Treatment for joint disorders Field of the invention The present invention relates to methods of treating joint disorders, particularly disorders characterised by hypervascularity, inflammation and/or fibrosis of the joint capsule. Cross-reference to earlier application This application claims priority from Australian provisional application AU 2022902097, the contents of which are hereby incorporated by reference in their entirety. Background of the invention Adhesive capsulitis or frozen shoulder, is a disorder that manifests with pain and restricted active as well as passive range of motion of the shoulder. The diagnosis of this condition is based on clinical criteria. Frozen shoulder is common, with a reported prevalence of 2% to 5% in the general population. Patients who have, have had, or are risk of having an autoimmune disease, diabetes, stroke, heart attack, thyroid disease, and/or prolonged immobilization are at higher risk of developing joint disorders such as frozen shoulder. Its prevalence is even higher (10% to 36%) in patients with diabetes. Frozen shoulder most commonly occurs in working-age patients who are forty to sixty years of age, with the peak age in the mid-fifties. Women are affected more often than men. The condition is often bilateral, and, in 6% to 17% of patients, it affects one shoulder first and the contralateral side within five years. Adhesive capsulitis can be either primary or secondary. In cases of primary or idiopathic frozen shoulder, no findings in the clinical history or physical examination explain the onset of disease. In cases of secondary frozen shoulder, the patient may have a history of trauma or surgery (particularly at the site of the joint disorder), cardiac disease (such as myocardial infarction or pulmonary disease), diabetes mellitus, thyroid disease (particularly hypothyroidism), stroke, autoimmune and/or inflammatory disease (such as rheumatoid arthritis, fibromyalgia, lupus), Dupuytren's disease, Parkinson’s disease, or barbiturate use. Frozen shoulder leads to substantial functional loss, with impairment of activities of daily living (dressing, washing, driving, self-care). It also adversely affects both patients and society by impairing the ability to work. Even though frozen shoulder traditionally has been considered to be a self-limited disease, with a natural history lasting two to three years, it is increasingly recognized that, for many patients, frozen shoulder is a chronic disease. Previous studies have shown that up to 40% of patients have symptoms and restriction of movement that persist beyond three years40 and that 15% have long-term disability. In a Dutch study, the health loss for patients with frozen shoulder was estimated to be 0.048 quality-adjusted life year (QALY) and the societal costs were estimated at €4521 ($AUD6500) per patient, of which 47% were health-care costs and 53% were non- health-care costs. The aims of treatment for frozen shoulder are to decrease pain and to improve the range of motion. Current treatments include both non-invasive options and invasive options. Treatment regimens for adhesive capsulitis begin with a trial of conservative therapy, including anti-inflammatory medications, glenohumeral joint corticosteroid injections, and physical therapy in the later stages. However, residual pain is one of the most important issues in the treatment of adhesive capsulitis. After nonsurgical treatment, 27% of patients had mild or moderate pain at 1.8 years’ follow-up, and another study reported that 35% of patients had mild pain at 7 years. When conservative therapy is not effective, more invasive approaches are sometimes required, such as capsular hydrodilatation, manipulation under anesthesia, or arthroscopic capsular release. Nevertheless, a consensus has not been reached on the optimal treatment for adhesive capsulitis that is resistant to traditional conservative treatments. There is a need for alternative therapies for capsulitis and other joint disorders characterised by inflammation, fibrosis, adhesions and tendinitis. Reference to any prior art in the specification is not an acknowledgment or suggestion that this prior art forms part of the common general knowledge in any jurisdiction or that this prior art could reasonably be expected to be understood, regarded as relevant, and/or combined with other pieces of prior art by a skilled person in the art. Summary of the invention The present invention provides a method of treating or preventing an individual suffering from a joint disorder characterised by hypervascularity, inflammation and/or fibrosis of the joint capsule, wherein the method comprises: administering to an individual in need thereof, a therapeutically effective amount of an inhibitor of angiogenesis, thereby treating the joint disorder in the individual. It will be appreciated that any inhibitor of angiogenesis may be used. In preferred embodiments, the inhibitor of angiogenesis is an inhibitor of vascular endothelial growth factor (VEGF). Accordingly the present invention provides a method of treating an individual suffering from a joint disorder characterised by hypervascularity, inflammation and/or fibrosis of the joint capsule, wherein the method comprises: administering to an individual in need thereof, a therapeutically effective amount of a vascular endothelial growth factor (VEGF) inhibitor, thereby treating the joint disorder in the individual. The present invention also provides a method of preventing a joint disorder characterised by hypervascularity, inflammation and/or fibrosis of the joint capsule, wherein the method comprises: administering to an individual at risk of suffering from a joint disorder characterised by hypervascularity, inflammation and fibrosis of the joint capsule, a therapeutically effective amount of a VEGF inhibitor, thereby preventing the joint disorder from developing in the individual. In any embodiment of the invention, the joint disorder may comprise hypervascularity, or hypervascularity and inflammation, or hypervascularity, inflammation and fibrosis. The joint disorder that may further be characterised by one or more of: tissue adhesions (scar tissue), synovial proliferation, capsulitis, bursitis and/or tendonitis. In any embodiment, the joint disorder may further be characterised by pain and/or reduced motion and stiffness of the joint. The joint requiring treatment according to the present invention may be characterised by hypervascularity that includes abnormal, excessive and/or disorganised neoangiogenesis and/or may include arteriovenous shunts. In any embodiment of the invention, the neoangiogenic vessels of the joint may further include neural ingrowth. Typically, the joint disorder requiring treatment according to the present invention can be defined as capsulitis. Accordingly, the present invention provides a method of treating an individual suffering from capsulitis of a joint, wherein the method comprises: administering to an individual suffering from or suspected of having capsulitis of a joint, a therapeutically effective amount of VEGF inhibitor, thereby treating the capsulitis in the joint of the individual. Preferably, the VEGF inhibitor is administered directly to the joint of the individual that is or is suspected of having capsulitis. The present invention also provides a method of preventing capsulitis of a joint in an individual, wherein the method comprises: administering to an individual at risk of suffering from capsulitis of a joint, a therapeutically effective amount of a VEGF inhibitor, thereby preventing the capsulitis from developing in a joint of the individual. Preferably, the VEGF inhibitor is administered directly to the joint of the individual that is at risk of developing capsulitis. In any embodiment, the capsulitis of the joint may be primary, secondary or idiopathic capsulitis. In further embodiments, the capsulitis may be secondary to a trauma or injury to the joint. In certain embodiments, the capsulitis arises following a surgery or other medical procedure to the joint (e.g., post-operative capsulitis of the joint). In any embodiment, the individual suffering from the joint disorder or at risk of suffering from the joint disorder does not have diabetes mellitus. Optionally, the individual is not at risk of having diabetes mellitus. Optionally, the individual does not have a medical history of diabetes mellitus. Alternatively, the individual has diabetes mellitus. Optionally, the individual is at risk of developing diabetes mellitus. Optionally, the individual has a medical history of diabetes mellitus. In any embodiment, the individual at risk of suffering from a joint disorder as described herein may be an individual who has a medical history of (or has, or is at risk of having) trauma or surgery (particularly at the site of the joint disorder, such as to the shoulder joint), cardiac disease (such as myocardial infarction or pulmonary disease), stroke, autoimmune and/or inflammatory disease (such as rheumatoid arthritis, fibromyalgia, lupus), Dupuytren's disease, diabetes mellitus, thyroid disease (especially hypothyroidism), Parkinson’s disease and/or barbiturate use. The individual at risk of suffering from a joint disorder as described herein may be an individual who is about to undergo surgery of the shoulder joint. In that context, the VEGF inhibitor may be administered pre-operatively. Alternatively, the individual at risk of a joint disorder as described herein may receive the VEGF inhibitor post-operatively so as to avoid the risk of secondary adhesive capsulitis or subacromial bursitis. In any embodiment, the joint disorder, or the joint that has or is at risk of capsulitis, is any joint comprising a capsule. Preferably the joint is selected from: a shoulder, knee, hip, ankle or a joint in the hand or wrist. Preferably, the capsulitis is of the shoulder. When the disorder or capsulitis is in the shoulder joint (i.e., the glenohumeral joint) this may also be referred to as adhesive capsulitis. When the disorder or capsulitis is of the knee, this may also be referred to as plica syndrome. Where the affected joint is the shoulder, the disorder may in a region of the shoulder selected from: the glenohumeral joint capsule, the rotator interval, the subacromial bursa, the coracohumeral ligament, the superior, middle and inferior glenohumeral ligaments or the coracoid process (particularly, the fat triangle under the coracoid process). Accordingly, the present invention also provides a method of treating a disorder of the shoulder joint, wherein the disorder is characterised by hypervascularisation, inflammation and/or fibrosis of the shoulder joint capsule, the method comprising: