Tenosynovial Giant Cell Tumors of the Temporomandibular Joint and Lateral Skull Base: Review of 11 Cases

Transcription

1 The Laryngoscope VC 2016 The American Laryngological, Rhinological and Otological Society, Inc. Tenosynovial Giant Cell Tumors of the Temporomandibular Joint and Lateral Skull Base: Review of 11 Cases Matthew L. Carlson, MD; L. Mariel Osetinsky, MD; Eran E. Alon, MD; Carrie Y. Inwards, MD; John I. Lane, MD; Eric J. Moore, MD Objectives: To elucidate the clinical behavior, treatment, and outcomes of tenosynovial giant cell tumors (TGCT) involving the temporomandibular joint (TMJ) and adjacent temporal bone. Study Design: Retrospective case series with histopathologic review. Methods: A retrospective chart review was performed identifying and collecting data from all cases of TGCT involving the TMJ and adjacent temporal bone that were treated at the authors center between January 1960 and December Results: Eleven histopathologically confirmed cases met inclusion criteria. The median age at diagnosis was 49 years, eight patients were men, and the median follow-up was 116 months. Computed tomographic (CT) imaging revealed a lytic expansile mass centered on the TMJ. Magnetic resonance imaging (MRI) most commonly exhibited hypointense signal on precontrast T1- and T2-weighted sequences and variable postcontrast enhancement. The median delay in diagnosis was 24 months, and the most common presenting symptoms were hearing loss and pain. All patients underwent surgical resection, eight receiving gross total removal, one receiving near total removal, and two patients from early in the series receiving subtotal resection with neoadjuvant or adjuvant radiation. Histopathological review of surgical specimens revealed chondroid metaplasia in seven tumors. Eight of nine cases receiving gross total or near total resection have no evidence of recurrence to date. Conclusions: TGCT of the TMJ and temporal bone are rare and locally aggressive tumors that commonly present with nonspecific symptoms. A careful review of CT and MRI followed by early biopsy is critical in establishing an accurate diagnosis and facilitating appropriate treatment. TGCT of the TMJ more commonly contain chondroid metaplasia when compared to TGCT at other anatomic locations. Gross total resection is achievable in most cases and offers long-term cure. Radiation may be considered for recurrent disease or adjuvant therapy following subtotal resection. Key Words: Tenosynovial giant cell tumor, chondroblastoma, pigmented villonodular synovitis, temporomandibular joint, lateral skull base, temporal bone, mandible. Level of Evidence: 4. Laryngoscope, 127: , 2017 INTRODUCTION Tenosynovial giant cell tumors (TGCT) represent an enigmatic family of tumors that arise from the synovial membrane of joints, tendon sheaths, and bursae. 1 5 Broadly, TGCT are classified according to anatomical site of involvement (intra-articular and extra-articular) and growth pattern, including localized and diffuse forms of disease. The localized form of TGCT is most prevalent and generally follows an indolent course, frequently affecting the tendon sheath and joints of the hands. In contrast, diffuse-type TGCT are less common and typically affect the knee, hip, or shoulder. Only rare From the Department of Otorhinolaryngology (M.L.C., L.M.O., E.E.A., E.J.M.) and Radiology (C.Y.I., J.I.L.), Mayo Clinic School of Medicine, Rochester, Minnesota, U.S.A.; and Department of Otolaryngology Head and Neck Surgery, Sheba Medical Center at Tel Hashomer, Tel Aviv, Israel (E.E.A.). Editor s Note: This Manuscript was accepted for publication October 31, The authors have no funding, financial relationships, or conflicts of interest to disclose. Send correspondence to Matthew L Carlson, MD, Department of Otorhinolaryngology, Mayo Clinic, 200 First St. SW, Rochester, MN carlson.matthew@mayo.edu DOI: /lary examples have been reported in other sites such as the temporomandibular joint (TMJ) and spinal facet joints. Although histologically benign and usually monoarticular, the diffuse form of disease is characterized by locally aggressive growth and a higher propensity for recurrence following surgery. Defining the clinical behavior and optimal treatment of TGCT of the skull base is challenged by the rare incidence of disease, variable nomenclature in the literature, and the presence of several conditions with overlapping clinical, radiological, and histological features. 