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Professional Reference articles are designed for health professionals to use. They are written by UK doctors and based on research evidence, UK and European Guidelines. You may find the Osteomyelitis article more useful, or one of our other health articles.

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What is osteomyelitis?

Osteomyelitis is an inflammatory bone disease that is caused by an infecting micro-organism, leading to progressive bone destruction and loss and, if the periosteum becomes involved, necrosis. The most common causative species are the usually commensal staphylococci, with Staphylococcus aureus and Staphylococcus epidermidis responsible for the majority of cases.1 When dead bone becomes detached from healthy bone, it is known as a sequestrum.

A large sequestrum that remains in situ acts as a focus for ongoing infection. An involucrum refers to viable periosteum that has become separated from the underlying bone and which forms new bone around it. In acute and chronic disease, there is subsequent bone remodelling and often, associated deformity. The most common site of infection is the distal femur and the proximal tibia in children and cancellous bone in adults. However, ultimately any bone may be affected.

Osteomyelitis may be acute or chronic (evolving over months or even years) and can be further categorised into two main subgroups2 3 :

Haematogenous osteomyelitis

  • This is an infection resulting from haematological bacterial seeding from a remote source.

  • Acute haematogenous osteomyelitis is the most frequent form of osteomyelitis in children, when it tends to occur in the rapidly growing and highly vascular metaphysis of growing bones.4

  • Haematogenous osteomyelitis is also seen in patients with distant foci of infection, such as those with infected urinary catheters.

Direct (contiguous) osteomyelitis

  • This type of infection occurs where there is direct contact of infected tissue with bone - as may occur during a surgical procedure or following trauma.

  • Clinical signs tend to be more localised and there are often multiple organisms involved.

Chronic non-bacterial osteomyelitis5

Although chronic in nature, chronic non-bacterial osteomyelitis can present with episodic flares and phases of remission, which have led to the name 'chronic recurrent osteomyelitis', with its severe multifocal form 'chronic recurrent multifocal osteomyelitis'. An infectious aetiology had been considered, since especially Propionibacterium acnes had been isolated from bone lesions of individual patients. However, long-term antibiotic therapy did not alter the course of disease and modern microbiological techniques (including PCR) failed to confirm bone infection as an underlying cause.


There are a number of possible pathogens but Staphylococcus aureus is by far the most common. More than one organism may be involved.

  • S. aureus including strains of meticillin-resistant S. aureus (MRSA).

  • Haemophilus influenzae.

  • Streptococcus spp.

  • Escherichia coli.

  • Proteus spp.

  • Pseudomonas spp.

  • Coagulase-negative Staphylococcus spp.

  • Mycobacteria.

  • Fungi.

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  • The incidence of chronic osteomyelitis is increasing because of the prevalence of predisposing conditions such as diabetes mellitus and peripheral arterial disease.

  • There is a bimodal age distribution with acute, haematogenous osteomyelitis occurring predominantly in children. Contiguous osteomyelitis (often associated with direct trauma) is more frequently seen in adolescents and adults.

Risk factors

  • Trauma (orthopaedic surgery or open fracture).

  • Prosthetic orthopaedic device.

  • Diabetes: clinically unsuspected osteomyelitis is frequent in persisting diabetic foot ulcers and is a high risk factor for adverse outcome. Early diagnosis is crucial to ensure correct management.7

  • Peripheral arterial disease.

  • Chronic joint disease.

  • Alcohol dependency.

  • Intravenous drug misuse.

  • Chronic steroid use.

  • Immunosuppression.

  • Tuberculosis.

  • HIV and AIDS.

  • Sickle cell disease.

  • Presence of catheter-related bloodstream infection.

Osteomyelitis symptoms6

Haematogenous osteomyelitis

Long bone

  • Classic presentation:

    • The acutely febrile and bacteraemic patient presents with a markedly painful, immobile limb.

    • There may be swelling and extreme tenderness over the affected area with associated erythema and warmth.

    • The pain is exacerbated by movement and there may be sympathetic effusion of neighbouring joints.

    • In neonates and infants, there may be an associated septic arthritis.

  • Other presentations:

    • Occasionally, the patient may present with mild symptoms, perhaps a history of blunt trauma to the area which may or may not be remembered (eg, a bump against a hard surface) 24-48 hours previously and mild or no pyrexia.

