Pigmented Villonodular Synovitis (PVS) is a proliferative disease that often occurs in synovial joints, tendon sheaths, and bursae and has an unknown etiology. The lesions often present as villi or nodular fibrous connective tissue protrusions, or both.
Research on the etiology and pathogenesis of PVNS is still a hot area. Several etiologies have been described, including disorders of lipid metabolism, trauma and hemorrhage, inflammation, and tumors, and in recent years, genetic abnormalities and their expression products, as well as inhibition of apoptosis, have been reported in the literature. The abnormalities of synovial cell genes induce the production of some abnormal expression products, which inhibit the apoptosis of synovial cells and trigger the hemorrhage of synovial tissue; the hemorrhage leads to the deposition of iron-containing heme, and the excessive iron deposition produces lipid peroxidation, damages the lysosomal membrane, releases tissue oxidase, and eventually leads to cell death, tissue damage, inflammation and foam cells; the synovial cells are protected by the inhibition of apoptosis. In contrast, synovial cells are protected from iron deposition by the inhibition of apoptosis and exhibit tumor-like proliferation.
Overview
In addition, histological features such as proliferation of mononuclear macrophage-like cells, proliferation of fibroblasts, multinucleated giant cells and lipid-containing foam cells, and deposition are also present. Thus, hyperpigmented villous nodular synovitis is a macroscopic description of the end result of chronic synovitis and recurrent hemorrhage.
In 1852, Chassaignac first described a nodular lesion of the flexor tendons of the fingers. Subsequently, in 1865, Simon reported a case of limited lesion of the joint PVS, and in 1909, Moser depicted a diffuse lesion. During this period, authors considered the lesions to be neoplastic and there was confusion over the names of the lesions, with names such as synovial yellow tumor, yellow tumor-like giant cell tumor, giant peritendinous tumor of the tendon sheath, chronic hemorrhagic villous synovitis, and benign synovial pleomorphic tumor being used. It was not until 1941 that Jaffe et.al unified several previously isolated described lesions under the name PVS, a name that emphasized the proliferation of villi and nodules, the deposition of iron-containing hemoglobin, and favored an inflammatory etiology.
Granowitz et al then further divided the lesions into two types.
(i) diffuse type ;
(ii) the limited type.
Epidemiology
Pigmented villous nodular synovitis is most common in young adults between the ages of 20 and 40 years, and most lesions involve the subsynovial tissues of the large joints of the lower extremities, but rarely the upper extremities. The knee is the most commonly affected area, followed by the hip, ankle, and foot in that order. The histopathology of dysplastic villous nodular synovitis is similar to that of giant cell tumors of the tendon sheaths that occur in the hands and feet. Commonly, the synovial membrane is hypertrophic and the knee joint is swollen, with progressive swelling associated with intermittent joint hemorrhage.
Inflammatory synovium can lead to bone erosion in the proximal joint at the point of attachment of the joint capsule, which is also seen in other chronic proliferative synovitis, for example. Less than 10% of hyperpigmented villonodular synovitis is more limited and presents as a localized soft tissue mass in the suprapatellar capsule or N-fossa without diffuse swelling of the knee joint. At this point, the mass may resemble a soft tissue sarcoma such as that seen in older adults in their 50s, and MRI may confirm the diagnosis.
Pathogenesis
The etiology of PVS varies from one school of thought to another. In summary, there are four main types: (1) disorders of lipid metabolism; (2) trauma and bleeding; (3) inflammation; and (4) tumor.
Due to the observation of elevated intracellular lipid levels in PVS lesions and intracellular cholesterol concentrations in tissues, Hirohata suggested that local disorders of lipid metabolism are the etiology of PVS. He believed that foam cells were involved in the abnormal synthesis of cholesterol and phospholipids and were the primary causative cells; whereas inflammation was a secondary alteration to this abnormality and the hemorrhage was due to inflammatory vascular injury. However, Granowitz later found that alterations in lipids were associated with lesions in bone and that experiments with injected lipids could no longer produce PVS lesions.