3,6 Compared to other anatomic sites, TGCT of the TMJ uniquely exhibit a tendency for chondroid metaplasia, thus mimicking other chondroid neoplasms, particularly chondroblastoma. To date, less than 60 cases of TGCT involving the TMJ have been published in the English literature, and only 10 recent cases have described the presence of chondroid metaplasia. 3 7 Accordingly, the objectives of the current study are to describe the clinical, radiological, and histopathological features of 11 cases evaluated between 1960 and 2015 at a single tertiary academic referral center, and to raise awareness in the otolaryngology and neurotology literature regarding the unique histopathological features of TGCT of the TMJ and temporal bone. 2340

2 TABLE I. Baseline Demographics and Presenting Symptoms of 11 Patients With Tenosynovial Giant Cell Tumors of the Temporomandibular Joint and Temporal Bone. No. Age Sex Side Duration of Symptoms, mo Primary Symptom(s) Hearing Loss Pure Tone Audiometry, db Word Recognition Score, % 1 43 F R 24 TMJ swelling, pain None NA 2 40 M R NR Hearing loss CHL 17 BC PTA, 53 AC PTA, 35 ABG M L 24 Aural fullness CHL 20 BC PTA, 52 AC PTA, 32 ABG M L 3 Hearing loss, pain, MHL 45 BC PTA, 75 AC PTA, 30 ABG 72 aural fullness 5 57 M L 12 Hearing loss, tinnitus, CHL 20 BC PTA, 43 AC PTA, 23 ABG 76 aural fullness 6 31 M R 15 TMJ swelling, pain None NA NA 7 42 F R 0 (incidental) Incidental None NA NA 8 49 M L 24 Trismus, pain None NA M R 24 Hearing loss, aural MHL 45 BC PTA, 72 AC PTA, 27 ABG 60 fullness, otorrhea M R 36 Hearing loss, otorrhea CHL 13 BC PTA, 40 AC PTA, 27 ABG F R 15 Jaw pain, otalgia None NA NA ABG 5 air bone gap; AC 5 air conduction; BC 5 bone conduction; CHL 5 conductive hearing loss; F 5 female; L 5 left; M 5 male; MHL 5 mixed hearing loss; NA 5 not applicable; NR 5 not recorded; PTA 5 pure tone average (0.5, 1, 2, 3 khz average); R 5 right; TMJ 5 temporomandibular joint. MATERIALS AND METHODS Following institutional review board approval (IRB ), a retrospective chart review was performed to identify all cases of TGCT involving the TMJ and adjacent temporal bone that were treated at the authors center between January 1960 and December Given overlapping histological features and variation in terminology over time, all surgical pathology reports with a diagnosis of tenosynovial giant cell tumor, giant cell tumor, pigmented villonodular synovitis, chondroblastoma, and chondrosarcoma were identified. In each case, histologic sections were reviewed by a senior musculoskeletal pathologist (C.Y.I.). All cases with histological evidence of alternate diagnoses, equivocal findings, or insufficient material were excluded. All confirmed cases of TGCT of the TMJ and temporal bone were reviewed, and the following variables were collected and presented in tabular form: baseline demographics, including age at diagnosis, and sex; presenting signs and symptoms; radiological features and extent of disease; results of audiometric testing; management strategy, including surgical approach, extent of resection, and use of adjuvant therapy; complications from treatment; recurrence; details regarding salvage therapy; and length of follow-up. Descriptive statistics were utilized, including the median and range, or frequency count and percentage. RESULTS Demographics and Presentation A total of 11 patients with TGCT of the TMJ and temporal bone underwent treatment at the authors center between 1960 and 2015 and met study criteria. Histologically, nine of the 11 tumors were originally diagnosed as chondroblastoma and subsequently reclassified as TGCT. The remaining two tumors were classified as TGCT at initial diagnosis. Four additional patients were excluded from the study for the following reasons: two cases did not have archived