Frozen shoulder, or adhesive capsulitis, is a common condition characterized by progressive stiffness and a significant loss of motion in the shoulder joint. This ailment affects an estimated two to five percent of the general population, most commonly striking adults between the ages of 40 and 60. In many cases, the exact cause is unknown, leading doctors to categorize it as idiopathic, meaning it appears spontaneously without a clear preceding injury or event. Research suggests a complex interplay of systemic health issues and inherited traits, raising the question of whether a genetic predisposition makes certain individuals more susceptible.
Understanding Adhesive Capsulitis
The physical mechanism involves changes to the glenohumeral joint capsule, the connective tissue sac surrounding the shoulder joint. In adhesive capsulitis, this capsule becomes inflamed, thickens, and contracts, reducing the space available for the upper arm bone (humerus) to move. This process involves the formation of thick bands of scar tissue, called adhesions, which severely restrict both active and passive range of motion.
The condition generally progresses through three distinct stages, which can collectively last from several months up to three years.
- The initial “freezing” stage is marked by a gradual onset of pain and a steady loss of movement, typically lasting two to nine months.
- The “frozen” stage follows, where pain may lessen, but stiffness and limited mobility remain the primary symptoms, usually persisting for four to twelve months.
- The “thawing” stage sees a slow, gradual improvement in both pain and shoulder motion, which can take six months to two years to resolve.
The Role of Genetics
While frozen shoulder is not a classically hereditary disorder determined by a single gene, strong familial aggregation suggests a significant genetic component. Studies indicate that 20 to 29 percent of patients report having a first-degree relative who also experienced the condition. A twin study supported this finding, calculating the heritability of frozen shoulder to be as high as 42 percent.
Recent research using Genome-Wide Association Studies has identified specific genetic markers that significantly increase the risk. Three locations on the human genome, near the genes WNT7B, POU1F1, and MAU2, show a significant association with adhesive capsulitis. The strongest link was found near WNT7B, a gene known to be involved in regulating fibrosis (scar tissue formation).
The collective risk associated with these genetic variations is substantial, estimated to be nearly six times that of the general population. This highlights that genetic factors create a biological susceptibility to the condition. However, it is often a combination of environmental or systemic health factors that initiate the disease process.
Associated Health Conditions and Risk Factors
Beyond genetics, several systemic health conditions significantly increase the risk of developing frozen shoulder. The most prominent association is with Diabetes Mellitus, where patients are estimated to be two to four times more likely to develop adhesive capsulitis. The prevalence in people with diabetes is reported to be between 10 and 30 percent.
This connection is related to chronic high blood sugar levels, which cause chemical reactions that change the structure of collagen. This altered collagen matrix makes the connective tissue within the shoulder capsule more rigid, promoting the fibrosis and contracture seen in the disorder. Thyroid dysfunction, including both hypothyroidism and hyperthyroidism, is another established systemic risk factor.
Additional factors that increase the likelihood of developing frozen shoulder include general demographics and prior physical trauma. The condition predominantly affects individuals between 40 and 60 years old and shows a higher incidence in women.
Other Risk Factors
- History of a shoulder injury or surgery.
- A period of prolonged immobilization, such as wearing a sling or brace.
Diagnosis and Treatment Pathways
Diagnosing adhesive capsulitis primarily relies on a thorough clinical assessment, as the symptoms are distinct from other shoulder problems. A doctor performs specific range-of-motion tests, observing both the active movement the patient achieves and the passive movement the doctor achieves. A defining characteristic is a significant restriction in both active and passive motion.
Imaging tests, such as X-rays or MRI, are used to rule out other potential causes of pain and stiffness, such as arthritis or a rotator cuff tear. Once diagnosed, the standard treatment is conservative, aiming to manage pain while restoring mobility. This typically involves nonsteroidal anti-inflammatory drugs (NSAIDs) for pain relief and a structured physical therapy program focusing on gentle, progressive stretching exercises.
Injections of corticosteroids directly into the shoulder joint are a common intervention, particularly during the initial painful stages, to reduce inflammation and improve motion. For cases that do not respond to conservative measures, other procedures may be considered. These include hydrodilatation (injecting sterile fluid to stretch the joint capsule) or manipulation under anesthesia. While recovery can be slow, most patients eventually regain a functional level of motion.