Epidemiology and risk factors for cranial osteomyelitis
After the development of antibiotics, cranial osteomyelitis became a rare event. However, the use of antibiotics has not resulted in complete eradication of cranial osteomyelitis in developed and underdeveloped nations.[12,13,15] In developing countries with limited access to antibiotics, the most common causes of cranial osteomyelitis are paranasal sinuses, direct head injuries, and scalp infections. In developed nations, postoperative craniotomy infections are the predominant source.[12,18,19,20,21]
In a 10-year retrospective study spanning from 1994 to 2004, 84 cases of osteomyelitis involving the head and neck were observed. Of the 84 cases, 24 required a cranial vault, 20 cases of frontal bone osteomyelitis involved chronic sinusitis, and 4 cases of temporal bone osteomyelitis occurred secondary to MOE. There was a 1.7:1 male-to-female ratio, with an age range of 15-70 years. However, according to two recent studies, the overall incidence rate of cranial osteomyelitis is reportedly higher in developing countries, with Tanzania reporting 12.7% and South Africa reporting 6.7%.[21,23] Furthermore, it is estimated that the incidence of cranial vault tuberculosis ranges from 0.2%-1.3% of all cases of skeletal tuberculosis. The most important risk factor for cranial osteomyelitis with frontal bone involvement is frontal sinusitis, especially in children and adolescents.[14,15,16,17,25,26] In addition to the frontal sinus, any paranasal sinus, such as orbital, oral, or dental, infections impose a significant risk of cranial osteomyelitis.[27,28]
At present, SBO is still a rare event and mainly involves the temporal bone and the sphenoidal bone. SBO commonly occurs as a complication of MOE and chronic mastoid infections or secondary to sphenoidal sinusitis.[29,30,31] MOE primarily affects the temporal bone and is the most frequent cause of SBO. A large study at the University of California Irvine from 1990 to 2000 reported a male-to-female ratio of 1:1 in 820 patients with SBO. The researchers reported the overall incidence of SBO as 69.3% in whites, 13.2% in Native Americans, 6.5% in African Americans, and 2.9% in Asians.
A new, rare clinical entity, central or atypical SBO may begin with otitis externa.[33,34] Central or atypical SBO primarily affects the sphenoidal bone and the occipital bone; the latter is often affected around the clivus bone.[33,32] A review of case study series from 1946 to 2013 revealed 42 cases of central or atypical SBO unrelated to ear infection, with a mean age of 52 years and a male-to-female ratio of 2.2: 1.
Surgical site infections (SSIs) are infections that occur in the wound, secondary to an invasive surgical procedure. Erman et al. estimated that the frequency of SSIs after a clean neurosurgical procedure in randomized controlled trials would be 4.0% to 12.0% without prophylactic antibiotics and 0.3% to 3.0% with prophylactic antibiotics. There are no available data related to prevalence and correlation of specific risk factors with iatrogenic cranial osteomyelitis.[36,37,38] However, procedure-related risk factors were reported as the strongest predictors of SSIs.[37,38] These risk factors often include longer operation time, craniotomy, dural substitute, CSF leak, and staples in wound closure.[37,38,39] Furthermore, prolonged initial hospitalizations and readmissions are significantly associated with SSIs.[37,38,39]
Many cases of cranial osteomyelitis have been reported from posttraumatic injuries secondary to minor scalp wounds such as human bites, scalp wound/laceration, and needle insertions.[19,40,41] Other direct injuries causing cranial osteomyelitis include cephalohematoma infection (particularly after vacuum extraction), craniofacial injuries, penetrating craniocerebral injury, traumatic scalp hematoma, and contaminated war wounds.[42,43,44,45,46,47]
In addition to the above-mentioned etiologic factors, cranial osteomyelitis is influenced by systemic diseases that decrease bone vascularity, the course of illness, and alter the host defense mechanism.[12,22,48,49,50,51,52,53,54,55,56,57,58] The causative infections and predisposing comorbidities are summarized in Table 1.