tissue slides available for review, in one case the histopathological findings were atypical and indeterminate, and in one case the patient was referred following treatment elsewhere and did not receive primary treatment at the authors center. Of the 11 included cases, the median age at diagnosis was 49 years (range years), eight were men, and seven were right-sided. The most common presenting symptoms were hearing loss (n 5 5; 45%), pain (n 5 5; 45%), and aural fullness or pressure (n 5 4; 36%). None of the patients presented with facial nerve paresis. The median delay between symptom onset and diagnosis was 24 months (range months). Details regarding baseline demographic data, disease presentation, and type and severity of hearing loss are further outlined in Table I. Extent of Disease and Radiological Features In all cases, the lesion was centered on the TMJ and glenoid fossa and did not extend medial to the petrous carotid, foramen spinosum, or foramen ovale. Two common patterns of growth were observed: 1) anterior and medial spread from the glenoid fossa, involving the zygomatic and squamosal portions of the temporal bone, the infratemporal fossa, and the greater wing of the sphenoid; and 2) circumferential growth from the glenoid fossa, involving the aforementioned regions, but additionally including the external auditory canal, middle ear, and often the mastoid. In all cases, the mandibular condyle was partially displaced by the lesion; however, the condyle was only grossly involved in two cases. Tumor routinely exhibited intracranial extension abutting the temporal lobe dura, but dural transgression was only seen in one case. The otic capsule appeared resistant to bony invasion in most cases; however, labyrinthine fistulas were present in two cases with extensive disease. The most common location of facial nerve involvement was the region of the geniculate ganglion and horizontal tympanic segment. Erosion of the ossicles was variable in cases of middle ear extension. With more 2341

3 TABLE II. Details Regarding Extent of Disease, Treatment, and Follow-up of 11 Index Patients With Tenosynovial Giant Cell Tumors of the Temporomandibular Joint and Temporal Bone. No. Extent of Disease Treatment Notable Operative Findings Length of Follow-up, mo 1 GF, Co, MF, ITF 1960: Preauricular infratemporal fossa approach, condylectomy with resection of glenoid fossa; GTR. 2 GF, MF, ITF, 3 GF, MF, ITF, 4 GF, MF, EAC, ME, Ma 5 GF, MF, EAC, ME, Ma 1970: Middle fossa craniotomy; STR. 1971: CWD tympanomastoidectomy; STR for adherent dural disease. 1973: External beam radiation, 60 Gy. 1972: Transmastoid biopsy. 1972: External bean radiation, 60 Gy. 1975: Subtotal temporal bone resection; STR for adherent carotid disease. 1977: Middle fossa craniotomy with CWD tympanomastoidectomy; GTR. 1979: Middle fossa craniotomy with CWD tympanomastoidectomy; GTR. 6 GF, Co, MF, ITF 1986: Preauricular infratemporal fossa approach, condylectomy with resection of glenoid fossa; GTR. 7 GF, MF, ITF 1993: Modified infratemporal fossa type B approach; GTR. 8 GF, MF, ITF, EAC, ME 9 GF, MF, ITF, 10 GF, MF, ITF, 2005: Middle fossa craniotomy with subtotal petrosectomy and blind sac closure of the external auditory canal; GTR. 2006: Transantral resection of infratemporal fossa recurrence. 2007: Transpalatal resection of infratemporal fossa recurrence. 2009: Middle fossa craniotomy with subtotal petrosectomy and blind sac closure of the external auditory canal; GTR. 2011: Middle fossa craniotomy with subtotal petrosectomy and blind sac closure of the external auditory canal; NTR for adherent disease at geniculate ganglion. 