In addition, there was no corresponding disturbance in serum triglyceride and cholesterol levels in PVS patients. Therefore, it is less likely that this theory is valid.
Research on trauma and bleeding leading to PVS has been extensive. Researchers have injected a variety of substances, such as blood and colloidal iron, into the synovial membranes of experimental animals. Although similar lesions have occurred, they have been relatively transient and not long lasting. Such similar lesions, which appear pigmented due to iron-containing heme, lack the typical gross morphology and cellular structure characteristic of PVS. Some authors have reported that injection of saline into the synovial membrane of dogs also produces this similar synovial lesion, suggesting that the response of the synovial membrane to hemorrhage is not specific. The relatively low incidence of PVS in patients with coagulation abnormalities and frequent bleeding has been reported to call into question the “bleeding etiology” theory from the opposite side.
Flandry et al. reported that only one third of 25 patients with knee PVS had a history of trauma, suggesting that the relationship between trauma and disease onset is ambiguous and that it is likely that trauma exacerbated the lesion and led to clinical symptoms, but that trauma was not the original cause. However, Myers identified a history of chronic repetitive trauma and repetitive bleeding in PVS patients based on demographic data and anatomical sites, thus supporting trauma as the pathogenesis of PVS.
Since 1941, inflammation has become the most widely accepted pathogenesis of PVS. Jaffe et al drew this conclusion from the histological observation that highly proliferative phagocytic stromal cells rich in collagen and vitreous degeneration most closely resemble the inflammatory process. Electron microscopic studies have revealed two types of proliferating monocytes: one rich in lysosomes with phagocytic function and the other rich in rough endoplasmic reticulum with collagen-synthesizing function.
These cells are morphologically similar to synovial layer type A and B cells. This finding supports Jaffe’s suggestion that PVS originates from “highly proliferating undifferentiated cells of the synovial membrane”. Since 1990, immunohistochemical studies of PVS lesions have been performed, reporting positive HAM56, CD68, and Vimentin in proliferating monocytes, and the use of CD68 and CD68 as macrophage markers. HAM56 were macrophage markers and concluded that the proliferating cells were monocyte-macrophage lineage.
In contrast, O’Connell et al. performed an immunohistochemical study of PVS and reactive synovitis cases against each other and found that CD68, HAM56, and Vimentin were positive in proliferating monocytes of PVS and their superficial synovial cells and reactive synovitis cells. The authors concluded that CD68 and HAM56 are non-specific macrophage markers because they also showed positivity in many non-vascular-derived cells, such as hepatocytes and renal tubular cells. In this way, having the same immune antigen type, O’Connell et al suggest that the proliferating monocytes are derived from synoviocytes, thus supporting the inflammatory etiology of PVS in terms of immunohistochemistry. Despite numerous studies on the etiology of inflammation, the causative agent and initiating mechanism leading to the inflammatory process had not been identified by the beginning of the 21st century.
The gradual re-acceptance of tumor as the etiology of PVS by many researchers, Rao and Vigorita concluded that PVS is a benign neoplastic process by carefully looking at the comprehensive histological material. They found that.
(i) proliferating cells located in the subsynovial layer are distinctly different from the cells in the synovial layer and enter the connecting tissue layer;
(ii) these areas contain a large number of synovial fibroblasts or primitive mesenchymal cells, which have the function of secreting collagen and transforming into histiocyte-like cells;
(iii) The mitotic activity was relatively increased in recurrent cases of PVS;
(iv) the degree of inflammation of the lesion was mild. Accordingly, they concluded that PVS is a tumorigenic proliferation of synovial fibroblasts and histiocytes.
