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60=6�2T;�(f;D3;�D3D�* # # #�5�5d*j # # #=6 # # # #����hd���h���@@@@@@����Pigmented Villonodular Synovitis of the Temporomandibular Joint: A Case Report and Literature Review

Zain H. Rizvi1, Mahdi A. Shkoukani, MD1,3, Senja Tomovic2, Kailash Narasimhan, MD1, Lewis Clayman, MD, DMD1*, Robert H. Mathog, MD1

1Department of Otolaryngology-Head and Neck Surgery, Wayne State University, Detroit, MI
2Department of Surgery, Division of Otolaryngology � Head and Neck Surgery, University of Medicine and Dentistry of New Jersey, Newark, NJ 
* Just retired

3To whom all correspondence should be addressed at:
4201 St. Antoine, 5E University Health Center John R,
Detroit, MI 48201
Phone: 313-577-0804
Fax: 313-577-8555
Email:  HYPERLINK "mailto:mshkouka@med.wayne.edu" mshkouka@med.wayne.edu



Financial Support: None




Abstract

Pigmented villonodular synovitis (PVNS) is a benign proliferation of tissues within a joint.  It most frequently affects large joints but rarely involves the temporomandibular joint (TMJ). Radical excision with wide margins is the recommended treatment. PVNS is resistant to radiotherapy. Herein we report a case involving the TMJ causing pain and trismus and its management that appears to be successful. Superficial parotidectomy was done to identify and protect facial nerve branches during tumor resection. Intraoperatively, the tumor was destroying the condyle, invading into the meniscus, and extending to the masseter and pterygoid muscles as well as skull base. Following radical excision with wide margins, the patient experienced right-sided facial paralysis postoperatively but had eventual recovery of facial nerve function.

Key words: pigmented villonodular synovitis, PVNS, temporomandibular joint, TMJ, facial nerve, facial paresis, parotidectomy





Introduction
Pigmented villonodular synovitis (PVNS) is a benign proliferation of synovial tissue [1]. It can be either local or diffuse, depending on the extent of involvement of the joint space, bursae and tendon sheath. It occurs most commonly in the knees, hips, and wrist joints of middle-aged people. However occurrence of PVNS in the temporomandibular joint is extremely rare, with less than 30 cases reported to date in the English literature [2,3]. 
Patients with PVNS of the TMJ most often present with a preauricular mass that is often misdiagnosed pre-operatively as a parotid tumor. Some patients may also experience localized pain and trismus. The differential diagnosis of this entity is extensive. A combination of fine needle aspiration biopsy (FNA) and imaging with computerized tomography (CT) and magnetic resonance imaging (MRI) are recommended to establish the diagnosis. Definitive treatment is wide local excision. 
Case Report
A 74-year-old female presented to the university clinic complaining of a right pre-auricular mass that she had noticed for a few months. She admitted that the mass was painful and had been enlarging in the few weeks prior to her first visit. This mass was preventing her from opening her mouth widely and taking big bites. On physical examination, she was noted to have 2.0 X 3.0 cm firm mass in the right pre-auricular area that was tender to palpation. Her maximal interincisal opening (MIO) was about 10 mm with deviation to the right about 5 mm at MIO. There was no facial paresis.
	The CT-neck with IV contrast (Figure 1) showed an enhancing mass surrounding the right mandibular condyle, with expansion of the TMJ space with slight anterior subluxation of the condyle. There were subcortical erosions within the mandibular condyle and mandibular ramus.  The adjacent bone appeared thickened and sclerotic.
 The MRI-neck with gadolinium (Figure 2) showed a 3.6 x 2.3 x 2.1 cm well defined mass with T1/T2 hypointense signal in the right TMJ region with subtle postcontrast enhancement. It also showed fine erosions of the mandibular condyle. At this point, the differential diagnosis included PVNS, arthritides (Calcium Pyrophosphade Dehydrate or gout), synovial chondromatosis, sarcoma, chronic osteomyelitis and metastasis from a distant site. A CT-guided fine needle aspiration (FNA) was performed showing moderate cellularity and loosely cohesive groups of oval to spindle cells with bland nuclei, prominent nucleoli, and intracytoplasmic hemosiderin pigmentation, consistent with histiocytes. Numerous multinucleated giant cells with similar nuclear features were also present. These histologic features strongly favored a diagnosis of PVNS.
After obtaining informed consent, the following procedures were performed: Tracheostomy, superficial parotidectomy, condylectomy and menisectomy. The tracheostomy was done to protect the airway post-operatively. The superficial parotidectomy was performed to identify the facial nerve branches and protect them during the resection of the tumor. Intraoperatively, the tumor was destroying the condyle and invading the meniscus with extension to the masseter muscle, medial pterygoid muscle, lateral pterygoid muscle and extending medially to the skull base and sphenoid spine. The final pathology report (Figure 3) showed an infiltrate of dense mononuclear cells that was associated with hemosiderosis, multinucleate giant cells, and fibrosis. The abnormal tissue replaced joint capsule, adjacent connective tissue and skeletal muscle, and it occupied the marrow space. This was consistent with a final diagnosis of PVNS.
Postoperatively, the patient had a complete right facial paralysis. To address incomplete right eye closure, she underwent a gold weight placement and lateral canthoplasty. After several months, however, movement did return in the right face with eye closure and mouth opening markedly improved. There was no evidence of recurrent tumor and the patient no longer had pain or trismus. A maxillofacial prosthesis with a guide plane was later used to improve her post-resection jaw deviation. 
 Discussion
PVNS is a benign proliferation of tissues within a joint. It most frequently affects large joints such as the knees, hips and hands. Jaffe et al [1] had been credited with coining the term pigmented villonodular synovitis in 1941, though it had been originally described by Chassiagnac in 1852 [4]. More than a century after the first description of PVNS, Lapayowker et al [5] reported the first case of PVNS in the TMJ in 1973. 
Jaffe et al [1] proposed that PVNS was a chronic inflammatory process. Since then, several theories have been set forth, including the other widely accepted theory that this is a benign neoplasm owing to evidence of cellular monoclonality and chromosomal abnormalities [6]. There are also a few reported cases of metastatic disease implying a malignant potential [7]. Other more controversial theories describe it as a lipid metabolism disturbance, or a reaction to blood products [3]. 
Grossly, the lesion appears dark to yellow-brown in color, with a nodular and villous texture. Histologically the mass contains finger-like projections that consist of multinucleated giant cells, histiocytes and hemosiderin concentrated in stromal cells. The mononuclear histiocytes show positive immunoreactivity for CD68 and are negative for S-100, thus differentiating it from chondroblastoma cells, which are positive for S-100 [8]. Immunophenotypic staining has also suggested the cells are of synovial origin [9].    
The most prevalent symptom of PVNS of the TMJ is a preauricular mass. Pain and discomfort of the jaw and trismus can also occur. Less commonly patients may present with hearing loss or tinnitus. The differential diagnosis for a preauricular mass includes a parotid tumor, gout or pseudogout of the TMJ, cutaneous metastases, or a cyst. 
In addition to a FNAB, imaging is a key component of the diagnostic work-up. CT will often show bony erosions, and cyst formation. The concentrated hemosiderin in the lesions lends PVNS to evaluation by MRI as well, though the results can be more variable. The hemosiderin dense parts will have low signal intensity on both T1 and T2 weighted images, while the cystic and eroded areas will have high signal intensity on T2 images. 
Conventional treatment for PVNS is radical excision with wide margins. The local recurrence rate has been reported to be about 9% [3]. There has only been one reported case of malignant PVNS of the TMJ with metastasis [7]. A few select cases were successfully treated with radiation therapy, none of which occurred at the TMJ. The most common complication after surgical treatment is facial paralysis, which resolves in most cases. In our case we chose to perform a superficial parotidectomy to expose and protect the facial nerve during TMJ resection, nevertheless our patient still initially suffered a complete paralysis, which resolved during subsequent follow-up visits.
Conclusion
Although more common in other joints, PVNS is a rare entity in the TMJ. Pre-auricular mass, pain, and trismus are common presenting symptoms. Diagnostic workup of this lesion includes fine needle biopsy and CT scan of the neck. Resection with wide margins remains the standard treatment. The facial nerve is at risk because of its proximity to the tumor, and while paralysis is a common complication, adequate exposure and judicious handling of tissues will provide a higher chance of return of function. 