11 GF, MF, ITF 2015: Middle fossa craniotomy with infratemporal fossa dissection; GTR. None 166 Disease inseparable from temporal lobe dura; ossicles eroded from disease; lateral semicircular canal fistula present Disease adherent but separable from temporal lobe dura; disease surrounding ossicles without erosion Disease separable from temporal lobe dura; ossicles eroded from disease Disease separable from temporal lobe dura; disease surrounding ossicles without erosion None 73 Adherent disease required resection of portion of involved temporal lobe dura Disease adherent but separable from temporal lobe dura; disease surrounding ossicles without erosion Disease transgressed middle fossa dura; ossicles eroded from disease Adherent disease required resection of involved temporal lobe dura; ossicles eroded from disease; cochlear fistula present; disease adherent to geniculate ganglion Adherent disease required resection of involved temporal lobe dura Co 5 condyle; CWD 5 canal wall down; EAC 5 external auditory canal; GF 5 glenoid fossa; GTR 5 gross total resection; ITF 5 infratemporal fossa; Ma 5 mastoid; ME 5 middle ear; MF 5 middle fossa; NTR 5 near total resection; STR 5 subtotal resection. limited involvement the ossicles remained intact; however, with extensive disease the ossicles were eroded (Table II). All 11 cases received preoperative imaging according to the diagnostic imaging modalities available at the time of evaluation. As the study period spanned 55 years, high-resolution computed tomographic (CT) imaging of the temporal bone was only available for review in the four most recent cases (Figs. 1 and 2), and contrastenhanced magnetic resonance imaging (MRI) in three. Within this more limited set, CT commonly demonstrated a lytic and expansile lesion with a spiculated pattern of erosion at the tumor periphery and central scattered calcifications likely corresponding to free-floating fragments of bone located within the substance of the tumor. On MRI, all three cases demonstrated characteristic precontrast T1 and T2 hypointense signal, and contrast uptake on T1-weighted imaging was minimal and heterogeneous. T2 hypointensity is related to the magnetic susceptibility effects of iron within the hemosiderinladen tumor and was accentuated with the use of gradient-recall echo (GRE or T2*) or susceptibilityweighted imaging (SWI; Fig. 3). Finally, secondary effusion or inflammatory changes were commonly found in the mastoid resulting from eustachian tube and antral blockage. Assessment of preoperative growth rate was limited, since only one patient had any period of radiological surveillance prior to treatment. In this one case, the lesion demonstrated 3 mm of growth over a period of 4 months. Management and Outcomes All patients underwent surgical management with or without radiation therapy. Surgical approach and degree of resection varied by extent of disease as well as era of treatment as outlined in Table II. In most cases, a combined mastoid and subtemporal middle fossa craniotomy was utilized. Three patients underwent boneanchored hearing aid placement following resection. 2342

4 Fig. 1. (A, B) Axial and (C) coronal temporal bone computed tomography demonstrating a left-sided expansile, lytic lesion centered at the glenoid fossa. A spiculated pattern of bony erosion is evident at the tumor margin (arrows). The lesion extends just to the foramen ovale and spinosum (A, white arrowhead and black arrowhead, respectively). The ossicles are enveloped without radiological evidence of erosion (B, arrowhead). The cortex of the mandibular condyle is preserved (C, arrowhead). (D) Surgical specimen demonstrating a reddish brown villous appearance. [Color figure can be viewed in the online issue, which is available at com.] Subtotal resection with neoadjuvant or adjuvant external beam radiation was used in two early cases in the 1970s. In one recent case, near total resection was performed given adherent disease at the geniculate ganglion, with no evidence of growth to date. The eight remaining cases underwent gross total resection. Regarding postoperative complications, one patient experienced transient facial nerve paresis with full recovery after resection of tumor involving the geniculate ganglion, and a second case with otic capsule erosion and a cochlear fistula experienced postoperative profound sensorineural hearing loss. Four patients experienced postoperative malocclusion; in two cases the malocclusion was self-resolving with time, whereas the remaining two patients had persistent symptoms. Of the nine patients who underwent