Other authors who support a tumorigenic origin have proposed the idea of malignant PVS lesions. Malignant PVS lesions have been reported whether they occur in the tendon sheath or synovium. Some of these cases are primary and others are secondary to a PVS lesion that existed several years earlier (i.e., malignant in origin), and both primary and recurrent tumors show characteristic PVS on histological examination. Patients mostly die of pulmonary metastases. bertonietal reported 8 patients with malignant PVS and suggested that all histological features of malignant PVS are.
(i) lesions with a nodular isolated growth pattern ;
(ii) large, full round cells with eosinophilic deep staining of the cytoplasm;
(iii) large nuclei with distinct nucleoli;
(iv) necrotic areas. These investigators have suggested the presence of malignant PVS, and others have suggested that PVS includes different lesions: one part is inflammatory and the other is neoplastic.
In addition, from the perspective of cytogenetic studies, some authors have found chromosomal abnormalities in PVS lesion cells, with chromosome 7 and chromosome 5 being more frequently reported. Although the presence of chromosomal trisomes does not definitely classify a lesion as a neoplasm, the presence of certain oncogenes on the chromosome and the overexpression of collagen-promoting growth factors may provide a reasonable explanation for proliferative lesions.Choongetal reported a case of recurrent PVS in which a subcutaneous metastatic nodule was found on the contralateral thigh and was histologically confirmed as a PVS nodule. The findings in this case supported the tumor origin of the lesion from a clinical point of view.
Pathology
Microscopic pathology of pigmented villous nodular synovitis
The gross pathological presentation of the two types of PVS lesions is markedly different. In diffuse lesions, villi and nodules involving the entire synovial membrane, the lesions are yellow, brown, and reddish-brown in color. There are two types of villi, one long and slender, intertwined, and the other relatively short, with bulbous, rough ends, resulting in a “mossy” surface. The nodules vary in size and can be isolated or in patches. The nodules have a short base, and the nodules and villi are mixed with each other. Most of the limited lesions are solitary nodules, ranging from a few mm to several cm in diameter as a brownish-red or reddish-brown tough mass with no abnormal changes in the surrounding synovial membrane or a yellowish color with pigmentation.
The light microscopic structure was the same for all lesion types. Microscopically, the villi consisted of reticular tissue, collagen matrix, and various cell types. The most superficial layer is composed of several layers of hyperplastic and hypertrophic synovial cells with iron-containing haematoxylin deposits. The subsynovial tissue is rich in capillaries and has a large number of large round, prismatic mononuclear cells proliferating in a nodular pattern. These cells are the most characteristic cells of PVS lesions. They are rich in cytoplasm and contain large amounts of iron-containing heme, with ovoid nuclei and light staining.
These proliferating nodules are surrounded by lipid-engulfing foam cells, multinucleated giant cells, scattered or focal aggregates, extracellular iron-containing heme deposits, paravalvular lymphocytes, plasma cell infiltration, and cystic collagen fibers.
Electron microscopic studies have revealed two sources of proliferating mononuclear cells. One is rich in macrophage-like cells with active lysosomal phagocytosis and is derived from synovial A cells, while the other is rich in rough endoplasmic reticulum and is derived from synovial B cells. Foam cells are formed by phagocytosis of lipids by A or B cells; giant cells are formed by fusion of A cells. The transformation of multinucleated giant cells from monocytes has been confirmed by the latest immunohistochemical aspects.
The mechanisms of PVS lesion erosion of cartilage and bone are variously described. McMaster suggests that the proliferating lesion expands tongue-like, directly erodes the articular cartilage and penetrates the cortical bone, and then produces a cystic lesion in the softer cancellous bone. This account emphasizes the neoplastic erosive character of PVS, while Chung and Janes suggest that the highly hyperplastic synovium causes increased pressure within the joint cavity, leading to localized osteoporosis. In subchondral bone cystic degeneration, the hyperplastic synovium will further invade the cancellous bone when the capsule wall is fractured.