References

Jaffe HL, Lichtenstien L, Sutro CJ (1941) Pigmented villonodular synovitis, bursitis and tenosynovitis. Arch Pathol 31:731-765.

Tosun F, Carrau RL, Weissman J (2005) Pigmented villonodular synovitis of the temporomandibular joint: an extensive case with skull-base involvement. Am J Otolar 25:204-7.
	http://www.ncbi.nlm.nih.gov/pubmed/15124172

Lee JH, Kim YY, Seo BM, Baek SH, Choi JY, Choung PH, Kim MJ (2000) Extra-articular pigmented villonodular synovitis of the temporomandibular joint: case report and review of the literature. Int J Oral Maxillofac Surg 29:408-15.
	http://www.ncbi.nlm.nih.gov/pubmed/11202319�

Chassaignac M (1852) Cancer de la gaine des tendons. Gazette des H�pitaux Civils et Militaires 47:185-186.

Lapayowker MS, Miller WT, Levy WM, Harwick RD (1973) PVNS of temporomandibular joint. Radiology 108:313-6. 
	http://www.ncbi.nlm.nih.gov/pubmed/4719033

Choong PF, Willen H, Nilbert M, Mertens F, Mandahl N, Carlen B, Rydholm A (1995) Pigmented villonodular synovitis. Monoclonality and metastasis � a case for neoplastic origin? Acta Orthop Scand 66:64-8.
	http://www.ncbi.nlm.nih.gov/pubmed/7863772

Bertoni F, Unni KK, Beabout JW, Sim FH (1997) Malignant giant cell tumor of the tendon sheaths and joints (malignant pigmented villonodular synovitis). Am J Surg Pathol 21:153-63. 
	http://www.ncbi.nlm.nih.gov/pubmed/9042281�

Kilpatrick SE, Parisien M, Bridge JA (2002) World Health Organization Classification of Tumours: Pathology and Geneteics of Tumours of Soft Tissue and Bone. International Agency for Research on Cancer Press: Lyon, France.

O�Connel JX, Fanburg JC, Rosenberg AE (1995) Giant cell tumor of tendon sheath and pigmented villonodular synovitis; immunophenotype suggests a synovial cell origin.  Hum Pathol 26:771-5.
	http://www.ncbi.nlm.nih.gov/pubmed/7628850














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