administering to an individual in need thereof, a therapeutically effective amount of a VEGF inhibitor, thereby treating the shoulder disorder in the individual. In any embodiment, the disorder of the shoulder may be selected from the group consisting of: shoulder joint contracture, adhesive capsulitis, subacromial bursitis, arthrofibrosis, tendonitis or tendinopathy (for example, tendonitis/tendinopathy of the rotator cuff). The present invention also provides a method of treating adhesive capsulitis in the glenohumeral joint of an individual, the method comprising: administering to an individual in need thereof, a therapeutically effective amount of a VEGF inhibitor, thereby treating the adhesive capsulitis in the glenohumeral joint in the individual. The adhesive capsulitis may be primary, secondary or idiopathic. Preferably, the VEGF inhibitor is administered directly to the glenohumeral joint capsule, the rotator interval, the subacromial bursa, the coracohumeral ligament, the superior, middle and inferior glenohumeral ligaments or the coracoid process (particularly the fat triangle under the coracoid process). The individual is preferably characterized as having a global restriction of active and passive range of motion in all planes of should motion with pain on passive stretching. Preferably the restriction and pain observed is when compared to the contralateral shoulder of the individual. The present invention also provides a method of preventing a disorder of the shoulder joint in an individual, wherein the method comprises: administering to an individual at risk of suffering from a shoulder disorder characterised by hypervascularity, inflammation and fibrosis of the shoulder joint capsule, a therapeutically effective amount of a VEGF inhibitor, thereby preventing the joint disorder from developing in the individual. The shoulder disorder for which the individual may be at risk may be selected from the group consisting of: shoulder joint contracture, adhesive capsulitis, subacromial bursitis, arthrofibrosis tendonitis or tendinopathy (for example, tendinopathy of the rotator cuff). Where the shoulder joint disorder is adhesive capsulitis, the disorder may be primary, secondary or idiopathic adhesive capsulitis. The present invention further provides a method comprising: - selecting an individual diagnosed with a joint disorder (preferably frozen shoulder), characterised by hypervascularity, inflammation and/or fibrosis of the joint capsule, by mechanical manipulation of the joint to assess passive and active ranges of motion, optionally an arthrogram or an MRI scan is used to confirm the diagnosis - administering a therapeutically effective amount of an inhibitor of angiogenesis, preferably a vascular endothelial growth factor (VEGF) inhibitor to the individual (preferably in the shoulder of the individual) thereby treating the joint disorder in the individual. In any embodiment, the therapeutically effective amount of an inhibitor of angiogenesis, preferably a VEGF inhibitor, is administered in combination with a pharmaceutically acceptable excipient or carrier. The present invention also provides a use of an angiogenesis inhibitor, preferably a VEGF inhibitor, in the manufacture of a medicament for the treatment or prevention of a joint disorder characterised by hypervascularisation, inflammation and/or fibrosis of the joint capsule. The medicament is preferably for use in the treatment or prevention of a joint disorder in a joint selected from the group consisting of: the shoulder joint, knee, hip, ankle or the joints of the hands/writs. In any embodiment of the invention, the medicament is for the treatment or prevention of a joint disorder that is characterised by one or more of: tissue adhesions (scar tissue), synovial proliferation, capsulitis, bursitis and/or tendonitis. Further, the joint disorder may be characterised by pain and/or reduced motion and stiffness of the joint. In any embodiment, the medicament may be for the treatment or prevention of a joint characterised by abnormal, excessive and/or disorganised neoangiogenesis and/or arteriovenous shunts. In any embodiment of the invention, the neoangiogenic vessels of the joint may further include neural ingrowth. Where the affected joint is the shoulder, the medicament is preferably for the treatment or prevention of a condition selected from the group consisting of: shoulder joint contracture, adhesive capsulitis, subacromial bursitis, arthrofibrosis or tendinopathy (for example, tendinopathy of the rotator cuff). In any embodiment, the medicament is for the treatment of adhesive capsulitis of the shoulder, wherein the adhesive capsulitis is selected from primary, secondary or idiopathic adhesive capsulitis. In further embodiments, the adhesive capsulitis may be postoperative adhesive capsulitis. In any embodiment of the invention, the medicament is adapted for administration directly into the affected joint. For example, preferably, the medicament is adapted for administration to: the glenohumeral joint capsule, the rotator interval, the subacromial bursa, the coracohumeral ligament, the superior, middle and inferior glenohumeral ligaments or the coracoid process (particularly the fat triangle under the coracoid process) or may be for intracapsular, intratendinous or peritendon administration. The present invention also provides an inhibitor of angiogenesis, preferably a VEGF inhibitor, or a pharmaceutical composition comprising a VEGF inhibitor, optionally in combination with a pharmaceutically acceptable excipient or carrier, for use in the treatment or prevention of a joint disorder characterised by hypervascularisation, inflammation and/or fibrosis of the joint capsule. In any embodiment of the invention, the use is for the treatment or prevention of a joint disorder that is characterised by one or more of tissue adhesions (scar tissue), synovial proliferation, capsulitis, bursitis and/or tendonitis. Further, the joint disorder may be characterised by pain and/or reduced motion and stiffness of the joint. In any use or medicament or method as described herein, the VEGF inhibitor is selected from the group consisting of: aflibercept, bevacizumab, ranibizumab, prolactin and brolucizumab. Preferably the VEGF inhibitor is aflibercept. Preferably the VEGF inhibitor is aflibercept or bevacizumab. Preferably the VEGF inhibitor is bevacizumab. In any embodiment of the invention, the use includes administration directly into the affected joint (also known as intraarticular administration). For example, preferably, the administration may be to: the glenohumeral joint capsule, the rotator interval, the subacromial bursa, the coracohumeral ligament, the superior, middle and inferior glenohumeral ligaments or the coracoid process (particularly the fat triangle under the coracoid process), or may be for intracapsular, intratendinous or peritendon administration. In any embodiment of the invention, the VEGF inhibitor is administered percutaneously. When the administration is to the glenohumeral joint capsule, preferably administration is by posterior approach. The administration can be controlled or visualised using real-time ultrasound. As used herein, except where the context requires otherwise, the term "comprise" and variations of the term, such as "comprising", "comprises" and "comprised", are not intended to exclude further additives, components, integers or steps. Further aspects of the present invention and further embodiments of the aspects described in the preceding paragraphs will become apparent from the following description, given by way of example and with reference to the accompanying drawings. Brief description of the drawings Figure 1: Example schema for a clinical protocol administering the VEGF inhibitor bevacizumab for the treatment of adhesive capsulitis. Detailed description of the embodiments It will be understood that the invention disclosed and defined in this specification extends to all alternative combinations of two or more of the individual features mentioned or evident from the text or drawings. All of these different combinations constitute various alternative aspects of the invention. For purposes of interpreting this specification, terms used in the singular will also include the plural and vice versa. Reference will now be made in detail to certain embodiments of the invention. While the invention will be described in conjunction with the embodiments, it will be understood that the intention is not to limit the invention to those embodiments. On the contrary, the invention is intended to cover all alternatives, modifications, and equivalents, which may be included within the scope of the present invention as defined by the claims. One skilled in the art will recognize many methods and materials similar or equivalent to those described herein, which could be used in the practice of the present invention. The present invention is in no way limited to the methods and materials described. It will be understood that the invention disclosed and defined in this specification extends to all alternative combinations of two or more of the individual features mentioned or evident from the text or drawings. All of these different combinations constitute various alternative aspects of the invention. All of the patents and publications referred to herein are incorporated by reference in their entirety. The present inventor has identified a new approach for treating and preventing certain joint disorders that are characterised by hypervascularisation, inflammation and fibrosis. The present invention is based on the finding by the inventor that inhibition of angiogenesis, especially with anti-VEGF (anti-vascular endothelial growth factor) therapy is useful for the treatment of adhesive capsulitis (commonly known as frozen shoulder), and for related joint pathologies characterised by capsulitis of the joint, such as: subacromial bursitis, arthrofibrosis or capsulitis of the knee, hip, hand/wrist or ankle. Most orthopaedic conditions are a manifestation of a mechanical aberration and therefore those who are tasked with treating these conditions, including orthopaedic surgeons are trained to think in the realm of biomechanics. Solutions for these problems therefore tend to have a strong focus on restoration of appropriate mechanics to a disordered anatomical system. Put simply, if a bone is broken it gets fixed it, if a tendon is torn, it gets repaired and if joint is worn, it is replaced. However, there is relatively little research into conditions such as adhesive capsulitis and its potential treatment compared to most other orthopaedic conditions for several reasons. Firstly, it is not a