Frozen Shoulder: Physiology, Stages, and Its Impact on Movement

What is the physiology of a frozen shoulder?

Frozen shoulder, medically known as adhesive capsulitis, is a debilitating condition characterized by progressive pain and stiffness in the glenohumeral joint, primarily due to a complex inflammatory and fibrotic process leading to thickening and contraction of the joint capsule.

Understanding the Shoulder Joint Anatomy

To grasp the physiology of a frozen shoulder, it's essential to briefly review the normal anatomy of the glenohumeral (shoulder) joint. This ball-and-socket joint is formed by the head of the humerus (upper arm bone) fitting into the glenoid cavity of the scapula (shoulder blade). Encasing this joint is the joint capsule, a strong, fibrous sac that provides stability and contains synovial fluid. The synovial fluid lubricates the joint, reduces friction, and nourishes the articular cartilage. The capsule itself is lined by the synovial membrane and is normally thin, pliable, and spacious, allowing for a wide range of motion.

The Pathophysiological Process of Adhesive Capsulitis

Frozen shoulder is fundamentally a disorder of the glenohumeral joint capsule, involving a cascade of events that transform a normally supple structure into a rigid, contracted one.

Inflammation as the Initiating Factor

The precise trigger for frozen shoulder is often unknown (idiopathic), but the initial phase typically involves inflammation of the synovial membrane and the surrounding joint capsule. This inflammation is characterized by:

• Increased vascularity (blood flow) to the joint capsule.
• Infiltration of inflammatory cells (e.g., macrophages, lymphocytes).
• Release of pro-inflammatory cytokines (e.g., TNF-alpha, IL-1 beta), which promote pain and further tissue damage.

Fibrosis and Scar Tissue Formation

Following the inflammatory phase, or sometimes concurrently, the hallmark of frozen shoulder is the development of fibrosis. This involves an abnormal healing response within the joint capsule, leading to:

• Fibroblast Proliferation: An excessive increase in the number of fibroblasts, the cells responsible for producing connective tissue.
• Collagen Deposition: Overproduction and disorganized deposition of collagen fibers, particularly Type I and Type III collagen. This forms dense, unyielding scar tissue.
• Cross-linking: Abnormal cross-linking between collagen fibers, making the tissue less elastic and more rigid.
• Myofibroblast Presence: The transformation of fibroblasts into myofibroblasts, cells that possess contractile properties similar to smooth muscle cells. These myofibroblasts actively pull on the collagen matrix, contributing to the capsule's contraction.

Capsular Thickening and Contraction

The cumulative effect of inflammation and fibrosis is a dramatic thickening and contraction of the joint capsule. This process significantly reduces the internal volume of the joint capsule, effectively "shrinking" the space available for the humeral head to move within the glenoid. The normal folds and recesses of the capsule, particularly in the axillary fold (lower part of the capsule), become obliterated and adhere to each other.

Loss of Synovial Fluid and Cartilage Health

While not the primary pathology, the chronic inflammatory environment and reduced capsular volume can secondarily impact the quality and quantity of synovial fluid. A decrease in healthy synovial fluid can further contribute to increased friction and stiffness within the joint, potentially affecting the health of the articular cartilage over time.

The Stages of Frozen Shoulder and Their Physiological Basis

The physiological changes manifest clinically through distinct stages, though the progression can vary between individuals.

1. Freezing Stage (Painful Stage)

• Physiology: Characterized by active inflammation of the synovial membrane and early fibrotic changes. Pain is often severe and worsens at night or with movement.
• Clinical Presentation: Gradual onset of pain with progressive loss of range of motion.

2. Frozen Stage (Stiff/Adhesive Stage)

• Physiology: Inflammation begins to subside, but fibrosis and capsular contraction dominate. The joint capsule becomes significantly thickened, stiff, and adhered.
• Clinical Presentation: Pain may decrease, but stiffness becomes the predominant symptom, with severe restriction in all planes of motion, particularly external rotation and abduction.

3. Thawing Stage (Recovery Stage)

• Physiology: A gradual process of capsular remodeling and resolution of fibrosis. The dense scar tissue slowly loosens and becomes more pliable.
• Clinical Presentation: Gradual, spontaneous return of range of motion, though full recovery may take months or even years, and some residual stiffness can persist.

Implications for Movement and Function

The physiological changes directly impair the biomechanics of the shoulder joint. The contracted capsule restricts the normal gliding and rolling motions of the humeral head within the glenoid, leading to:

• Restricted External Rotation: Often the first and most severely limited movement.
• Restricted Abduction: Difficulty lifting the arm away from the body.
• Restricted Internal Rotation and Flexion: Also limited, impacting daily activities like reaching behind the back or overhead.
• Compensatory Movements: The body compensates by increasing movement at the scapulothoracic joint (movement of the shoulder blade on the rib cage), which can lead to secondary issues or muscle imbalances.

In conclusion, the physiology of a frozen shoulder is a complex interplay of inflammation and an aggressive, self-limiting fibrotic process within the glenohumeral joint capsule. This leads to a profound thickening, contraction, and loss of elasticity of the capsule, ultimately resulting in the characteristic pain and severe restriction of shoulder movement.