacter species
Children, adolescents (aged 4 y to adult) S. aureus (80%), group A Streptococcus species, H. influenzae, and Enterobacter species
Adult S. aureus and occasionally Enterobacter or Streptococcus species
Sickle Cell Anemia Patients Salmonella species

In children, the long bones are usually affected. In adults, the vertebrae and the pelvis are most commonly affected.

Acute osteomyelitis almost invariably occurs in children. When adults are affected, it may be because of compromised host resistance due to debilitation, intravenous drug abuse, infectious root-canaled teeth, or other disease or drugs (e.g., immunosuppressive therapy).

Osteomyelitis is a secondary complication in 1–3% of patients with pulmonary tuberculosis.[1] In this case, the bacteria, in general, spread to the bone through the circulatory system, first infecting the synovium (due to its higher oxygen concentration) before spreading to the adjacent bone.[1] In tubercular osteomyelitis, the long bones and vertebrae are the ones that tend to be affected.[1]

Staphylococcus aureus is the organism most commonly isolated from all forms of osteomyelitis.[1]

Bloodstream-sourced osteomyelitis is seen most frequently in children, and nearly 90% of cases are caused by Staphylococcus aureus. In infants, S. aureus, Group B streptococci (most common[6]) and Escherichia coli are commonly isolated; in children from 1 to 16 years of age, S. aureus, Streptococcus pyogenes, and Haemophilus influenzae are common. In some subpopulations, including intravenous drug users and splenectomized patients, Gram-negative bacteria, including enteric bacteria, are significant pathogens.[7]

The most common form of the disease in adults is caused by injury exposing the bone to local infection. Staphylococcus aureus is the most common organism seen in osteomyelitis, seeded from areas of contiguous infection. But anaerobes and Gram-negative organisms, including Pseudomonas aeruginosa, E. coli, and Serratia marcescens, are also common. Mixed infections are the rule rather than the exception.[7]

Systemic mycotic (fungal) infections may also cause osteomyelitis. The two most common are Blastomyces dermatitidis and Coccidioides immitis.

In osteomyelitis involving the vertebral bodies, about half the cases are due to Staphylococcus aureus, and the other half are due to tuberculosis (spread hematogenously from the lungs). Tubercular osteomyelitis of the spine was so common before the initiation of effective antitubercular therapy that it acquired a special name, Pott's disease.

Following laboratory analysis of clinical data and studied literature, we can say that the bone pathological changes are induced by several interrelated mechanisms the drug components, produced clandestinely.[8] The Burkholderia cepacia complex have been implicated in vertebral osteomyelitis in intravenous drug users.[9]

Diagnosis

Diagnosis of osteomyelitis is often based on radiologic results showing a lytic center with a ring of sclerosis.[1] Culture of material taken from a bone biopsy is needed to identify the specific pathogen; alternative sampling methods such as needle puncture or surface swabs are easier to perform, but do not produce reliable results.[10]

Factors that may commonly complicate osteomyelitis are fractures of the bone, amyloidosis, endocarditis, or sepsis.[1]

Treatment

Osteomyelitis often requires prolonged antibiotic therapy, with a course lasting a matter of weeks or months. A PICC line or central venous catheter is often placed for this purpose. Osteomyelitis also may require surgical debridement. Severe cases may lead to the loss of a limb. Initial first-line antibiotic choice is determined by the patient's history and regional differences in common infective organisms. A treatment lasting 42 days is practiced in a number of facilities.[11] Local and sustained availability of drugs have proven to be more effective in achieving prophylactic and therapeutic outcomes.[12]

In 1875, American artist Thomas Eakins depicted a surgical procedure for osteomyelitis at Jefferson Medical College, in a famous oil painting titled The Gross Clinic.

Prior to the widespread availability and use of antibiotics, blow fly larvae were sometimes deliberately introduced to the wounds to feed on the infected material, effectively scouring them clean.[13][14]

Hyperbaric oxygen therapy has been shown to be a useful adjunct to the treatment of refractory osteomyelitis.[15][16]

Open surgery is needed for chronic osteomyelitis, whereby the involucrum is opened and the sequestrum is removed or sometimes saucerization[17] can be done

Fossil record

Main article: Paleopathology

Evidence for osteomyelitis found in the fossil record is studied by paleopathologists, specialists in ancient disease and injury. Osteomyelitis has been reported in fossils of the large carnivorous dinosaur Allosaurus fragilis.[18]