biomechanical problem that can therefore have a mechanical solution. Second, although it is known as one of the most painful conditions of the shoulder with significant debilitation due to pain and stiffness, it is viewed as a benign condition as it mostly resolves with time. But, this can take up to two years in a non-diabetic and up to three to four years in a diabetic patient. Thirdly, a lot of the research has been carried out by a few scattered groups around the world but there has been no concerted effort to understand what the underlying molecular pathology really-is and how it can be treated. The present inventor is the first to recognise a common factor among joint pathologies that manifest as biomechanical problems, but likely have a molecular cause. Currently, the mainstay of treatment for conditions such as capsulitis is the use of intraarticular corticosteroid injections to dampen the degree of inflammation. If given in the first three to four months of developing the condition, it may improve pain but it does not alter the natural history of the condition and its prolonged course. Unfortunately, the pain returns several weeks after corticosteroid treatment. The other common solution is surgical release of the fibrotic joint capsule to improve range of motion in the later stages of the condition when stiffness is the predominant symptom, as opposed to pain in the early inflammatory phase. The surgical release is a late therapeutic option which incises the thickened fibrotic shoulder joint capsule but does not address the underlying pathology. Accordingly, a significant advantage of the present invention over previous treatment approaches is that it addresses the underlying cause of the pathology rather than masking it (as is the case with corticosteroid injections). A further advantage, is that is avoids or reduces the need for invasive procedures such as surgeries, since the treatment (ie, the VEGF inhibitor), can be administered directly into the joint by intraarticular injection. The rotator interval Adhesive capsulitis involves abnormalities of the coracohumeral ligament and rotator interval. Zhao et al. found that the most characteristic magnetic resonance imaging findings in patients with adhesive capsulitis were thickening of the coracohumeral ligament and the capsule at the rotator interval and complete obliteration of the fat triangle under the coracoid process. Open surgical exploration has shown that the coracohumeral ligament is the most palpably thickened and abnormal part of the capsule. Open surgery and arthroscopic observation have confirmed that angiogenesis most commonly affects the rotator interval. Berghs et al. reported findings of abundant angiogenesis, especially in the rotator interval area; they also found that arthroscopic excision of this area resulted in rapid pain relief. Anecdotally, some investigators have described hypervascularity at the rotator interval with adhesive capsulitis. Some groups have histologically confirmed increased vascularity in fibrotic tissues from the rotator interval of patients with adhesive capsulitis. Bunker and Anthony described 12 patients who did not have improvement after manipulation. The patients were treated by surgical release of the coracohumeral ligament, and this tissue was hypervascular in all of them. Ryu et al. described more intense immunostaining for general markers for blood vessels in the synovium of the rotator interval in patients with diabetic adhesive capsulitis compared with a control group. In a recent study, Okuno et al. also found that all patients with adhesive capsulitis had abnormal neovessels that were excessive, disorganized and contained arteriovenous shunts. Their angiographic findings showed abnormal neovessels at the rotator interval and the fat triangle under the coracoid process. They safely performed transcatheter arterial embolization using Imipenem (IPM) and Cilastatin Sodium (CS) with significant improvements in pain, range of motion and shoulder function at short-term follow-up in patients with adhesive capsulitis. The results of this study indicate that hypervascularity at the rotator interval and surrounding tissues plays an important role in adhesive capsulitis, and the occlusion of these abnormal vessels produces therapeutic effects. Abnormal neovessels and accompanying nerves are likely sources of pain in adhesive capsulitis. Alfredson and colleagues showed vascular/neural ingrowth in areas associated with chronic painful tendinopathy, and immunohistochemically identified substance P–positive nerves located near the newly formed blood vessels. Gotoh et al. measured levels of substance P in the subacromial bursa of patients with rotator cuff disease and found that the amount of nerve fibers immunoreactive to substance P was increased around the vessels. Xu et al. immunohistochemically analyzed shoulder capsule tissues collected from patients with adhesive capsulitis and from patients with rotator cuff tears without stiffness. They found significantly higher expression levels of nerve markers in capsule tissue associated with adhesive capsulitis than with rotator cuff tears. Furthermore, nerve fibers were often located close to small blood vessels in adhesive capsulitis tissues. This indicates that abnormal blood vessels and accompanying nerves at the rotator interval are possible sources of pain. Another possible mechanism of the transcatheter arterial embolization therapy in the study by Okuno et al., is the suppression of inflammation induced by occlusion of blood vessels. Costa et al. reported that angiogenesis and inflammation are often closely integrated and that angiogenesis could facilitate inflammation. Despite anecdotal information implicating a potential role for increased vascularity in the pathophysiology of adhesive capsulitis, current approaches to treating this condition continue to focus on administration of anti-inflammatory medication, or the use of surgical intervention. The present inventor has concluded that VEGF expression is associated with vascularity, synovial proliferation and shoulder motion pain in the rotator cuff disease. Thus, the present invention is based on a detailed understanding by the inventor, of the molecular culprits associated with joint conditions such as adhesive capsulitis and a recognition that abnormal neoangiogenesis and accompanying nerves are the likely sources of pain in adhesive capsulitis and subacromial bursitis. Angiogenesis and inflammation are often closely integrated and angiogenesis facilitates inflammation. The inventor believes that this implicates VEGF as an integral factor in the development of adhesive capsulitis. The inventor recognises that VEGF likely provides the angiogenetic infrastructure that instigates and propagates adhesive capsulitis causing pain and stiffness. The inventor also recognises that VEGF also has a role in the pain and loss of range of motion associated with subacromial bursitis. Critically, the present inventor identified that inhibition of VEGF activity in the joint capsule provides a novel approach by which to reduce the development and progression of various capsular conditions, particularly conditions arising from hypervascularity, leading to inflammation and fibrosis of the joint capsule. Thus, the present inventor has developed a novel approach for the treatment and prevention of debilitating conditions that prior to now, had only been treated using anti-inflammatory and other interventions that provide for limited to no benefit to patients. Importantly, the findings of the inventor find application in joint disorders other than those arising in the shoulder (ie frozen shoulder). Indeed, by inhibiting VEGF in the capsule of other joints, such as the hip, knee, ankle or joint of the wrist and hand, the inventor believes that it is also possible to mitigate or reduce the development and progression of capsulitis in those joints. Angiogenesis and VEGF Vascular Endothelial Growth Factor (VEGF) is one of the most important angiogenesis factors, and it consists of a homodimeric heparin-binding glycoprotein with a molecular weight of 34 to 42 kDa. VEGF is expressed during hypoxia to promote oxygen delivery and to encourage neoangiogenesis by selectively simulating the growth of endotheliocytes, and it also occurs as a genetic factor in the consequent fibrous restoration process. A variety of cytokines and growth factors are involved in the regulation of angiogenesis, and the most potent agent that acts specifically on vascular endothelium is VEGF. VEGF is an endothelial-specific growth factor that potently increases microvascular permeability, stimulates endothelial cell proliferation, and induces proteolytic enzyme expression and the migration of endothelial cells, monocytes, and osteoblasts, all of which are essential for angiogenesis. Diabetes and VEGF The association between diabetes mellitus and the frozen shoulder has been well documented. Approximately 10% of patients that have frozen shoulder are found to have diabetes mellitus (some of whom are diagnosed with diabetes mellitus following investigation prompted by the frozen shoulder diagnosis). Thus, the inventor believes that the methods of the present invention also find particular utility in preventing and treating capsulitis of the shoulder and other joints, in patients who are at increased risk, particularly patients that have or are at risk of having diabetes mellitus. Recent studies have suggested a major role for VEGF in diabetes mellitus because microangiopathy and an increased angiogenic response are the main characteristics of this disease. The cause for the upregulation of VEGF in diabetes remains speculative, but multiple factors may be involved. Several factors relevant to the pathogenesis of diabetic complications have been shown to promote VEGF expression in a variety of cell types and tissues, including the advanced glycation end products, angiotensin II, and reactive oxygen species. It is important to note that protein kinase C, which is increasingly being recognized as a central mediator for the damaging effects of hyperglycemia, has been shown to upregulate VEGF. Previous studies have shown a close relationship between neovascularization and VEGF in diabetes mellitus. Duh and Aiello have reported that VEGF can cause endocrine changes that stimulate systemic neovascularization in diabetes mellitus, thereby inducing microangiopathy. Conversely, about 90% of patients diagnosed with frozen shoulder do not have diabetes mellitus. Conditions for treatment according to the invention Accordingly, the present invention provides a method of treating an individual suffering from a joint disorder characterised by