Osteomyelitis of the ribs in children: a rare and potentially challenging diagnosis.

BACKGROUND: Rib osteomyelitis is rare in children and can mimic other pathologies. Imaging has a major role in the diagnosing rib osteomyelitis. OBJECTIVE: To evaluate clinical presentation and imaging findings in children with rib osteomyelitis. MATERIALS AND METHODS: We performed a retrospective (2009-2018) study on children with rib osteomyelitis verified by either positive culture or pathology. We excluded children with multifocal osteomyelitis or empyema necessitans. We reviewed medical charts for clinical, laboratory and pathology data, and treatment. All imaging modalities for rib abnormalities were evaluated for presence and location of osteomyelitis and abscess. We calculated descriptive statistics to compare patient demographics, clinical presentation and imaging findings. RESULTS: The study group included 10 children (6 boys, 4 girls), with an average age of 7.3 years (range, 3 months to 15.9 years). The most common clinical presentations were fever (n=8) and pain (n=5). Eight children had elevated inflammatory indices (leukocytosis, erythrocyte sedimentation rate [ESR], C-reactive protein [CRP]). Localized chest wall swelling was found initially in six children and later in two more children. Rib osteomyelitis was suspected on presentation in only two children. All children had chest radiographs. Rib lytic changes were found on only one chest radiograph, in two of the four ultrasound studies, and in four of eight CTs. Bone marrow signal abnormalities were seen in all eight MRIs. In nine children the osteomyelitis involved the costochondral junction. Six children had an associated abscess. Staphylococcus aureus was cultured in eight children. Osteomyelitis was diagnosed based on pathology in one child with negative cultures. CONCLUSION: While rib osteomyelitis is rare, imaging findings of lytic changes at the costochondral junction combined with a history of fever, elevated inflammatory markers or localized soft-tissue swelling in the chest should raise suspicion for this disease.

Human adipose stromal cell therapy improves survival and reduces renal inflammation and capillary rarefaction in acute kidney injury.

Damage to endothelial cells contributes to acute kidney injury (AKI) by causing impaired perfusion, while the permanent loss of the capillary network following AKI has been suggested to promote chronic kidney disease. Therefore, strategies to protect renal vasculature may impact both short-term recovery and long-term functional preservation post-AKI. Human adipose stromal cells (hASCs) possess pro-angiogenic and anti-inflammatory properties and therefore have been tested as a therapeutic agent to treat ischaemic conditions. This study evaluated hASC potential to facilitate recovery from AKI with specific attention to capillary preservation and inflammation. Male Sprague Dawley rats were subjected to bilateral ischaemia/reperfusion and allowed to recover for either two or seven days. At the time of reperfusion, hASCs or vehicle was injected into the suprarenal abdominal aorta. hASC-treated rats had significantly greater survival compared to vehicle-treated rats (88.7% versus 69.3%). hASC treatment showed hastened recovery as demonstrated by lower creatinine levels at 48 hrs, while tubular damage was significantly reduced at 48 hrs. hASC treatment resulted in a significant decrease in total T cell and Th17 cell infiltration into injured kidneys at 2 days post-AKI, but an increase in accumulation of regulatory T cells. By day 7, hASC-treated rats showed significantly attenuated capillary rarefaction in the cortex (15% versus 5%) and outer medulla (36% versus 18%) compared to vehicle-treated rats as well as reduced accumulation of interstitial alpha-smooth muscle actin-positive myofibroblasts. These results suggest for the first time that hASCs improve recovery from I/R-induced injury by mechanisms that contribute to decrease in inflammation and preservation of peritubular capillaries.

Endothelial colony-forming cells ameliorate endothelial dysfunction via secreted factors following ischemia-reperfusion injury.

Damage to endothelial cells contributes to acute kidney injury (AKI) by leading to impaired perfusion. Endothelial colony-forming cells (ECFC) are endothelial precursor cells with high proliferative capacity, pro-angiogenic activity, and in vivo vessel forming potential. We hypothesized that ECFC may ameliorate the degree of AKI and/or promote repair of the renal vasculature following ischemia-reperfusion (I/R). Rat pulmonary microvascular endothelial cells (PMVEC) with high proliferative potential were compared with pulmonary artery endothelial cells (PAEC) with low proliferative potential in rats subjected to renal I/R. PMVEC administration reduced renal injury and hastened recovery as indicated by serum creatinine and tubular injury scores, while PAEC did not. Vehicle-treated control animals showed consistent reductions in renal medullary blood flow (MBF) within 2 h of reperfusion, while PMVEC protected against loss in MBF as measured by laser Doppler. Interestingly, PMVEC mediated protection occurred in the absence of homing to the kidney. Conditioned medium (CM) from human cultured cord blood ECFC also conveyed beneficial effects against I/R injury and loss of MBF. Moreover, ECFC-CM significantly reduced the expression of ICAM-1 and decreased the number of differentiated lymphocytes typically recruited into the kidney following renal ischemia. Taken together, these data suggest that ECFC secrete factors that preserve renal function post ischemia, in part, by preserving microvascular function.