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Year : 2022  |  Volume : 9  |  Issue : 2  |  Page : 141-144

Brown's tumor of mandible as a manifestation of primary hyperparathyroidism: A case report and review of literature

Department of Oral Medicine and Radiology, Institute of Dental Sciences, Bareilly, Uttar Pradesh, India

Date of Submission20-Feb-2022
Date of Decision19-Jun-2022
Date of Acceptance01-Aug-2022
Date of Web Publication31-Aug-2022

Correspondence Address:
Dr. Samia Seraj
Department of Oral Medicine and Radiology, Institute of Dental Sciences, Bareilly, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/sjoralsci.sjoralsci_8_22

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Hypercalcemia and increased or abnormal serum levels of parathyroid hormone are indicators of primary hyperparathyroidism (HPT). Brown tumor of bone is a rare nonneoplastic lesion that arises due to abnormal bone metabolism caused by HPT. The reported prevalence of brown tumor is 0.1%. In today's world, however, skeletal illness caused by primary HPT is quite rare. Patient consent was obtained. Here, we present a rare case of bony lytic lesion in the mandible that raised suspicion of giant cell lesion, compelling further investigations. The patient underwent blood investigations which revealed hypercalcemia. Ultrasonography revealed a hypoechoic mass on the left inferior thyroid lobe. An incisional biopsy was done which revealed hemorrhagic fibrovascular connective tissue in a background of multinucleated giant cells; the mandibular lesion was classified as a giant cell lesion. A final diagnosis of Brown tumor of the mandible was made based on the investigations. The left parathyroidectomy was done. Curettage of the mandibular lesion was done surgically. The patient was on follow-up for 6 months and showed no signs of recurrence. Although Brown tumor of mandible is a rare lesion, it should be considered a differential diagnosis for osteolytic lesions of the jaw. Early diagnosis can help to prevent late outcomes of the disease.

Keywords: Browns tumor, giant cell lesion, hyperparathyroidism

How to cite this article:
Seraj S, Aggarwal A, Upadhyay N, Agarwal N, Vishnurao SG, Rathore AS. Brown's tumor of mandible as a manifestation of primary hyperparathyroidism: A case report and review of literature. Saudi J Oral Sci 2022;9:141-4

How to cite this URL:
Seraj S, Aggarwal A, Upadhyay N, Agarwal N, Vishnurao SG, Rathore AS. Brown's tumor of mandible as a manifestation of primary hyperparathyroidism: A case report and review of literature. Saudi J Oral Sci [serial online] 2022 [cited 2023 Apr 2];9:141-4. Available from: https://www.saudijos.org/text.asp?2022/9/2/141/355228

  Introduction Top

The overproduction of parathyroid hormones (PTH) causes hyperparathyroidism (HPT), which causes an increase in calcium release from bone, which has a direct impact on the skeletal system. Calcium absorption by the kidneys and intestine is affected as the concentration of calcium in plasma rises. This causes skeletal demineralization, allowing multinucleated large cells known as osteoclasts to replace bone, causing the skeletal structure to deteriorate.[1]

Hypersecretion of PTH, which is produced by hyperplastic or tumoral alterations in one of the four parathyroid glands (PTGs), causes primary HPT. The resulting condition is hypercalcemia.[2] End-stage renal illness is the most common cause of secondary HPT end-stage renal disease. In reaction to the hypocalcemia, normal PTG release an increase in PTH. In patients with long-term secondary illness, tertiary HPT is defined by PTG hyperplasia and a loss of responsiveness to serum calcium levels.[3] There is increased activity of osteoclasts and bone resorption when there is PTH overload. The trabecular and cortical bones are removed, followed by loose connective tissue filling their place. Brown's tumor of HPT is a collection of hemorrhagic debris and osteoclasts that form a unique mass in some cases.[1]

Only a few cases of Brown tumor have been reported in literature. This example emphasizes the need of thoroughly examining every osteolytic lesion in the maxillofacial region, as it is rightly stated, “Oral Health is the Mirror of General Health.” In this case, the patient had an osteolytic lesion that turned out to be Brown tumor of Primary HPT, a rare condition with a prevalence of roughly 0.1%.

  Case Report Top

A 40-year-old male patient presented with a complaint of swelling on the right side of his face that had been present for 2 months. As per the patient, the swelling was small in size initially and progressed to its present size gradually. All the vital signs were within normal limits. Since a few months, the patient had generalized weakness, fatigue, and weight loss. His medical history and family history were both noncontributory.

Extraoral examination revealed a single diffuse swelling on the middle and lower third of right side of face, extending superioinferiorly from the right infraorbital margin to 2 cm below the inferior border of the mandible and mediolaterally from the preauricular region to the symphysis region, measuring about 6 cm × 4 cm. The overlying skin was stretched [Figure 1]. On palpation, all inspectory findings were confirmed. The swelling firm and tender with slightly raised temperature. The right submandibular and submental nodes were tender and palpable. The mouth opening was reduced to 12 mm.
Figure 1: Image showing extraoral swelling

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Intraoral examination revealed a single well-defined ulceroproliferative growth, noted over the alveolar ridge in relation to 46.47 region measuring about 3 cm × 2.5 cm in its greatest dimension. The surface was ulcerated and the margins were well defined. It had firm consistency and was tender on palpation. The borders of the lesion were indurated. A provisional diagnosis of central giant cell granuloma involving the right side of the jaw was made based on the clinical examination.