hypervascularisation, inflammation and/or fibrosis of the joint capsule, wherein the method comprises: administering to an individual in need thereof, a therapeutically effective amount of a vascular endothelial growth factor (VEGF) inhibitor, thereby treating the joint disorder in the individual. The present invention also provides a method of preventing a joint disorder characterised by hypervascularity, inflammation and/or fibrosis of the joint capsule, wherein the method comprises: administering to an individual at risk, a therapeutically effective amount of a VEGF inhibitor, thereby preventing the joint disorder from developing in the individual. It will be understood that the methods of the present invention extend to the treatment of any joint disorder where there is one or more of fibrosis, tissue adhesions (scar tissue), synovial proliferation, inflammation, capsulitis, bursitis and/or tendonitis. More specifically, the joint requiring treatment according to the present invention may be the shoulder joint, knee joint, hip joint, a joint in the hand/wrist, or the ankle. The joint disorder will typically be characterised by pain, and a reduction in joint movement. For example, with adhesive capsulitis of the shoulder, the reduction in the range of movement may be such that the individual requiring treatment has a global restriction of active and passive range of motion in all planes of shoulder motion with pain on passive stretching when compared to the contralateral shoulder. Similarly, where the capsulitis is in the knee, hip, hand/wrist or ankle, the range of movement may be significantly restricted compared to normal. As will also be understood, the pathologies of the joint disorders described herein involve abnormal, excessive and/or disorganised neoangiogenesis and/or may include arteriovenous shunts. In any embodiment of the invention, the neoangiogenic vessels of the joint may further include neural ingrowth. The individual receiving treatment according to the present invention may be any animal, preferably a mammal or human patient. Examples of animals that can be treated according to the invention include domestic animals (such as cats, dogs, etc.), farm or competitive animals (such as horses, cows, pigs, etc.), and exotic animals (such as monkeys, apes, etc.). Regions of the shoulder that are known to be affected by capsulitis, bursitis, fibrosis, tissue adhesions (scar tissue), synovial proliferation, inflammation, and/or tendonitis or reduced movement, pain, inflammation, include the rotator interval, the subacromial bursa, the coracohumeral ligament or the coracoid process (particularly, the fat triangle under the coracoid process). Pathologies in these regions of the shoulder may present as: shoulder joint contracture, adhesive capsulitis, subacromial bursitis, arthrofibrosis, tendonitis or tendinopathy (for example, tendonitis/tendinopathy of the rotator cuff). The pathologies may be primary, secondary or idiopathic. In cases of secondary pathologies, the individual may have had a recent trauma to the joint (including surgical trauma), a period of inconsistent/intermittent movement of the joint, rheumatic disease progression or a history of diabetes mellitus, cardiac disease such as myocardial infarction, thyroid disease such as hypothyroidism, Parkinson’s Disease or barbiturate use. More specifically, the methods of the present invention may be useful for the treatment or prevention of: - primary idiopathic adhesive capsulitis/frozen shoulder; - secondary adhesive capsulitis/frozen shoulder; - postoperative adhesive capsulitis/frozen shoulder; - Post-operative capsulitis of the knee or hip; - subacromial bursitis; - primary idiopathic arthrofibrosis or capsulitis of other joints in the musculoskeletal system, such as the knee, hip, ankle, hand or wrist joints; - secondary arthrofibrosis or capsulitis of other joints in the musculoskeletal system, such as the knee, hip, ankle, hand or wrist joints; - tendinopathy of the Rotator Cuff Tendons; - tendinopathy of the long head of the biceps. The skilled person will be familiar with methods for identifying an individual in need of treatment according to the methods and uses described herein. For example, one sign of a shoulder joint (adhesive capsulitis) is that the joint becomes so tight and stiff that it is nearly impossible to carry out simple movements (for example, in the case of adhesive capsulitis of the shoulder, raising the arm.) The individual requiring treatment may be characterized as having extremely decreased shoulder motion in all planes to include active elevation, active internal rotations (spine level reached by the thumb behind the back), active external rotation, passive elevation, passive external rotation at the side, passive external rotation at 90 degrees, function scores. As indicated above, the stiffness in the joint is frequently accompanied by pain that worsens at night. Pain due to a frozen joint is usually dull or aching. It can be worsened with attempted motion, or if bumped. Pain may be to a level where it interferes with activities of daily living and diminishes the quality of life. A frozen joint can be diagnosed if limits to the active range of motion (range of motion from active use of muscles) are the same or almost the same as the limits to the passive range of motion (range of motion from a person manipulating the arm and shoulder). An arthrogram or an MRI scan may confirm the diagnosis. A standard X-ray may also be used to confirm the diagnosis. The normal course of a frozen shoulder has been described as having three stages: • Stage one: The "freezing" or painful stage, which may last from six weeks to nine months, and in which the patient has a slow onset of pain. As the pain worsens, the shoulder loses motion. • Stage two: The "frozen" or adhesive stage is marked by a slow improvement in pain but the stiffness remains. This stage generally lasts from four to nine months. • Stage three: The "thawing" or recovery, when shoulder motion slowly returns toward normal. This generally lasts from about 5 to about 26 months. A clinical diagnosis of frozen shoulder may be made based on progressive pain and stiffness of greater than about 2 months but less than about 6 months. Preferably, progressive pain and stiffness are observed for a period of at least about 2 months, for example about 2 months, about 3 months, about 4 months, about 5 months or about 6 months. Diagnosis may also involve physiotherapist and orthopaedic surgeon evaluation of: • the percentage of passive range of motion loss (comparing to contralateral side) ^ Global (external rotation, abduction, elevation) ^ External Rotation ^ Abduction ^ Elevation ^ Addutction + internal rotation • visual analogue scale (VAS) for pain on passive stretching • Standardized shoulder functional scores • Severity of frozen shoulder (% of global range of motion loss compared to contralateral side) ^ Mild (<30%) ^ Moderate (30-60%) ^ Severe (>60º%) Diagnosis may also include: plain radiograph (AP, Lat outlet, axillary) to confirm diagnosis and exclude bony glenohumeral pathology, MRI to confirm radiologic signs of capsulitis: • Thickening: • coracohumeral ligament • axillary pouch • rotator interval joint capsule • obliteration of the subcoracoid fat triangle • T2 signal hyperintensity and post-contrast enhancement of the joint capsule The methods of the present invention may have utility in shortening the course of frozen shoulder pathology, for example by shortening the length of or avoiding any of the stages above such that the patient has a return to normal range of joint movement within a shorter period of time. Further, the methods of the present invention are have utility in reducing the level of pain associated with the joint disorders described herein. Angiogenesis and VEGF inhibitors As used herein, an inhibitor of angiogenesis includes any molecule that inhibits the formation and growth of new blood vessels (angiogenesis). Angiogenesis inhibitors are well known to the skilled person, and include agents in the class of VEGF and VEGFR, agents that inhibit proliferation and migration of endothelial cells, and agents which downregulate or inhibit stimulators of angiogenesis. A particularly preferred class of angiogenesis inhibitor for use according to the present invention is a VEGF inhibitor. As used herein, a VEGF inhibitor is any compound that inhibits the activity of vascular endothelial growth factor (VEGF). The inhibitor may be a direct inhibitor and be specific for VEGF – i.e., it may bind specifically to VEGF and thereby inhibit the normal signalling or activity of VEGF. Alternatively, the inhibitor may inhibit indirectly by binding to a receptor of VEGF (e.g., VEGFR), thereby preventing VEGF from binding to its receptor, and blocking or inhibiting the activity of VEGF. In such instances, the VEGF inhibitor may in fact be a VEGFR inhibitor and as such, the present invention contemplates uses of VEGFR inhibitors in any method or use described herein. Preferably, the inhibitor is an exogenous inhibitor that directly binds VEGF or VEGFR. Alternatively, the exogenous inhibitor indirectly inhibits VEGF by inducing the endogenous expression of anti-VEGF proteins and/or nucleic acids. The inhibition of VEGF activity may be at least 10%, 20%, 30%, 40%, 50%, 60% or greater inhibition of VEGF. In preferred forms, the inhibitor may be a small molecule chemical compound or interfering RNA (e.g. siRNA). The inhibitor may also be a peptide, an antibody such as a monoclonal antibody, or a fusion protein that binds to VEGF directly or to a VEGFR. Preferably, the inhibitor is an exogenous anti-VEGF or anti-VEGFR protein, peptide, or antigen-binding fragment thereof. It will be understood that the inhibitor may be any suitable polypeptide capable of binding to an antigen, preferably a VEGF or VEGFR antigen. For example, the inhibitor may be an antigen binding protein that is an antibody, an antibody fragment, a genetically engineered antibody, a chimeric antibody, a heteroconjugate antibody, or a combination thereof. In certain embodiments, the inhibitor is an antibody. Inhibitors of VEGF and VEGFR are known in the art and are commercially available. Certain non-limiting examples follow although it will be appreciated that the scope of the present invention should not be limited to the specific inhibitors described herein. Moreover, once the skilled person has determined a suitable joint disorder requires treating, the skilled person can then readily determine a suitable inhibitor to perform the present invention, with reference to the known literature regarding VEGF and VEGFR inhibitors. Non-limiting examples of suitable VEGF