Table 1

- Demonstration of pathophysiological mechanisms involvement in osteonecrosis of the femoral head in sickle cell disease.

AuthorYearStudy designStudy PopulationAgeMethod usedMechanisms associated with ON pathophysiologyP-value
Daltro et al232020Case–control9 SCD patients, 15 SCD-ON patients, 19 control10-55 yearflow cytometryCD4+T lymphocytes raised circulatory levels of simultaneously produced pro-inflammatory cytokines IL-17+-IL4+ and IFN-γ+-IL4+ contributing to ON inflammation at target organ site. The polyclonal stimulation with phorbol myristate acetate/ inomycin in vitro in SCD, SCD-ON showed significantly raised IL4+TCD4+ cells.p=0.0016,
Al-Ghaithi et al242021Experimental7 SCD patients22–32 yearsRaman SpectroscopyDecline in bone quality and drop in mineral volume due to decrease in bone phosphate to amide ratio, carbonate to amide ratio carbonate-to-phosphatep=0.01
Adesina and Neumayr252019Case study1 SCD patient19 year-Progression of R-ONFH with decreased joint space, cysts (Steinberg stage V) and sclerosis; and minimal flattening (Steinberg stage II) at the left femoral headp<0.05
Chaouch et al82015Case–control100 SCD patients30±5 yearPCR/sequencingBMP6 polymorphisms in articular cartilage destruction during pathogenesis of ON in SCA patients showed significant association between osteonecrosis and alleles G of rs267201 and A of 267196p=0.04

SCD: sickle cell disease, SCD-ON: sickle cell disease with osteonecrosis, IL: interleukin, IFN-γ: Interferon gamma, ONFH: osteonecrosis of the femoral head, PCR: polymerase chain reaction, ON: osteonecrosis, BMP: bone morphogenetic protein