    • There may be nonspecific systemic malaise attributed to a viral illness and suspicions are only raised as the symptoms localise after several days.


  • Vertebral osteomyelitis is a potentially fatal infection which is insidious, presenting with back pain. Fever is present in about 60% of patients.

  • Neurological deficits, including radiculopathy, urinary retention, limb weakness, paralysis, dysaesthesia, or sensory loss are less common.

  • There may be localised oedema, erythema and tenderness ± associated contiguous vascular insufficiency.

  • Prompt diagnosis is very important to prevent permanent neurological deficit or death.

  • Pott's disease:

    • Pott's disease refers to vertebral osteomyelitis resulting from the haematogenous spread of tuberculosis.

    • There is damage to the bodies of two neighbouring vertebrae, leading to vertebral collapse and subsequent abscess formation (known as a 'cold abscess').

    • Pus can track out from there into adjacent structures, leading to systemic symptoms of malaise, fever and night sweats.

Contiguous osteomyelitis

  • Patients tend to present in the classic manner with fever, pain and erythema (see above).

  • However, they may have an associated history of accidental or surgical trauma (including dental procedures).

Diabetic foot ulcers

  • These may be present and the pain masked by neuropathy.

  • Clinical diagnosis may be complicated by the absence of local signs of infection, such as purulent drainage and local erythema, warmth, and tenderness.

  • Often the only systemic sign of diabetic foot osteomyelitis is recalcitrant hyperglycaemia; fever and chills are absent in up to two thirds of patients.

Chronic osteomyelitis

Patients may have all or only a few of the following:

  • Previous acute infection (either unresponsive to treatment or relapsing following treatment).

  • Localised bone pain.

  • Erythema and swelling over the affected area.

  • Non-healing ulcer.

  • Draining sinus tracts.

  • Decreased range of motion of adjacent joints.

  • Chronic fatigue.

  • Generalised malaise.

Occasionally, the infection becomes localised to form a chronic abscess (Brodie's abscess) within the bone. These patients may be asymptomatic for months or years or may have a history of intermittent, localised pain.

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Differential diagnosis

Patients presenting with a history of trauma may pose a diagnostic difficulty, as the initial symptoms may be similar to early osteomyelitis. The key is that symptoms should rapidly settle following minor trauma; continued pain and swelling to the initial injury as well as raised inflammatory markers can help confirm clinical suspicion of osteomyelitis. It is therefore important to tell patients being discharged with a history of minor trauma to return if their symptoms do not settle or if they become systemically unwell.


Laboratory tests

  • FBC (white cells are usually up) and inflammatory markers.

  • Blood cultures are mandatory and positive in ~60% of cases (unless there is localisation of the infection into an abscess or where there is underlying vascular insufficiency).

  • Any expressed pus needs to be cultured, as do samples from joint effusion taps and any potential primary sources (eg, urine).

  • Bone cultures (or curettage where there are associated ulcers) provide the gold standard for diagnosis, with a positive test in ~90% of patients.

  • Specifically inform the laboratory if you suspect mycobacterial or fungal infections, as these require different growth media.

  • Where chronic osteomyelitis is suspected, diagnosis may be a little more tricky, as blood cultures are rarely positive and samples from sinus tracts are unreliable.

  • S. aureus serodiagnosis using the anti-staphylolysin test ± the anti-nuclease test. If a bone biopsy is performed, it should be done through non-infected tissue.


  • MRI is the imaging modality of choice for investigation of acute osteomyelitis, allowing good visualisation of even subtle abnormalities9 .

  • Plain X-ray films:

    • May be helpful in the diagnosis of chronic osteomyelitis (look for patchy osteopenia and signs of bone destruction) but its use is limited in acute cases where early signs of soft tissue swelling only become apparent after at least two to three days.

    • A periosteal reaction cannot be seen until about seven days and bone necrosis after ten days.

Osteomyelitis treatment and management

The success of osteomyelitis treatment, particularly in cases related to implants, is closely linked to extensive surgical debridement and adequate antibiotic therapy. Adjuvant therapies may also be used - eg, hyperbaric oxygenation.

