Frozen shoulder is commonly encountered in general orthopaedic practice. It may arise spontaneously without an obvious predisposing cause, or be associated with a variety of local or systemic disorders. Diagnosis is based upon the recognition of the characteristic features of the pain, and selective limitation of passive external rotation. The macroscopic and histological features of the capsular contracture are well-defined, but the underlying pathological processes remain poorly understood. It may cause protracted disability, and imposes a considerable burden on health service resources. Most patients are still managed by physiotherapy in primary care, and only the more refractory cases are referred for specialist intervention. Targeted therapy is not possible and treatment remains predominantly symptomatic. However, over the last ten years, more active interventions that may shorten the clinical course, such as capsular distension arthrography and arthroscopic capsular release, have become more popular. This review describes the clinical and pathological features of frozen shoulder. We also outline the current treatment options, review the published results and present our own treatment algorithm.

Perivascular stem cells (PSCs) are the natural ancestors of mesenchymal stem cells (MSCs) and are the stem cells responsible for homeostasis and repair in vivo. Prospectively identified and isolated PSCs have demonstrated increased plasticity and osteogenic potential. Cells from the infrapatellar fat pad (IFP) have demonstrated increased chondrogenic potential compared with those from subcutaneous fat. This research assessed the chondrogenic potential of IFP PSCs compared with MSCs from the IFP and bone marrow. Immunohistochemistry demonstrated the location of perivascular markers (CD146, CD34, neural/glial antigen 2 [NG2], platelet‐derived growth factor receptor‐β [PDGFRβ], and α‐smooth muscle actin [α‐SMA]) in relation to endothelial markers (CD31, CD144, von Willebrand factor [vWF]). Pericytes and adventitial cells were isolated from the stromal vascular fraction (3.8% and 21.2%, respectively) using flow cytometry with a viability of 88%. The mean numbers of pericytes and adventitial cells isolated were 4.6 ± 2.2 × 104 and 16.2 ± 3.2 × 104, respectively, equating to 7.9 ± 4.4 × 103 and 20.8 ± 4.3 × 103 cells per gram of harvested tissue. Fluorescence‐activated cell sorting demonstrated that cultured PSCs were CD44+CD90+CD105+; polymerase chain reaction and immunocytochemistry demonstrated that pericytes retained their CD146+ phenotype and expressed the pericyte markers PDGFRβ and NG2. Differentiation was confirmed using histochemical stains and genetic expression. Using a pellet model, the IFP PSCs and the MSCs generated significantly more extracellular matrix than bone marrow MSCs (p < .001 and p = .011, respectively). The IFP PSCs generated significantly more extracellular matrix than IFP MSCs (p = .002). Micromass culture demonstrated that differentiated PSCs were upregulated compared with MSCs for COL2A1, ACAN, and SOX9 expression by factors of 4.8 ± 1.3, 4.3 ± 0.9, and 7.0 ± 1.7, respectively. The IFP was a significantly better source of chondrogenic stem cells compared with bone marrow. PSCs generated significantly more extracellular matrix than culture‐derived MSCs. Stem Cells Translational Medicine 2017;6:77–87

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