inhibitors for use in accordance with the methods of the present invention include: - Aflibercept (trade name Eylea, CAS number 862111-32-8), a recombinant fusion protein consisting of vascular endothelial growth factor (VEGF)-binding portions from the extracellular domains of human VEGF receptors 1 and 2, that are fused to the Fc portion of the human IgG1 immunoglobulin. A biosimilar of aflibercept, Ziv-aflibercept (trade name Zaltrap), is also available. - Bevacizumab, (trade name Avastin), a recombinant humanized monoclonal antibody that blocks angiogenesis by inhibiting vascular endothelial growth factor A (VEGF-A). A biosimilar of bevacizumab, bevacizumab-awwb (Amgen; trade name MVASI) is also available. Biosimilars of bevacizumab, bevacizumab-bvzr (trade name Zirabev), bevacizumab-adcd (trade name Vegzelma) and bevacizumab-maly (trade name Alymsys) are also available. - Ranibizumab, (trade name Lucentis, among others), a monoclonal antibody fragment (Fab) created from the same parent mouse antibody as bevacizumab. Ranibizumab inhibits angiogenesis by inhibiting Vascular endothelial growth factor A. - Brolucizumab, (trade name Beovu), a monoclonal antibody that binds to VEGF- A and thereby prevents VEGF-A from binding to its receptor. - Ramucirumab (trade name Cyramza), a monoclonal antibody that is a direct VEGFR2 antagonist, binding to the extracellular domain of VEGFR and thereby blocking the binding of ligands VEGF-A, VEGF-C and VEGF-D to the receptor. The commercially available VEGF inhibitors are all available as injectable formulations and can therefore be easily used in the methods of the present invention. Other inhibitors which may be used include VEGFR inhibitors including: pazopanib, sunitunib, sorafanib, regorafenib, cabozantinib, lenvantinib, panatinib, axitinib, tivozanib, and vandetanib. The skilled person can make use of the antigen binding domains from any known antibody for the methods of the present invention. Method of administration/dosing The phrase ‘therapeutically effective amount’ as used herein, generally refers to an amount of one or more inhibitors, or, if a small molecule inhibitor, a pharmaceutically acceptable salt, polymorph or prodrug thereof of the present invention that (i) treats the particular disease, condition, or disorder, (ii) attenuates, ameliorates, or eliminates one or more symptoms of the particular disease, condition, or disorder, or (iii) delays the onset of one or more symptoms of the particular disease, condition, or disorder described herein. As used herein, "preventing" or "prevention" is intended to refer to at least the reduction of likelihood of the risk of (or susceptibility to) acquiring a disease or disorder (i.e., causing at least one of the clinical symptoms of the disease not to develop in a patient that may be exposed to or predisposed to the disease but does not yet experience or display symptoms of the disease). This includes preventing the recurrence of one or more of the clinical symptoms of a disease or disorder. Biological and physiological parameters for identifying such patients are provided herein and are also well known by physicians. For example, prevention of a joint disorder as described herein, may be characterised by an absence of, or reduced levels of tissue adhesions, fibrosis, or inflammation if the individual has preliminary signs of these disorders, or has a history of developing similar joint disorders. Similarly, the individual may be in a high risk category for the development of a joint disorder as described herein, such as having, having had, or being at risk of having diabetes mellitus, trauma or surgery at the site of the joint disorder, cardiac disease (e.g. myocardial infarction, pulmonary disease), stroke, autoimmune and/or inflammatory disease (e.g. rheumatoid arthritis, fibromyalgia, and/or lupus), diabetes mellitus, thyroid disease (e.g. hypothyroidism), Dupuytren's disease, Parkinson’s disease and/or barbiturate use. The terms "treatment" or "treating" of a subject includes the application or administration of a compound of the invention to a subject (or application or administration of a compound of the invention to a cell or tissue from a subject) with the purpose of delaying, slowing, stabilizing, curing, healing, alleviating, relieving, altering, remedying, less worsening, ameliorating, improving, or affecting the disease or condition, the symptom of the disease or condition, or the risk of (or susceptibility to) the disease or condition. The term "treating" refers to any indication of success in the treatment or amelioration of an injury, pathology or condition, including any objective or subjective parameter such as abatement; remission; lessening of the rate of worsening; lessening severity of the disease; stabilization, diminishing of symptoms or making the injury, pathology or condition more tolerable to the subject; slowing in the rate of degeneration or decline; making the final point of degeneration less debilitating; or improving a subject's physical or mental well-being. It will be understood that a preferred method for administering the VEGF inhibitors in accordance with the present invention, is local administration (i.e., direct injection) into the joint requiring treatment. The potential anatomical targets for Anti-VEGF therapy in Adhesive Capsulitis and Subacromial Bursitis of the Shoulder are: - rotator interval tissue (Between the Supraspinatus and Subscapularis Rotator Cuff Tendons) - coracohumeral ligament - subcoracoid space - subcoracoid fat triangle - subacromial space - subacromial bursa - intracapsular - intratendinous - peritenon/peritendon The skilled person will be familiar with methods for injection of a therapeutic agent into a joint requiring treatment. Conveniently, the site of administration would mirror the site where current corticosteroid treatments are administered. Moreover, anti-VEGF therapies could be administered into the above anatomical sites under the guidance of radiological imaging or ultrasound imaging, as well as under direct vision during arthroscopic or open surgical procedures. Typically a healthy shoulder will accommodate 8-15 ml of fluid, however, in the context of the joint disorders to be treated according to the present invention, this amount is likely to be reduced to around 7 ml. Accordingly, preferably, the total volume of liquid injected into a shoulder requiring treatment, does not exceed about 7 ml, or 5 ml, or 2.5 ml. Preferably, the total volume of liquid injected into a shoulder requiring treatment, does not exceed about 6 ml, 4 ml, 3 ml or 2 ml. A smaller volume down to about 1 ml may also be used. It will be well within the purview of the skilled person to determine the appropriate dosage and treatment regimen for administering VEGF inhibitors according to the present invention. It will be understood, that the specific dose level for any particular patient will depend upon a variety of factors including the activity of the specific compound employed, the age, body weight, general health, sex, diet, time of administration, route of administration, and rate of excretion, drug combination (i.e. other drugs being used to treat the patient), and the severity of the particular disorder undergoing therapy. The total dosage is preferably injected in one portion, although two or more portions at the same or different points into the joint capsule are possible, preferably intralesionally, or intra-adhesionally. The objective of these procedures is to assure good distribution of the VEGF inhibitor within a small volume of the adhesion. In some embodiments, the VEGF inhibitor is administered intra-articularly. In some embodiments, the VEGF inhibitor is administered at a dose of at least 50 mg to about 200 mg or at least 100 to about 200 mg; for example about 50 mg, about 75 mg, about 100 mg, about 125 mg, about 150 mg, about 175 mg, or about 200 mg. In some embodiments, the VEGF inhibitor is administered intra-articularly at a dose of at least 100 mg. Preferably, the individual receiving treatment will have their arm (or leg as the case may be) immobilized for approximately 5-6 hours post injection. (Use of a sling may facilitate this). In certain embodiments, the injection of VEGF inhibitor is preceded by an anaesthetic injection of lidocaine (for example 5-10 mml 1% lidocaine). In certain embodiments, the injection of VEGF inhibitor is preceded by an anaesthetic injection of lignocaine (for example 5-10 mml 2% lignocaine). Preferably, the anaesthetic injection is subcutaneous local injection. Anti-VEGF therapy may be administered preoperatively – for example in patients at risk of developing adhesive capsulitis/frozen shoulder or subacromial bursitis. And postoperatively – for example in patients undergoing shoulder surgery (arthroscopic or open) as a treatment for secondary adhesive capsulitis/frozen shoulder or subacromial bursitis. In cases where results of a single treatment are considered inadequate, the same procedures, total amount of VEGF inhibitor and concentration may be repeated. For example, the VEGF inhibitor may be administered with repeated injections at 2 to 6 week intervals, or more (such as once a month, once every 2 months, once every 3 months or less frequently). In some embodiments, the VEGF inhibitor may be administered with repeated injections at about 2, 3, 4, 5 or 6 week intervals. In some embodiments, the VEGF inhibitor is administered monthly. The skilled person will also be familiar with methods for determining successful treatment, or prevention of a joint disorder, following performing a method or use of the invention as described herein. For example, successful treatment may be observed as a decrease in pain and/or increase in range of joint motion. For example, successful treatment may include wherein after one month of receiving at least one administration of VEGF inhibitor, the patient achieves an active and passive range of motion and/or reduced pain on passive stretching compared to baseline. For example, prevention may be observed as no increase in pain, and/or (i) no decrease in range of joint motion, or (ii) an increase in range of joint motion from a subclinical symptomatic level of joint restriction. Optionally, the prevention is measured as an increase in range of joint motion from a subclinical symptomatic level of joint restriction. For example, successful prevention may include wherein after one month of receiving at least one administration of VEGF inhibitor, the patient exhibits no reduction in active and passive range of motion and/or no increase in pain on passive stretching compared to baseline. Optionally, the patient has a medical history of a joint disorder, preferably