gross total or near total resection, without radiation, only one recurrence has occurred. The median duration of follow-up for all patients was 116 months (range months). Histopathology Microscopically, at low-magnification the tumors had an infiltrative growth pattern with diffuse sheets of tumor cells, a feature resembling what is seen in diffuse-type TGCT at other anatomic locations. Cleft-like spaces were common, and two tumors had focal areas with a distinct villous pattern. Bands of dense fibrosis traversed throughout the tumors, oftentimes creating partial or completely formed nodules of tumor cells. Zones of prominent stromal hyalinization were frequently seen, and all tumors contained numerous osteoclastlike giant cells (Fig. 4A). One tumor contained diffuse sheets of foamy macrophages, whereas in the others they were sprinkled among the mononuclear tumor cells. Scattered trabeculae of reactive woven bone were present in 10 tumors. Seven tumors contained a small to moderate amount of chondroid matrix with zones of dystrophic calcification, oftentimes deposited in a lacelike pattern similar to what is seen in chondroblastoma (Fig. 4B). Modest to abundant amounts of hemosiderin deposition were observed in all tumors. The mononuclear tumor cells ranged from small cells with round to ovoid nuclei surrounded by pale cytoplasm, to plump epithelioid cells with eosinophilic to amphophilic cytoplasm, frequently containing intracytoplasmic hemosiderin (Fig. 4C). Eight of 11 tumors displayed abundant epithelioid cells arranged in broad sheets or variably sized clusters. DISCUSSION The current study of 11 patients adds to the growing body of literature characterizing the clinical features 2343

5 Fig. 2. (A C) Axial and (D) coronal temporal bone computed tomography demonstrating a right-sided expansile, lytic lesion centered at the glenoid fossa with destruction of the squamosal portion of the temporal bone. A reticular pattern of bony erosion is evident at the tumor margin (A C, arrows). There is tumor extension into the middle ear cavity with destruction of the head of the malleus and preservation of the body of the incus (A, black arrowhead). The petrous portion of the carotid canal remains intact (A, white arrowhead). Tumor extends to involve the lateral margin of the geniculate ganglion (B, arrowhead). The cortex of the mandibular condyle is preserved (D, arrowhead). and treatment of TGCT of the TMJ and temporal bone. In a comprehensive literature review performed by Safaee et al. in 2015, a summary of 58 published cases was presented. 1 Corroborating the current study, they found that the mean age was 45 years, with a relatively even distribution between men and women. The mean duration between symptom onset and diagnosis was 15 months and the most common presenting symptom was pain. The great majority of patients received surgical resection, and the rate of recurrence in patients with at least 1 year of follow-up was 15%; however, in a limited cohort of seven cases with extended follow-up, the rate of recurrence at 5 years was 29%. With a broad differential diagnosis and rare incidence, the radiological features of TGCT of the TMJ and temporal bone provide valuable information for establishing an accurate clinical diagnosis. 7 9 Diagnostic considerations include osteoarthritic change, chondroblastoma, chondrosarcoma, aneurysmal bone cyst, rhabdomyosarcoma, plasmacytoma, cholesteatoma, intraosseous meningioma, reparative granuloma, tumoral calcium pyrophosphate dihydrate crystal deposition disease, and metastasis. CT findings suggestive of TGCT include a lytic juxta-articular lesion with irregular bony margins and areas of central calcification. On MRI, marked hypointensity on T2 or T2* sequences is highly characteristic of these tumors. Specifically, heavy hemosiderin deposition results in focal or diffuse low signal within the lesion on T1- and T2-weighted imaging that is markedly accentuated ( blooming artifact) on GRE and SWI sequences. Contrast uptake is variable. 