Acute infections can be treated initially with extensive surgical cleaning associated with antibiotic therapy lasting four to six weeks. Chronic infections should be treated with extensive surgical debridement, removal of any implants and antibiotic therapy lasting three to six months.3

The local treatment itself is based on five principles:10

  • Local bone and soft tissue debridement.

  • Stabilisation of the bone.

  • Local antibiotic therapy.

  • Reconstruction of the soft tissue.

  • Reconstruction of the osseous defect zone.

Antimicrobial therapy is now complicated by the increasing prevalence of antibiotic-resistant organisms, especially MRSA.11

  • Early clinical suspicion, confirmation through imaging and microbiological tests and prompt treatment are the keys to a successful outcome.

  • Analgesia (and limb splinting if a long bone is involved) is an important part of symptom control.

  • Exact treatment varies according to the bones involved, the severity of the infection and the immune status of the patient.

  • Surgery may be needed to debride the bone and close any defects.

Antibiotic regimes12

Most antibiotics have good penetration into bone and joint tissues reaching concentrations exceeding the minimum inhibitory concentrations of common bone and joint infection pathogens. A few exceptions, which include penicillin and metronidazole, show a lower than optimum penetration into bones.13

  • Seek specialist advice if chronic infection or prostheses are present.

  • Flucloxacillin: consider adding fusidic acid or rifampicin for the initial two weeks. Suggested duration of treatment is six weeks for acute infection.

  • If penicillin-allergic, clindamycin. Consider adding fusidic acid or rifampicin for the initial two weeks. Suggested duration of treatment is six weeks for acute infection.

  • If MRSA is suspected, vancomycin (teicoplanin may also be used). Consider adding fusidic acid or rifampicin for the initial two weeks. Suggested duration of treatment is six weeks for acute infection.

The treatment for acute infection is usually for four to six weeks and chronic infection for at least 12 weeks. High doses are required to achieve suitable concentrations in necrotic avascular bone. Intravenous treatment is used initially and also to cover any surgical period, up to two weeks following surgery. The switch to oral therapy may happen once the clinical condition stabilises, the inflammatory markers are going down and there are reliable microbiology results.

Although treatment is guided by clinical response and the level of inflammatory markers, an early drop in CRP shouldn't tempt early discontinuation of antibiotics - expect to be treating the patient for no less than four weeks. Changes on plain X-ray lag at least two weeks behind normalisation of CRP.

Specifically consult the microbiologists if there is a risk of MRSA or if there is a prosthetic device in situ. Microbiologists will also be able to help in the case of polymicrobial infection. Rifampicin should not be used alone, as antimicrobial resistance rapidly develops.

Chronic osteomyelitis

  • It is usually appropriate to delay treatment until culture and sensitivity results are obtained, unless the infection is severe, in which case empirical treatment is started as above.

  • The standard recommendation for antibiotic treatment is six weeks of parenteral antibiotic therapy. However, the optimal duration of therapy for chronic osteomyelitis remains uncertain.14

  • Surgical debridement is the mainstay of treatment (it removes the necrotic tissue and provides an infection-free scaffold for future healing).

  • If surgery is not possible, indefinite antimicrobial therapy may be required but this is generally accepted to be less effective than surgery.

Osteomyelitis and the diabetic foot ulcer

People with diabetes are at increased risk of developing osteomyelitis, particularly in the foot, and of subsequent need for lower limb amputation. Antibiotic therapy and surgical treatment for diabetic foot osteomyelitis have similar outcomes in terms of healing rates, time to healing, and short-term complications in patients with neuropathic forefoot ulcers complicated by osteomyelitis without ischaemia or necrotising soft tissue infections.15

Osteomyelitis complications

  • Bone abscess.

  • Bacteraemia.

  • Fracture.

  • Growth arrest.

  • Septic arthritis.

  • Loosening of the prosthetic implant.

  • Overlying soft tissue cellulitis.

  • Chronic infection.


  • This is variable depending on the number of risk factors and the patient's general condition.

  • Timely diagnosis and intervention in an otherwise well patient should lead to full recovery, although follow-up over several months will be required to monitor for relapse.

  • Surgery combined with anti-infective chemotherapy leads to long-lasting containment of infection in 70% to 90% of cases of chronic osteomyelitis.16

  • However, chronic osteomyelitis can persist intermittently for years with frequent therapeutic failure or relapse.17

Prevention of osteomyelitis

It is not possible to prevent osteomyelitis but limitation of its effects is through awareness of risk factors, early suspicion and prompt treatment.