adhesive capsulitis. Optionally, prevention is in a subject that is one or more of (i) in a high risk category for the development of a joint disorder, (ii) predisposed to development of a joint disorder, (iii) has a history of joint disorder. For example, effective treatment may be assessed by using one or more of the following parameters: - reduction in passive global range of motion (ROM) loss of the affected shoulder against the unaffected contralateral shoulder, compared to baseline; and/or - reduction in pain levels compared to baseline; and/or - reduction in Shoulder Pain and Disability Index assessment compared to baseline; and/or - increase in ability to perform arm, shoulder or hand activities (eg using cutting utensils, heavy household chores, carrying bags, recreational sport) compared to baseline; and/or - reduction in severity classification of global range of motion loss compared to baseline. Percentage loss of ROM may be categorised as <30% loss of motion (mild), 30- 60% loss of motion (moderate), and >60% loss of motion (severe). Optionally, the treatment is successful due to a reduction in category from severe to moderate, mild or none; or from moderate to mild or none; or from mild to none. Optionally, the prevention is successful due to a reduced likelihood or reduced incidence of the loss of ROM category changing over time: from moderate to severe, mild to moderate, or from mild to severe. Optionally, the prevention is successful due to loss of ROM categorised as mild or moderate remaining unchanged (ie not progressing to a more severe category). Patient pain levels may be assessed by a visual analogue scale (VAS). For example, the scale may consist of a 100mm line which represents the continuum between “no pain” (mm) and “worst pain” (100mm). Participants self-report a measurement that aligns with their experienced symptoms. Markings may be categorised as follows: 0 to 4 mm (no pain), 5 to 44 mm (mild pain), 45 to 74 mm (moderate pain), and 75 to 100 mm (severe pain) (see for example, Jensen et al. (2003) Interpretation of visual analog scale ratings and change scores: a reanalysis of two clinical trials of postoperative pain. The Journal of Pain, 4(7) 407-414. https://doi.org/10.1016/s1526-5900(03)00716-8; incorporated herein by reference). Optionally, the treatment is successful due to a reduction in category from severe to moderate, mild or none; or from moderate to mild or none; or from mild to none. Optionally, the prevention is successful due to a reduction in category changing over time from moderate to severe, mild to moderate, or from mild to severe. Optionally, the prevention is successful due to mild or moderate VAS category remaining unchanged (ie not progressing to a severe category). Shoulder Pain and Disability Index (SPADI) methods can be found in the art (eg Roach et al. (1991) Development of shoulder pain and disability index. Arthritis Care Research 4(4):143-9; 9; Hill et al. (2011). Factor structure and validity of the shoulder pain and disability index in a population-based study of people with shoulder symptoms. BMC Musculoskeletal Disorders, 12(8); Brindisino et al. (2021). Shoulder Pain and Disability Index: Italian cross-cultural validation in patients with non-specific shoulder pain. Shoulder & Elbow, 13(4).433-444. https://doi.org/10.1177/1758573220913246; all of which are incorporated herein by reference). The SPADI assessment may comprise a patient-reported questionnaire (eg 13 questions) to measure the pain and viability associated with various shoulder pathologies, including adhesive capsulitis. Assessing increased ability to perform arm, shoulder or hand activities is known to the skilled person. This may comprise a patient-reported questionnaire (eg 11-30 questions) that measures physical function and symptoms in patients with musculoskeletal disorders of the upper extremity. Exemplary assessments include: Disabilities of the Arm, Shoulder and Hand assessment (DASH); and Quick Disabilities of the Arm, Shoulder and Hand assessment (QuickDASH) (Zwaan et al. (2022) Predictive Value of the (Quick)DASH Tool for Upper Extremity Dysfunction Following Percutaneous Coronary Intervention. Patient Related Outcome Measures, 13, 145-155. https://doi.org/10.2147/PROM.S353895; incorporated herein by reference Baseline is assessed prior to the treatment or the prevention. In some embodiments, the post-treatment assessment for comparison with baseline may occur at least about 3 days, about 4 days, about 5 days, about 6 days, about 7 days, about 10 days, about 14 days, about 28 days, about 1 month, about 2 months, about 84 days, about 3 months, about 4 months, about 5 months, about 6 months, about 168 days, about 364 days, about 52 weeks, or about 1 year after treatment. In another embodiment there is provided a kit or article of manufacture including one or more inhibitors of VEGF as described herein, or a pharmaceutically acceptable salt, polymorph or prodrug thereof and/or pharmaceutical composition as described above. In other embodiments there is provided a kit for use in a therapeutic or prophylactic application mentioned above, the kit including: - a container holding a therapeutic composition in the form of one or more inhibitors of VEGF as described herein, or a pharmaceutically acceptable salt, polymorph or prodrug thereof or pharmaceutical composition; - a label or package insert with instructions for use. In certain embodiments the kit may contain one or more further active principles or ingredients for treatment of a joint disorder as described herein. The kit or “article of manufacture” may comprise a container and a label or package insert on or associated with the container. Suitable containers include, for example, bottles, vials, syringes, blister pack, etc. The containers may be formed from a variety of materials such as glass or plastic. The container holds a therapeutic composition which is effective for treating the condition and may have a sterile access port (for example the container may be an intravenous solution bag or a vial having a stopper pierceable by a hypodermic injection needle). The label or package insert indicates that the therapeutic composition is used for treating the condition of choice. In one embodiment, the label or package insert includes instructions for use and indicates that the therapeutic or prophylactic composition can be used to treat a joint disorder described herein. The kit may comprise (a) a therapeutic or prophylactic composition; and (b) a second container with a second active principle or ingredient contained therein. The kit in this embodiment of the invention may further comprise a package insert indicating the composition and other active principle can be used to treat a disorder or prevent a complication stemming from a hypervascular disease described herein. Alternatively, or additionally, the kit may further comprise a second (or third) container comprising a pharmaceutically-acceptable buffer, such as bacteriostatic water for injection (BWFI), phosphate-buffered saline, Ringer's solution and dextrose solution. It may further include other materials desirable from a commercial and user standpoint, including other buffers, diluents, filters, needles, and syringes. In certain embodiments the therapeutic composition may be provided in the form of a device, disposable or reusable, including a receptacle for holding the therapeutic, prophylactic or pharmaceutical composition. In one embodiment, the device is a syringe. The device may hold 1-2 mL of the therapeutic composition. In some embodiments, the device may hold 1-16 mL of the therapeutic composition, optionally 4 mL, preferably 1-2 mL. The therapeutic or prophylactic composition may be provided in the device in a state that is ready for use or in a state requiring mixing or addition of further components. As used herein, the term "pharmaceutical composition" refers to a preparation which is in such form as to permit the biological activity of an active ingredient contained therein to be effective, and which contains no additional components which are unacceptably toxic to a subject to which the formulation would be administered. A "pharmaceutically acceptable carrier" refers to an ingredient in a pharmaceutical composition, other than an active ingredient, which is nontoxic to a subject. A pharmaceutically acceptable carrier includes, but is not limited to, a buffer, excipient, stabilizer, or preservative. Examples Example 1: A patient presents at a clinic with shoulder pain. A clinical diagnosis of frozen shoulder is made based on: progressive pain and stiffness of >2 months and <6 months. A physiotherapist and orthopaedic surgeon evaluate the patient for: ^ the percentage of passive range of motion loss (comparing to contralateral side) o Global (external rotation, abduction and elevation) o External rotation o Abduction o Elevation o Abduction and internal rotation ^ Visual analogue scale (VAS) for pain on passive stretching ^ Standardized shoulder functional scores (eg QuickDASH; SPADI) ^ Severity of frozen shoulder (% of global range of motion loss compared to contralateral side) o Mild (<30%) o Moderate (30-60%) o Severe (>60º%) Upon receipt of a positive diagnosis of adhesive capsulitis, the patient is recommended treatment with a VEGF inhibitor. VEGF is administered to the shoulder joint via injection by an interventional radiologist. The VEGF inhibitor is injected under image guidance (eg, radiological imaging or ultrasound imaging, as well as under direct vision during arthroscopic or open surgical procedures) into the glenohumeral joint. The total volume of VEGF inhibitor injected into the joint is approximately 5 ml. After a period of about 6-12 weeks, the patient reports increasing movement in the shoulder and reduction in pain on passive stretching. Example 2: SPADI assessment as provided to patient Purpose: This questionnaire will ask about your symptoms as well as your ability to perform certain activities. Instructions: Please answer every question, based on your condition during the last week, by circling the appropriate number. If you did not have the opportunity to perform an activity in the past week, please make your best estimate of which response would be the most accurate. It doesn’t matter which hand or arm you use to perform the activity; please answer based on your ability regardless of how you perform the task. 1. How severe is your pain? Circle the number that best describes your pain where: 0 = no pain and 10 = the worst pain imaginable. 2. How much difficulty do you have? Circle the number that best describes your experience where: 0 = no difficulty and 10 = so difficult it requires help