7 9 Currently, mainstay therapy for TGCT of the TMJ and temporal bone remains surgical. Similar to other major joints such as the knee and hip, TGCT of the temporal bone most commonly acquire the diffuse form of disease involving the contiguous synovial space with extension into adjacent structures. Accordingly, limited resection or curettage carries a high rate of recurrence, whereas wide local resection, when feasible, is usually curative. 1,3 5 Careful review of preoperative CT and MRI is critical for surgical planning, because growth patterns are variable and more extensive tumors may involve the facial nerve, labyrinth, trigeminal nerve, or petrous carotid artery or exhibit dural transgression. In most cases where disease is located anterior to the external auditory canal, a subtemporal middle cranial fossa approach with or without zygomatic osteotomy can provide sufficient surgical access. In cases with disease extending to the external auditory canal, middle ear, and mastoid, a combined mastoid middle cranial fossa approach or infratemporal fossa type B approach can be performed. As described in Table II, between 1960 and 2015 there was a gradual evolution in management of disease involving the external 2344

6 Fig. 3. (A, B) T1 axial, (C, D) T1 axial with contrast, and (E, F) fat-saturated T2 axial images in two patients with tenosynovial giant cell tumors. Both lesions are characterized by low T1 signal relative to adjacent brain (A, B, arrows) and modest inhomogeneous contrast enhancement (C, D, arrows). The smaller lesion (E) is characterized by T2 signal only slightly hypointense to adjacent brain (arrow), whereas the larger lesion (F) is markedly hypointense (arrow). (G, H) Gradient-recall echo and susceptibility weighted imaging, respectively, demonstrate markedly hypointense signal, reflecting the magnetic susceptibility effects of iron within the hemosiderin-laden tumor. auditory canal, middle ear, and mastoid. Prior to 1980, canal wall down cavities were utilized more frequently, given surgical preferences of the time, and also to assist with clinical surveillance, since imaging technologies were primitive. Beginning in the 1980s, extensive external auditory canal and tympanomastoid disease was managed with subtotal petrosectomy and blind sac closure of the external auditory canal. Despite primary involvement of the TMJ, condylectomy was only performed in two cases. In most patients, the glenoid fossa defect was reconstructed with a local muscle rotation flap. Only one of 11 patients was managed with perioperative intermaxillary fixation, and only two patients reported long-term malocclusion. Given the nonmalignant nature of disease, aggressive subtotal resection is indicated when complete removal carries high risk to critical neurovascular structures. Finally, salvage surgery or radiation may be utilized for recurrence depending upon location, tumor volume, and patientspecific factors. Given the rarity of the studied condition, establishing recommendations for optimal duration and frequency of radiologic follow-up remains challenging. In the current series, after a median follow-up of 116 months, only one patient experienced disease recurrence following gross total resection, 16 months after initial surgery. Paralleling TGCT at other anatomic sites, risk for recurrence Fig. 4. (A) Tenosynovial giant cell tumor containing histiocytelike mononuclear cells, osteoclastlike giant cells, fibrosis, hemosiderin, and a single trabecula of non-neoplastic woven bone. (B) Pale blue chondroid matrix with calcification embedded within the tumor. (C) Tumor cells have an epithelioid appearance characterized by abundant eosinophilic cytoplasm. [Color figure can be viewed in the online issue, which is available at