Further reading and references

  1. Kavanagh N, Ryan EJ, Widaa A, et al; Staphylococcal Osteomyelitis: Disease Progression, Treatment Challenges, and Future Directions. Clin Microbiol Rev. 2018 Feb 14;31(2). pii: 31/2/e00084-17. doi: 10.1128/CMR.00084-17. Print 2018 Apr.
  2. Lew DP, Waldvogel FA; Osteomyelitis. Lancet. 2004 Jul 24-30;364(9431):369-79.
  3. Lima AL, Oliveira PR, Carvalho VC, et al; Recommendations for the treatment of osteomyelitis. Braz J Infect Dis. 2014 Sep-Oct;18(5):526-34. doi: 10.1016/j.bjid.2013.12.005. Epub 2014 Apr 1.
  4. McNeil JC; Acute Hematogenous Osteomyelitis in Children: Clinical Presentation and Management. Infect Drug Resist. 2020 Dec 14;13:4459-4473. doi: 10.2147/IDR.S257517. eCollection 2020.
  5. Hedrich CM, Morbach H, Reiser C, et al; New Insights into Adult and Paediatric Chronic Non-bacterial Osteomyelitis CNO. Curr Rheumatol Rep. 2020 Jul 23;22(9):52. doi: 10.1007/s11926-020-00928-1.
  6. Hatzenbuehler J, Pulling TJ; Diagnosis and management of osteomyelitis. Am Fam Physician. 2011 Nov 1;84(9):1027-33.
  7. Gemechu FW, Seemant F, Curley CA; Diabetic foot infections. Am Fam Physician. 2013 Aug 1;88(3):177-84.
  8. Maamari J, Tande AJ, Diehn F, et al; Diagnosis of vertebral osteomyelitis. J Bone Jt Infect. 2022 Jan 27;7(1):23-32. doi: 10.5194/jbji-7-23-2022. eCollection 2022.
  9. Kapoor A, Page S, Lavalley M, et al; Magnetic resonance imaging for diagnosing foot osteomyelitis: a meta-analysis. Arch Intern Med. 2007 Jan 22;167(2):125-32.
  10. Tiemann AH, Hofmann GO; Wound irrigation within the surgical treatment of osteomyelitis. GMS Interdiscip Plast Reconstr Surg DGPW. 2012 Jan 9;1:Doc08. doi: 10.3205/iprs000008. eCollection 2012.
  11. Rao N, Ziran BH, Lipsky BA; Treating osteomyelitis: antibiotics and surgery. Plast Reconstr Surg. 2011 Jan;127 Suppl 1:177S-187S. doi: 10.1097/PRS.0b013e3182001f0f.
  12. British National Formulary (BNF); NICE Evidence Services (UK access only)
  13. Thabit AK, Fatani DF, Bamakhrama MS, et al; Antibiotic penetration into bone and joints: An updated review. Int J Infect Dis. 2019 Apr;81:128-136. doi: 10.1016/j.ijid.2019.02.005. Epub 2019 Feb 14.
  14. Spellberg B, Lipsky BA; Systemic antibiotic therapy for chronic osteomyelitis in adults. Clin Infect Dis. 2012 Feb 1;54(3):393-407. doi: 10.1093/cid/cir842. Epub 2011 Dec 12.
  15. Lazaro-Martinez JL, Aragon-Sanchez J, Garcia-Morales E; Antibiotics versus conservative surgery for treating diabetic foot osteomyelitis: a randomized comparative trial. Diabetes Care. 2014;37(3):789-95. doi: 10.2337/dc13-1526. Epub 2013 Oct 15.
  16. Walter G, Kemmerer M, Kappler C, et al; Treatment algorithms for chronic osteomyelitis. Dtsch Arztebl Int. 2012 Apr;109(14):257-64. doi: 10.3238/arztebl.2012.0257. Epub 2012 Apr 6.
  17. Conterno LO, Turchi MD; Antibiotics for treating chronic osteomyelitis in adults. Cochrane Database Syst Rev. 2013 Sep 6;(9):CD004439. doi: 10.1002/14651858.CD004439.pub3.

Article history

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