Score calculation and interpretation: Any unanswered question will be removed from the calculable score of that section. Minimum Detectable Change (90% confidence) = 13 points. Any change less than this may be attributable to measurement error Example 3: QuickDASH assessment as provided to patient Purpose: This questionnaire will ask about your symptoms as well as your ability to perform certain activities. Instructions: Please answer every question, based on your condition during the last week, by circling the appropriate number. If you did not have the opportunity to perform an activity in the past week, please make your best estimate of which response would be the most accurate. It doesn’t matter which hand or arm you use to perform the activity; please answer based on your ability regardless of how you perform the task. Module 1: Please rate your ability to do the following activities in the last week by circling the number below the appropriate response.

Module 2: Work (Optional – If you do not work you may skip this module) The following questions ask about the impact of your arm, shoulder or hand problem on your ability to work (including homemaking if that is your main work role). Please indicate what your job/work is. Please circle the number that best describes your physical ability in the past week. Module 3: Sports/Performing Arts (Optional – If you do not play a sport or an instrument you may skip this section) The following questions ask about the impact of your arm, shoulder or hand problem on playing your musical instrument or sport or both. If you play more than one sport or instrument (or play both), please answer with respect to that activity which is most important to you. Please indicate the sport or instrument which is most important to you. Please circle the number that best describes your physical ability in the past week.