Bone erosion in PVS is more common in the hip joint because of the narrow hip joint space, which does not have much room to accommodate the proliferating synovial membrane, resulting in a rapid increase in internal pressure. Intraoperative findings of significantly elevated pressure in the hip capsule of PVS patients have been made, and Scott has suggested that the lesions enter the bone through dilated vascular trophoblastic foramina. It is possible that bone erosion in PVS is caused by a combination of these pathways. The role of metalloproteinases in the destruction of cartilage and bone has also been suggested. It has been shown that PVS synovial layer cells can secrete two metalloproteinases as mediators of joint destruction, but the stimulating factors for enzyme production are not known.
Clinical manifestations and laboratory tests
Diffuse PVS occurs in adults aged 30-40 years, mostly in single joints, with no significant differences between men and women. It can also occur in children and is a very rare lesion characterized by polyarticular involvement, often with congenital anomalies and a family history. The focus here is on adult lesions. The knee is the most susceptible joint, followed by the hip, ankle, and shoulder joints. Other rare joints, such as the temporomandibular joint and small joints of the spine, have also been reported.PVS has an insidious onset, a long course, and a progressive development of symptoms. The most common knee symptom is swelling of one joint and progressively increasing painful discomfort and stiffness. Patients may or may not have a history of trauma. When the lesion involves cartilage and bone, symptoms such as painful walking up and down stairs, semi-squatting pain, ringing sounds in the joint during extension and flexion, and interlocking may occur. These symptoms of bone and cartilage lesions are not characteristic, but instead often confuse the diagnosis.
”Rao and Vigorita reported that about 50% of patients have localized pressure pain, sometimes synovial masses or nodules can be felt, and there may be a decrease in the range of motion of the joint. Laboratory tests, including serum cholesterol measurements, do not show any abnormalities. Dark red or brown bloody joint fluid extracted by arthrocentesis may reveal the disease, but it is not specific, and in some patients the joint fluid may be yellow-green, so the joint fluid examination should be combined with clinical examination. Some authors have suggested that arthrocentesis should not be used as a diagnostic method for PVS because of its low specificity and risk of infection. Laboratory analysis of synovial fluid is also not specific and is therefore not used as a diagnostic tool.
Limited PVS lesions can occur in both the tendon sheath and the joint, with the former being more prevalent than the latter. Restricted PVS lesions located in the tendon sheath differ from the diffuse type in the joints in several ways: (1) lesions in the tendon tend to occur in elderly patients, commonly aged 50-60 years; (2) tendon sheath PVS is most often seen in female patients; and (3) tendon sheath lesions are usually painless and present as progressively larger masses, involving the joints in the restricted type of lesions. It most commonly occurs in the knee, but has also been reported in the shoulder, ankle, wrist, and hip joints. Clinical symptoms are intermittent mild swelling and pain. The nodules are tough and may have a free body sensation. When the nodules are embedded in the bony ends of both joints, interlocking or limited extension may occur.
Arthroscopic presentation of pigmented villous nodular synovitis
PVS lesions most commonly appear on radiographs as swollen soft tissues with increased density due to iron-containing hemosiderin deposits, but without calcification. Sometimes nodular and lobulated masses within the joint capsule are seen. When the lesion involves cartilage and bone, there may be marginal jagged bone destruction and areas of cystic bone defects of varying sizes. When secondary to osteoarthritis, there is joint space narrowing, uneven joint surfaces, and intra-articular free bodies.
Arthrography provides a clearer picture of the intra-articular capsule changes. This may appear as an enlarged joint capsule with lobulated synovial tissue or multiple nodular shadows protruding into the joint capsule with wavy edges.
In addition, high-frequency ultrasound is a valuable imaging method for routine preoperative screening of PVS.
