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existence—of adhesions has since been challenged (Bunker 1997, Bunker 2009, Omari & Bunker
2001), but Neviaser and Cyriax were right to incriminate the joint capsule.
Since Neviaser’s study, the advent of arthroscopic (keyhole) techniques has made surgical
exploration of shoulder joints commonplace. As reviewed by Bunker (2009), one of the most
striking features on arthroscoping a contracted (frozen) shoulder is capsular contracture: the
capsule becomes tough and thickened, and its volume may shrink to as little as 3–4 ml. (This loss of
capacity is also obvious when attempting to inject moderate volumes of fluid into affected
shoulders.) Another striking feature is the formation of new blood vessels in the synovial
membrane, especially in the rotator interval area, but also in the superior capsule, the posterior
capsule and the redundant axillary fold. In cases where the pain is giving way to stiffness, these
new blood vessels become embedded in thick scar (Bunker 2009, Omari and Bunker 2001).
But the underlying pathology has been elusive. Some have argued that the fundamental process is
inflammation; others that it is scarring; yet others that it is scarring produced in reaction to
inflammation (Hand et al 2007). The last of these is logically appealing for a number of reasons:
because frozen shoulder causes both pain and stiffness, but the stiffness outlasts the pain; because
of the changes seen in relation to blood circulation; and also because painful contracted (frozen)
shoulder may respond to injections of corticosteroid (Buchbinder, Green & Youd 2003), a potent
suppressor of inflammation. Hand et al (2007) microscopically examined tissues from the rotator
interval of 22 patients with frozen shoulder. This examination, combined with novel staining
techniques, revealed large numbers of fibroblasts (cells that, among other things, produce scar);
cells associated with chronic inflammation (Hand et al 2007); and an increase in blood vessels. On
this basis, Hand et al (2007) have proposed that frozen shoulder does indeed represent a process in
which inflammation leads to scarring. They have tentatively implicated mast cells in this link. Mast
cells, which are among the inflammation-related cells they found, are known to control the
proliferation of fibroblasts. Myofibroblasts, another cell type—a cross between fibroblasts and
muscle cells, which cause scar to contract—may also be implicated in the pathology of frozen
shoulder. Bunker (1997) and Omari and Bunker (2001) resorted to open surgery in patients with
frozen shoulder that had responded to neither conservative measures nor manipulation under
anaesthesia, and found abundant myofibroblasts in tissue taken from the rotator interval. Clearly,
on a large scale, myofibroblasts could contribute to capsular contracture; and that Hand et al
(2007) did not find significant numbers of these cells may reflect the fact that their patient
population was less chronic. Another finding in capsular tissue from patients with frozen shoulder
is the absence of certain enzymes that would normally be involved in the remodelling of scar tissue
(Bunker 2009).
Regardless of the mechanism by which it comes about, contracture is such a striking feature of
frozen shoulder that Bunker (2009) has suggested a further redesignation, ‘contracted (frozen)
shoulder’, which we have adopted.
The subtypes of contracted (frozen) shoulder have also been inconsistently classified. Codman
(1934)—and indeed Duplay—noted that the condition could be insidious or secondary to trauma.
Cyriax called the former monarticular infective [sic] arthritis (Cyriax & Troisier 1953, Cyriax 1954)
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