1 2 3 4 5 or playing your instrument or sport?

Score calculation and interpretation

Module 1

A score cannot be calculated if more than one question is missing a response. A higher score is interpreted as higher disabilit

/sum of n responses \

Score = I - ^; - - 1 X 25

X n / where n is equal to the number of completed responses

Optional Modules

A score cannot be calculated if more than one question is missing a response. A higher score is interpreted as higher disability sum of n responses

Score - 1 X 25 n

Example 4: VAS pain scale assessment as provided to patient Score calculation and interpretation: Using a ruler, measure the distance from “0” to where the participant marked their line. The following table (Table 1) describes the categorisation of severity based on distance measured. Table 1: Scoring for VAS pain scale Example 5: A single-centred, open-label, dose-ranging clinical trial is proposed to assess the safety and efficacy of intra-articular bevacizumab in adults with adhesive capsulitis. Participants, aged 18 years and over, will be included in this study if they are diagnosed with adhesive capsulitis as defined in the inclusion criteria. Eligibility will be dependent on the exclusion of any previous shoulder trauma in the contralateral shoulder, previous adhesive capsulitis or any other differential diagnosis of the ipsilateral shoulder, and serology confirming absence of diabetes mellitus (defined by fasting glucose ≥7mmol/L and Hba1c ≥ 5.7%). The dose-ranging follows a classic “3+3 design” to establish dose-limiting toxicities and the recommended dose for future studies. All dose escalations will be determined after a safety evaluation of the prior cohort. The design will be conducted as follows: initially, three participants will be enrolled into cohort 1 and will receive a 50mg dose of bevacizumab. The occurrence of a single treatment-related dose limiting toxicity (defined as a grade 3 or higher adverse event as per Common Terminology Criteria for Adverse Events version 5.0 United States of Health and Human Services, 2017) will prompt enrolment of three additional participants into the same cohort. When more than one treatment-related dose limiting toxicity occurs in ≤ 6 patients in a dosing cohort, dose escalation will be stopped, and this dose level will be identified as the non- tolerated dose. Otherwise, if ≤ 1 treatment-related dose limiting toxicity occurs in ≤ 6 participants, three participants will be enrolled into the next cohort (cohort 2) and receive a sequentially higher dose of bevacizumab (100mg). This will continue at 50mg increases of bevacizumab for each cohort unless otherwise stopped due to dose- limiting toxicities or Sponsor discretion. The maximum planned dose will be cohort 4 (200mg dose). For this cohort, it is planned to enrol up to 10 participants unless dose- limiting toxicities (DLTs) are observed or enrolment is stopped. Number of Participants and Duration: Approximately 15-30 participants, preferably 20 participants, will be enrolled to determine dose-limiting toxicities (DLTs). The duration of each participant’s involvement in the trial is expected to be approximately 12 months: ^ Screening will last up to 28 days ^ Treatment will be administered as a single injection on Day 1 ^ Follow-up period will last up to 52 weeks Investigated Therapy: Participants will receive a single intra-articular dose of 50mg bevacizumab. This dose will increase sequentially by 50mg per treatment cohort, until otherwise stopped due to dose-limiting toxicities or Sponsor discretion. All treatment administration will be performed at the investigational site by healthcare professionals. Formulation: Bevacizumab (Avastin®) will be supplied to study site as a single 4mL vial containing 100mg of bevacizumab or 16mL vial containing 400mg of bevacizumab. Route of administration: Preliminary subcutaneous administration of local anaesthetic (lignocaine 2%). Intra-articular dose of bevacizumab then administered percutaneously under strict sterile conditions by a highly experienced musculoskeletal radiologist using a posterior approach to the glenohumeral joint under direct real-time ultrasound control. Correct placement of the needle tip that allows free flow of injectate without resistance will be confirmed prior to bevacizumab instillation with a small initial test injection of saline delivered via an attached 3-way stopcock. Table 2: Inclusion Criteria To be eligible for the study, participants must meet all the following criteria: IC1. Over 18 years of age (inclusive) at the time of signing informed consent IC2. Clinical diagnosis of adhesive capsulitis which is defined as: a. Progressive pain and stiffness for a period greater than 2 months but less than 6 months; and, b. Either thickening or signal hyperintensity associated with coracohumeral ligament, axillary pouch, or rotator interval joint capsule OR obliteration of the subcoracoid fat triangle as confirmed by radiological examination (magnetic resonance imaging); and, c. Normal x-ray of the shoulder with no evidence of glenohumeral joint degenerative changes or sequelae of previous trauma. IC3. Capable of giving signed informed consent as described in Section 14 of the protocol which includes compliance with the requirements and restrictions listed in the informed consent form and in this protocol IC41. Participants of child-bearing potential are eligible to participate if they agree to the following during the study intervention period and for a minimum of 120 days after the study intervention is administered: a. Female participants must not be pregnant or breastfeeding AND are either abstinent from heterosexual intercourse as their preferred usual lifestyle OR engage in an adequate method of contraception (i.e., the oral contraceptive pill, intrauterine device, or other) b. Male participants must refrain from donating sperm AND are either abstinent from heterosexual intercourse as their preferred usual lifestyle OR must agree to use an adequate method of contraception/barrier method (i.e. condom and/or heterosexual partner engaging in an adequate method of contraception as previously described) IC5. Participants who are not of child-bearing potential, defined as at least one or more of the following criteria, are eligible to participate in the study a. Female participants in a post-menopausal state (defined as not experiencing menses for 12 consecutive months without an alternative cause) b. Documented permanent sterilisation method (including, but not limited to, hysterectomy, bilateral salpingectomy, bilateral oophorectomy, and vasectomy) Table 3: Exclusion Criteria Participants who meet any of the following criteria are not eligible for the study: EC1. History of previous surgery or treatment with corticosteroid within 3 months prior to screening, platelet-rich plasma, or anti-VEGF injections in the ipsilateral shoulder EC2. History of adhesive capsulitis in ipsilateral shoulder EC3. Presence of trauma in the affected shoulder unrelated to adhesive capsulitis EC4 Advanced imaging features associated with calcific tendinopathy EC5. Presence of uncontrolled hypertension (defined as systolic pressure > 140mmHg and diastolic pressure > 100mmHg) EC6. Any medical history of cardiovascular disease, uncontrolled ischemic heart disease, acute myocardial infarction within 12 months of study entry, or any history of intracranial hemorrhage, stroke or a transient ischaemic attacks at any time EC7. Presence of inflammatory arthritis (such as but not limited to: systemic lupus erythematosus, rheumatoid arthritis, reactive arthritis, etc.), Parkinson’s disease, brain injury, osteoarthritis, bony glenohumeral pathology, hypothyroidism, neuromuscular disorders, or pre-diabetes or diabetes mellitus (defined by fasting glucose ≥7mmol/L and Hba1c ≥ 5.7%) EC8. Participants currently taking corticosteroids, monoclonal antibody therapy, or other immunosuppressants which are deemed to impact the study endpoints EC9. Planning to or have received treatment for the affected shoulder at any time during the study or prior to the study (within 60 days), included but not limited to: a. Intra-articular or intrabursal injection(s) of lidocaine, suprascapular nerve blocks; corticosteroids, electroanalgesic and/or thermoanalgesic modalities b. Intra-articular or intrabursal injection(s) of sodium hyaluronate and/or glenohumeral distension arthrography c. Surgical intervention EC10. Progressive pain and stiffness in the affected shoulder that is for a period less than 2 months or greater than 6 months EC11. Hypersensitivity to the study intervention, including any constituents thereof, or drug or other allergy that, in the opinion of the Investigator, contraindicates participation in the study EC12. Any active malignancy under treatment EC13. Women who are pregnant and/or breastfeeding, or who plan to be pregnant in the following six months after study intervention EC14. Participants not suitable for participation, whatever the reason, as judged by the Investigator, including medical or clinical conditions that might affect their safety or ability to complete the protocol or that may confound the efficacy or safety results of the trial EC15. Participants are employees of the clinical study site or other individuals directly involved in the conduct of the study, or immediate family members of such individuals (in conjunction with Section 1.61 of the ICH-GCP Ordinance E6) EC16. Individuals accommodated in an institution because of regulatory or legal order; prisoners or participants who are legally institutionalised EC17. Participants unable to provide written informed consent EC18. Participants who have participated in other clinical trial within 1 month, have participated in another study within 6 months from the date of selection, or have planned for participation in another trial during the follow up period of this trial which is deemed by the Investigator to impact the planned study endpoints of this study EC19. Acute illness within the 30 days prior to V1 that, in the opinion of the Investigator, affects the participant’s ability to participate in the study. EC20. Abnormal laboratory assessments defined as: alanine transaminase and/or aspartate transaminase > 3x upper limit of normal (ULN), Bilirubin T > 2, international normalise ratio > 1.6, estimated glomerular filtration rate < 60mL/min, absolute neutrophil count < 1.5 x 10 ⁹ /L, platelets < 100 x 10 ⁹ /L, haemoglobin < 10g/dL, and/or serum creatine > 1.5x ULN. EC21. Participants currently taking warfarin EC22. Participants deemed with any condition which would preclude their use for study-related magnetic resonance imaging procedures, including but not limited to: morbid obesity, severe claustrophobia, and/or permanent pacemaker). Table 4. Planned dose selections for cohorts. The duration of each participant’s involvement in the trial is expected to be approximately 12 months: • Screening will last up to 28 days • Treatment will be administered as a single injection on Day 1 • Follow-up period will last up to 52 weeks Bevacizumab will be supplied to all participants at a dose determined by the prior cohort. Participants enrolled into the first cohort will receive preliminary subcutaneous local anaesthetic (lignocaine 2%). A 50mg intra-articular dose of bevacizumab will then administered percutaneously under strict sterile conditions by a highly experienced musculoskeletal radiologist using posterior approach into the glenohumeral joint under direct real-time ultrasound control. Correct placement of the needle tip that allows free flow of injectate without resistance will be confirmed prior to bevacizumab instillation with a small initial test injection of saline delivered via an attached 3-way stopcock. Dose escalation will follow a “3+3” design, with each subsequent cohort receiving a 50mg dose increase. This will continue until either the maximum total dose (MTD) is established or the maximum planned dose of 200mg is reached.

Table 5: Objectives and endpoints

Fasting Glucose fest X

j j

X-Ray x ! X

Magnetic Resonance imaging X \ f X

Abbreviations for Table 6: DASH, Disabilities of the Arm, Shoulder, and Hand; EoS, end of study; Hba1c, haemoglobin A1c; SPADI, Shoulder Pain and Disability Index; TSH, thyroid stimulating hormone; VAS, visual analogue scale; VEGF, vascular endothelial growth factor. Footnotes for Table 6: ¹ Demographics include age, gender, race, and ethnicity. Participants are also required to provide their current phone number and emergency contact information. Contact information should be updated at subsequent visits if applicable. ² Prior and concomitant medications include all medications taken within 30 days of screening up until V8. ³ Pregnancy test requires a urine sample test to exclude pregnancy in females of child-bearing potential. ⁴ Safety laboratory tests include haematology parameters (white blood cell count, red blood cell count, platelet count, haematocrit, red blood cell volume, haemoglobin concentration, and differential white blood count), liver function tests (alanine transaminase, alkaline phosphatase, aspartate transaminase, gamma-glutamyltransferase, bilirubin, L-lactate dehydrogenase, serum albumin, prothrombin time/international normalised ratio), serum creatinine, and glomerular filtration rate. ⁵ A full physical examination is required at V0 and involves examination of the head and neck, lymph nodes, skin, chest, abdomen, and musculoskeletal system. Subsequent examinations may be symptom-lead only. ⁶ Vital signs include temperature, blood pressure (systolic and diastolic), respiration, and pulse. These can be measured when sitting after 5 minutes of rest, in the same arm. ⁷ Electrocardiogram assessment includes heart rate, PR and QTcF intervals, and QRS duration. These can be measured when in a supine position after at least 5 minutes. Repeated evaluation throughout the trial is at the discretion of the Investigator. ⁸ Adverse events will be collected from the signature of informed consent until at least V5. ⁹ V2 is a safety phone call rather than an in-clinic visit. Sites will confirm the presence of any adverse events or use of concomitant medications, and will confirm with participants the presence of any symptoms indicating septic arthritis or injection site reactions. An unscheduled in-clinic visit will be per investigator discretion. References Ashraf S, Mapp PI, Walsh DA. 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