See also

References

  1. ^ a b c d e f g h i j k Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; & Mitchell, Richard N. (2007). Robbins Basic Pathology (8th ed.). Saunders Elsevier. pp. 810–811 ISBN 978-1-4160-2973-1
  2. ^ Ellington Microb Pathog 1999
  3. ^ Ellington JBJS Br 2003
  4. ^ Ellington J Ortho Res 2006
  5. ^ King MD, Randall W. (2006-07-13). "Osteomyelitis". eMedicine. WebMD. Retrieved 2007-11-11. {{cite web}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  6. ^ Haggerty, Maureen (2002). "Streptococcal Infections". Gale Encyclopedia of Medicine. The Gale Group. Retrieved 2008-03-14.
  7. ^ a b Carek, P.J. (2001-06-15). "Diagnosis and management of osteomyelitis". Am Fam Physician. 63 (12): 2413–20. PMID 11430456. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  8. ^ Mihail Radzichevici, Dumitru Șcerbatiuc, Natalia Rusu (2010). "The complex treatment of steomyelitis" (HTML). Rev. chir. oro-maxilo-fac. implantol. (in Template:Ro icon). 1 (1): 36–40. ISSN 2069-3850. 13. Retrieved 2012-04-09. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link) CS1 maint: unrecognized language (link)(webpage has a translation button)
  9. ^ Weinstein, Lenny (2007-12-16). "Cervical osteomyelitis caused by Burkholderia cepacia after rhinoplasty". J Infect Developing Countries. 2 (1): 76–77. ISSN 1972-2680. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help) [dead link‍]
  10. ^ Senneville E, Morant H, Descamps D; et al. (2009). "Needle puncture and transcutaneous bone biopsy cultures are inconsistent in patients with diabetes and suspected osteomyelitis of the foot". Clin Infect Dis. 48 (7): 888–93. doi:10.1086/597263. PMID 19228109. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  11. ^ Putland M.D, Michael S., Hyperbaric Medicine, Capital Regional Medical Center, Tallahassee, Florida, personal inquiry June 2008.
  12. ^ Soundrapandian, C (2007). "Drug-eluting implants for osteomyelitis". Crit Rev Ther Drug Carrier Syst. 24 (6): 493–545. PMID 18298388. Retrieved 2010-09-27. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  13. ^ Baer M.D., William S. (1 July 1931). "The Treatment of Chronic Osteomyelitis with the Maggot (Larva of the Blow Fly)". Journal of Bone and Joint Surgery. 13 (3): 438–475. Retrieved 2007-11-12.
  14. ^ McKeever, Duncan Clark (2008). "The Classic: Maggots in Treatment of Osteomyelitis: A Simple Inexpensive Method". Clin. Orthop. Relat. Res. 466 (6): 1329–35. doi:10.1007/s11999-008-0240-5. PMC 2384033. PMID 18404291. {{cite journal}}: Unknown parameter |month= ignored (help)
  15. ^ Mader JT, Adams KR, Sutton TE (1987). "Infectious diseases: pathophysiology and mechanisms of hyperbaric oxygen". J. Hyperbaric Med. 2 (3): 133–140. Retrieved 2008-05-16.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  16. ^ Kawashima M, Tamura H, Nagayoshi I, Takao K, Yoshida K, Yamaguchi T (2004). "Hyperbaric oxygen therapy in orthopedic conditions". Undersea Hyperb Med. 31 (1): 155–62. PMID 15233171. Retrieved 2008-05-16.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  17. ^ http://medical-dictionary.thefreedictionary.com/saucerization
  18. ^ Molnar, R. E., 2001, Theropod paleopathology: a literature survey: In: Mesozoic Vertebrate Life, edited by Tanke, D. H., and Carpenter, K., Indiana University Press, p. 337-363.

Further reading

  • Mechanisms of Staphylococcus aureus invasion of cultured osteoblasts. Ellington JK, Reilly SS, Ramp WK, Smeltzer MS, Kellam JF, Hudson MC. Microb Pathog. 1999 Jun;26(6):317–23.
  • Intracellular Staphylococcus aureus. A mechanism for the indolence of osteomyelitis. Ellington JK, Harris M, Webb L, Smith B, Smith T, Tan K, Hudson M. J Bone Joint Surg Br. 2003 Aug;85(6):918–21.
  • Intracellular Staphylococcus aureus and antibiotic resistance: implications for treatment of staphylococcal osteomyelitis. Ellington JK, Harris M, Hudson MC, Vishin S, Webb LX, Sherertz R. J Orthop Res. 2006 Jan;24(1):87–93.
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