Since the 1990s, many articles have reported the use of magnetic resonance imaging (MRI) as a diagnostic tool for PVS. Kottaletal was the first to describe the characteristic presentation of PVS lesions on MRI: a hypointense signal area on T1- and T2-weighted images, which was thought to be associated with the deposition of iron-containing heme and lipids in the lesioned tissue. Subsequent studies have further confirmed this point. Whether the lesion is diffuse or confined, the MRI presentation corresponds to its corresponding pathological component.
On T1-weighted images, there are scattered areas of hypointense signal that resemble muscle density, representing iron-containing heme deposits in the hypertrophic synovium, while on T2-weighted images, there is even less density and signs such as joint effusion or joint space reduction may be present. Because of its characteristic presentation, MRI has been used as the most sensitive method for early diagnosis of PVS and is also helpful in pre-treatment evaluation.
The value of MRI in the diagnosis of PVS of the knee
The main manifestation of knee PVS on X-ray is joint swelling without calcification, and round-like erosive defects can be seen when the joint bone destruction is severe, but the imaging changes themselves lack specificity for a definite diagnosis. MRI has qualitative diagnostic significance for PVS of the knee, as it can clearly show the extent of the lesion, the degree of articular cartilage and bone destruction, and its characteristic performance is the low-density signal area on T1- and T2-weighted images.
Therefore, MRI has become the imaging method of choice after X-ray examination. Preoperative MRI examination not only helps to clarify the extent and scope of intra- and extra-articular lesions, but also, postoperative MRI examination is the most sensitive means to check the recurrence of lesions.
1.2 Differential diagnosis
1.2.1 Chronic synovitis Chronic synovitis has significant congestion, hypertrophy of villi, and infiltration of inflammatory cells without significant iron-containing heme deposits and granulomatous lesions formed by histiocyte proliferation.
1.2.2 Rheumatoid arthritis Rheumatoid arthritis is also common in which the synovium is villi-like in structure, but there is not much ischemic flavin deposition in the synovium, but characteristic lymphoid follicle formation and plasma cell infiltration, and the cellular components are not as diverse as in this disease, combined with clinical manifestations, multiple small joint lesions, and accelerated blood sedimentation.
1.2.3 Limited nodular synovitis also often involves the knee joint, and the microscopic findings are similar to this disease, but the synovial lesions are limited and isolated, with little iron-containing heme deposition, no recurrence of local excision, and no infiltration of bone.
1.2.4 Differentiation of synovial sarcoma from pigmented villous nodular synovitis.
① The cells of this disease are abundant and occasional nuclear division is seen, but the cellular components are more numerous and there are no malignant features such as deep staining of the nucleus, heterotypy and pathological nuclear division signs, whereas synovial sarcoma is dominated by rhombocytes and has malignant features.
②Some lacunae or small cystic cavities can be seen in this disease, but there is no pseudoepithelial structure of synovial sarcoma.
(3) The disease has obvious iron-containing heme deposits and choroidal nodular structures, whereas synovial sarcoma does not have this feature.
Differentiation
PVNS needs to be differentiated from the following diseases: gout, a group of diseases caused by increased tissue damage due to disorders of purine metabolism resulting in increased blood uric acid, with red, swollen, hot, painful joints, restricted movement, accompanied by fever, chills, fatigue, anorexia, headache, etc. Gout stones can be formed, and can be differentiated by X-ray and blood tests; ‘rheumatoid arthritis, which also starts in the synovium. The swelling, effusion, and muscle atrophy can be seen, but it is often a multi-joint disease, and the blood sedimentation, rheumatoid factor, and blood picture can be changed, while the pigmented villous nodular synovitis is mostly seen in a single joint, and there is no change in the above laboratory tests, and the fluid extracted by joint puncture can be distinguished; synovial tuberculosis, which also has features such as swelling, effusion, and chronic process, can be easily distinguished by X-ray and joint puncture.