7 is strongly driven by extent of the primary tumor and completeness of resection. 10 In the authors practice, a postoperative MRI is commonly obtained at approximately 3 months following surgery to serve as a baseline. In cases where gross total resection was achieved and no residual tumor is seen on the first postoperative MRI, biennial imaging could be considered early on, extending to larger imaging intervals over time. In cases where subtotal resection was performed, more frequent imaging follow-up is recommended. Until more data regarding risk for late recurrence are available, lifelong follow-up should be considered. A final important point of discussion is the evolution in disease nomenclature and overlapping histologic features with chondroblastoma. As has been pointed out by Oda et al., cases of TGCT with chondroid metaplasia resemble chondroblastoma of bone. 6 In general, chondroid metaplasia in TGCT is rare; however, recent literature demonstrates that TGCT of the TMJ have a unique predilection for chondroid metaplasia. 3,4,6,7 This observation is further substantiated by our series, in which the majority (seven of 11) of tumors contained chondroid metaplasia, often with foci of the lacelike ( chicken wire ) calcification seen in chondroblastoma. However, unlike chondroblastoma, the chondroid tissue in our cases often displayed, at least in part, the pale blue color of hyaline cartilage when compared to the pink chondroid matrix classically described in chondroblastoma. Whereas the tumor cells of chondroblastoma are comprised of eosinophilic cytoplasm, TGCT of the TMJ frequently contain cells with abundant eosinophilic cytoplasm and intracytoplasmic hemosiderin. Careful cytologic evaluation of the tumor cells, in combination with the clinical and radiologic findings, can also be helpful in separating these two entities. These findings create a heightened awareness of the possibility that some published reports of TMJ chondroblastoma may have actually been TGCT, as is the case with nine of the tumors in the current series. 11 CONCLUSION TGCT of the TMJ and temporal bone are rare and locally aggressive tumors that commonly present with nonspecific symptoms, including TMJ or ear pain and hearing loss. Careful review of CT and MRI, followed by preoperative biopsy, is critical for establishing an accurate diagnosis and facilitating appropriate treatment. TGCT of the temporal bone have a unique predilection for chondroid metaplasia with calcification and an abundance of epithelioid tumor cells, features that can lead to misdiagnosis of chondroblastoma. Gross total resection is achievable in most cases and offers long-term cure. Radiation may be considered for recurrent disease or adjuvant therapy following subtotal resection. BIBLIOGRAPHY 1. Safaee M, Oh T, Sun MZ, et al. Pigmented villonodular synovitis of the temporomandibular joint with intracranial extension: a case series and systematic review. Head Neck 2015;37: Romanach MJ, Brasileiro BF, Leon JE, Alves DB, de Almeida OP, Vargas PA. Pigmented villonodular synovitis of the temporomandibular joint: case report and review of the literature. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2011;111:e17 e Hoch BL, Garcia RA, Smalberger GJ. Chondroid tenosynovial giant cell tumor: a clinicopathological and immunohistochemical analysis of 5 new cases. Int J Surg Pathol 2011;19: Fisher M, Biddinger P, Folpe AL, McKinnon B. Chondroid tenosynovial giant cell tumor of the temporal bone. Otol Neurotol 2013;34:e49 e Damodar D, Chan N, Kokot N. Pigmented villonodular synovitis of the temporomandibular joint: case report and review of the literature. Head Neck 2015;37:E194 E Oda Y, Izumi T, Harimaya K, et al. Pigmented villonodular synovitis with chondroid metaplasia, resembling chondroblastoma of the bone: a report of three cases. Mod Pathol 2007;20: Pina S, Fernandez M, Maya S, et al. Recurrent temporal bone tenosynovial giant cell tumor with chondroid metaplasia: the use of imaging to assess recurrence. Neuroradiol J 2014;27: Kim KW, Han MH, Park SW, et al. Pigmented villonodular synovitis of the temporomandibular joint: MR findings in four cases. Eur J Radiol 2004; 49: Cheng XG, You YH, Liu W, Zhao T, Qu H. MRI features of pigmented villonodular synovitis (PVNS). Clin Rheumatol 2004;23: Ravi V, Wang WL, Lewis VO. Treatment of tenosynovial giant cell tumor and pigmented villonodular synovitis. Curr Opin Oncol 2011;23: Bertoni F, Unni KK, Beabout JW, Harner SG, Dahlin DC. Chondroblastoma of the skull and facial bones. Am J Clin Pathol 1987;88: