Open surgery is needed for chronic osteomyelitis, whereby the involucrum is opened and the sequestrum is removed or sometimes saucerization can be done. Hyperbaric oxygen therapy has been shown to be a useful adjunct to the treatment of refractory osteomyelitis.Before 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.There is tentative evidence that bioactive glass may also be useful in long bone infections. Support from randomized controlled trials, however, was not available as of 2015.Hemicorporectomy is performed in severe cases of Terminal Osteomyelitis in the Pelvis if further treatment won’t stop the infection. History
The word is from Greek words ὀστέον osteon, meaning bone, μυελό- myelo- meaning marrow, and -ῖτις -itis meaning inflammation. In 1875, American artist Thomas Eakins depicted a surgical procedure for osteomyelitis at Jefferson Medical College, in an oil painting titled The Gross Clinic. Fossil record
Evidence for osteomyelitis found in the fossil record is studied by paleopathologists, specialists in ancient disease and injury. It has been reported in fossils of the large carnivorous dinosaur Allosaurus fragilis. Osteomyelitis has been also associated with the first evidence of parasites in dinosaur bones. See also
References
External links

00298 at CHORUSAcosta, Chin;  et al. (2004). "Diagnosis and management of adult pyogenic osteomyelitis of the cervical spine" (PDF). Neurosurg Focus. 17 (6): E2. doi:10.3171/foc.2004.17.6.2. PMID 15636572.
About 50% of diabetics with diabetic cardiomyopathy show pathologic evidence for microangiopathy such as sub-endothelial and endothelial fibrosis, compared to only 21% of non-diabetic heart failure patients. Over the years, several hypotheses were postulated to explain the endothelial dysfunction observed in diabetes. It was hypothesized that the extracellular hyperglycemia leads to an intracellular hyperglycemia in cells unable to regulate their glucose uptake, most predominantly, endothelial cells. Indeed, while hepatocytes and myocytes have mechanisms allowing them to internalize their glucose transporter, endothelial cells do not possess this ability. The consequences of increased intracellular glucose concentration are fourfold, all resulting from increasing concentration of glycolytic intermediates upstream of the rate-limiting glyceraldehyde-3-phosphate reaction which is inhibited by mechanisms activated by increased free radical formation, common in diabetes. Four pathways, enumerated below all explain part of the diabetic complications. First, it has been widely reported since the 1960s that hyperglycemia causes an increase in the flux through aldose reductase and the polyol pathway. Increased activity of the detoxifying aldose reductase enzyme leads to a depletion of the essential cofactor NADH, thereby disrupting crucial cell processes. Second, increasing fructose 6-phosphate, a glycolysis intermediate, will lead to increased flux through the hexosamine pathway. This produces N-acetyl glucosamine that can add on serine and threonine residues and alter signaling pathways as well as cause pathological induction of certain transcription factors. Third, hyperglycemia causes an increase in diacylglycerol, which is also an activator of the Protein Kinase C (PKC) signaling pathway.