When treating PVNS arthroscopically, careful intraoperative examination is required to find the typical area of synovium for pathological examination first, then follow the sequence of intercondylar fossa – medial space – medial crypt – suprapatellar capsule – lateral crypt – lateral space -The synovial membrane should be shaved in the order of the posterior joint cavity, and the parts that are easily missed, such as the upper part of the posterior femoral condyle and the underside of the meniscus, should be cleared with attention and, if necessary, with forceps, for clean excision, and electrocautery can be given to prevent bleeding.
Although postoperative radiotherapy can reduce the recurrence rate, radiotherapy may cause stiffness of the joint, slow wound growth and healing, especially in young people, there is a chance of sarcoma [8], we believe that thorough removal of the diseased synovium can achieve good results. Postoperative rehabilitation is important, and early rehabilitation can lead to fast recovery of joint swelling, mobility and muscle strength.
Arthroscopic surgery is one of the effective treatment methods for PVNS. Arthroscopic treatment is as effective as incisional surgery, and arthroscopic subsurface resection is more effective than incisional surgery. There are many complications after incisional surgery, such as pain, joint swelling, and difficulty in flexion, and the surgical requirements for incisional synovial removal are high. Arthroscopic treatment can completely remove the synovial membrane in locations that cannot be reached by incisional surgery, and there is little damage, low recurrence rate and good functional recovery. Nodular PVNS has a very good follow-up prevention effect, and arthroscopic surgical treatment can be the first choice. Thorough removal of the diseased synovium is the key during surgery, and postoperative radiotherapy is not possible. Early postoperative rehabilitation is important for joint swelling and pain to subside and function to recover.
Synovial nodular pigmentation needs to be differentiated from joint diseases that can lead to joint swelling, joint effusion, and joint bone destruction. The soft tissue swelling in pigmented villous nodular synovitis is dense and nodular and predominantly intra-articular, with no osteoporosis, sclerotic edges of bone defects, and the joint space remains normal to help differentiate from joint tuberculosis, synovitis, synovial sarcoma, and RA. Calcification is mostly seen in tuberculosis and synovial sarcoma, but pigmented villonodular synovitis should not be completely excluded, and calcification should be analyzed in a comprehensive manner among all signs so as to reduce misdiagnosis.
(1) Charcot’s joint: early all appear to have joint swelling, effusion, painless, etc., but most have a history of trauma and more serious joint deformity. x-ray seen new bone formation, bone end disintegration, joint surface destruction, joint dislocation and other bone and joint damage is extremely inconsistent with clinical symptoms.
Synovial sarcoma: both have soft tissue masses, calcification, and bone destruction, but synovial sarcoma has a rapid development, short course, severe pain, and dissolving bone destruction without sclerotic margins.
(iii) Synovial tuberculosis: both have periarticular tissue swelling, joint surface destruction, and early widening and late narrowing of the joint space. The difference is that the tuberculosis has obvious osteoporosis, joint surface destruction involving both sides, no sclerotic edges, and no mass shadow in the soft tissue.
Rheumatoid arthritis monoarticular type: Mostly seen in elbow, wrist, knee, finger joints, joint swelling, soft tissue thickening, pain is not very obvious. Osteomalacia, narrowing of the joint space or even worm-like destruction appear earlier. The joint is punctured with clear fluid.
Complete removal of the diseased synovial tissue is the key to the treatment of PVS.
Since PVS lesions occurring at different anatomical sites respond differently to treatment, here we will only describe the knee joint as an example. The treatment and prognosis of diffuse and limited lesions are very different, with the latter having a more definitive treatment and a good prognosis, while the former has a variety of treatment options and a high recurrence rate.
Rao and Vigorita reported 8 patients with LPVS of the knee and only 1 recurrence at 6 years after 5-10 years of follow-up. Similar results have been reported by Johansson. In recent years, with the development of arthroscopic techniques, local excision of the lesion via arthroscopy for limited PVS has been reported, and the advantages of satisfactory efficacy, less trauma, fewer complications, and shorter recovery time are fully reflected in the excision of limited lesions and relatively simple operation. Therefore, it should be the preferred treatment method.
