Hartofilakidis typing divides DDH into three types, with type C being high dislocation of the hip; according to positional correlation between the femoral head and the true and false acetabulum, type C can be subdivided into type C1 (false acetabulum formation) and type C2 (no false acetabulum formation).[sup][1] Due to the high dislocation, normal anatomy of the hip changes, and bone and soft tissue deformities are obvious; the femoral head may form a
pseudarthrosis in the iliac wing, with the
pseudarthrosis located superior or posterior to the true acetabulum.
The differential diagnosis of hereditary multiple exostoses includes the enchondromatosis, which are a heterogeneous group of syndromes that present with multiple enchondromas associated with pathological fractures,
pseudarthrosis, limb shortening, malignant transformation risk, and scoliosis.
These include disuse atrophy, acute inflammatory atrophy associated with trauma (Sudeck's atrophy or algodystrophy), primary and metastatic tumours, hyperparathyroidism, gout, congenital
pseudarthrosis, granulomatous diseases, rheumatoid arthritis, diabetes mellitus, psoriatic arthritis, osteomyelitis, systemic mastocytosis, aseptic necrosis, neurogenic arthropathy, prolonged steroid therapy, bony aneurysm, and cystic angiomatous of bone.
No patients had evidence of
pseudarthrosis; typical case was shown as Figures 2 and 3.
Shortly after this procedure a postoperative
pseudarthrosis was observed, but causing no problems.
The syndrome can result from: mistaken diagnoses, technique error, poor application, inappropriate indication,
pseudarthrosis or continued natural progression of disease.
Three column osteotomy indications include
pseudarthrosis, sharp angular kyphosis, severe global positive sagittal malalignment, concomitant coronal deformity, and previous multilevel circumferential fusions.
Although good clinical results have been reported by some, this procedure has serious disadvantages: High
pseudarthrosis rate, postoperative progression by plastic bone remodeling despite consolidated fusion mass, and even neurological compromise as a late sequel [7,10-12].
There were no permanent neurological complications or
pseudarthrosis. The magnetic resonance imaging showed that there was no obvious disc degeneration in the adjacent segment.
In this paper, we focus our attention on the molecular mechanisms involved in osteogenic and chondrogenic differentiation of hMSC, and the potential clinical use of hMSCs in osteoarticular pediatric disease characterized by fracture nonunion and
pseudarthrosis.