Treatment
There are many ways to treat diffuse PVS lesions. Subtotal synovectomy, radiation therapy, surgery plus radiation therapy, arthrodesis, arthroplasty, etc. have been used. Total synovectomy is currently advocated. It has been reported that in 20 cases of diffuse PVS lesions in the knee, 11 total synovectomies and 9 partial synovectomies were performed, and after 4.5 years of follow-up, it was statistically confirmed that the recurrence rate and time to recurrence were lower in the former than in the latter.
However, neither open surgery nor transarthroscopic total synovectomy could completely cure the diffuse lesion. The range of recurrence rates reported in the literature is 8-50%, with a mean of 31.3%. Some authors attribute recurrence to the operational difficulty of performing an absolute total synovectomy with residual diseased tissue, but others believe that this is indicative of the oncologic nature of PVS.
Monoradiotherapy was reported as early as 1941. Researchers believe that the effectiveness of radiation therapy is related to the appropriate stage of the disease. MacMaster noted that the potential disadvantages of radiation therapy were stiffness of the joints and slow healing of wounds and bone graft growth.
In particular, there is a risk of sarcoma in young people, and subtotal synovectomy supplemented with radiation therapy can reduce complications and recurrence rates. From the 1960s to the present, the Institute of Sports Medicine at Beijing Medical University reported more than 30 cases of diffuse lesions treated with 4-5 weeks of radiotherapy after major synovectomy and silicone rubber membrane placement, all with satisfactory results and no recurrence.
Arthroplasty or arthroplasty has been used sparingly, and Rao and Vigorita have reported a case in which total knee arthroplasty was used as initial treatment. Because of the cruelty of this procedure, most patients are reluctant to use it as their first choice of treatment, limiting it to those cases where knee function cannot be preserved and where there are multiple recurrences.
Radiological synovectomy, in which radioactive yttrium gel 90 is injected into the joint to treat PVS lesions, has been used by Wiss to successfully treat a recurrent patient. It has the advantages of simple technique, short hospital stay, low cost and few complications. wiss concluded that the possible complications are chromosomal mutation, malignancy, needle tract necrosis and fever and pain reactions.
Postoperative braking, cautious use of this method in the elderly, saline flushing after injection, and administration of antipyretic and analgesic drugs are measures that can reduce complications. Chen DY et al. have since reported a case of intra-articular radiosynovectomy in a patient with relief of diseased knee symptoms at follow-up. This approach awaits further clinical studies.
Pigmented villous nodular synovitis is a highly proliferative disease involving the joints and synovial and tendon sheaths throughout the body. There is much controversy regarding the study of its etiology. The two most circulating theories are a chronic inflammatory response and a fibroblastic neoplastic lesion. Both theories are supported by histological, electron microscopic, or clinical evidence, but neither is complete enough to suggest an initiating stimulus for inflammatory or neoplastic lesions and to describe their specific pathogenesis.
Diagnostically, it presents with swelling of the joint or tendon sheath and progressive pain and discomfort. When the joints are involved, the knees and hips are more likely to be involved; when the tendon sheaths are involved, the ends of the hands and feet are more likely to be involved. The characteristic T1- and T2-weighted low-density signal areas are considered to be the most sensitive diagnostic method for PVS.
Focal or diffuse PVS lesions, although histopathologically consistent, respond very differently to treatment. Focal lesions can be treated satisfactorily with simple focal resection, and arthroscopic completion of this procedure should be the first method of treatment for the focal type. The diffuse type has many controversial methods of treatment, and none of them can be completely cured, with an average recurrence rate of 31.3%. The more popular treatment is total synovectomy. When there are new advances in the study of PVS etiology, its treatment will be improved accordingly, so PVS etiology and its pathogenesis should be a key area of investigation.