A computed tomographic scan (GE Medical Systems) of the face was acquired and reconstructed using Dentascan Software (Bareilly, Uttar Pradesh, India). The resultant images were evaluated. A well-defined multilocular lesion measuring about 70.9 mm × 24.2 mm was present on the right side body of the mandible with respect to 46 regions and involving the entire ramus of the mandible. The internal structure of the pathology was mixed radiopaque and radiolucent. The pathology was involving the right side inferior alveolar nerve [Figure 2]. Expansion of the buccal and lingual cortical plates was noted. The lower border of the mandible was thinned out. Perforation of the lingual and the buccal cortical plate was noted. The overall density of the mandible appeared to be reduced. The trabecular pattern appeared to be altered. The entire calvarium appeared granular, with no typical cortical bone at the inner and outer tables of the skull, as well as a generalized lack of distinct outer cortical boundaries of the osseous structures [Figure 3].
Figure 2: Panorex of the mandible

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Figure 3: Axial image showing the involvement of skull bones

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The patient's blood tests revealed 700 IU/L of alkaline phosphatase and 402.5 pg/ml of PTH, respectively. The calcium concentration in the blood (serum calcium) was 13.5 mg/dl. A hypoechoic mass on the left inferior thyroid lobe was found on ultrasonography.

After an incisional biopsy, which revealed hemorrhagic fibrovascular connective tissue in a background of multinucleated giant cells, the mandibular lesion was classified as a giant cell lesion [Figure 4]. A final diagnosis of browns tumour of HPT was made based on radiographic, biochemical, and histological findings.
Figure 4: Histopathology of the lesion

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The patient received left parathyroidectomy surgery. The pathological findings revealed the presence of chief cells with the tumor surrounded by a fibrous capsule, thereby confirming the diagnosis of parathyroid adenoma. Curettage was done to remove the bony lesion surgically. The patient was on follow-up for 6 months and showed no sign of recurrence.

  Discussion Top

Brown tumors are focal lesions of the bone that occur in people with uncontrolled HPT and are a result of increased activity of osteoclasts and fibroblasts. They can be found in any section of the skeleton, although the clavicles, ribs, pelvic girdle, and extremities are the most common sites. Lesions in the craniofacial bones that are clinically significant are infrequent.[4]

In 1891, Von Recklinghausen described HPT as a bone disease for the first time. Askanazy was the first to describe a patient who had both a cystic osteitis and parathyroid tumor in 1904. He did not, however, link the two entities. HPT can have three forms: primary, secondary, or tertiary.[5] The disorder is marked by an increase in PTH levels as well as calcium mobilization from the bones in all cases. Primary HPT can be caused by primary parathyroid hyperplasia, parathyroid adenoma, or parathyroid cancer. Secondary HPT is the outcome of a compensatory mechanism triggered by a primary illness that causes hypocalcemia, such as pregnancy, rickets, chronic renal failure, or osteomalacia.[6]

The PTGs synthesize and secrete PTH, and their activity is regulated by the amount of free (ionized) calcium in the blood.[7] Anomalies in one or more of the PTGs produce elevated PTH production in primary HPT. About 85% of primary HPT cases are caused by adenomas.[8] The presence of hypophosphatemia and hypercalcemia on regular multipanel serum tests detects the majority of individuals with primary HPT. Hypocalcemia or Vitamin D insufficiency stimulates excessive PTH generation, resulting in secondary HPT.[9] The most common cause of secondary HPT is chronic renal failure. Hypocalcemia is the result, and the PTG overwork to compensate for the low (serum) calcium level. The PTGs can sometimes become autonomous in long-term secondary HPT instances. This is referred to as tertiary HPT.[10] Literature mentions a fourth form of HPT, which is likely to be caused by elevated PTH levels in patients with malignancy. HPT can now be detected significantly earlier, usually in the asymptomatic period, thanks to recent breakthroughs in routine biochemical screening, whereas it was previously diagnosed as an aggressive disease with mostly skeletal indications in the 1970s. Various focal areas of skull demineralization, generalized osteoporosis, and osteitis fibrosa cystica are late bone symptoms of the disease (brown tumor).[1]

Jaffe created the term “brown tumor” to describe the bony lesions detected in HPT. The term derives from the tissue's reddish brown color, i.e., caused by hemorrhage, vascularity, and hemosiderin deposits.[1] It is an osteolytic lesion of the bone caused by a giant cells. It is a rare lesion and is estimated that 4.5% of people with primary HPT and 1.5%–1.7% of those with secondary HPT would develop it.[3] As in this case, it could be the first clinical sign of HPT. The mandible is more commonly afflicted than the maxilla. Brown tumors are nonneoplastic lesions caused by the aberrant metabolism of bone in HPT, which results in a focal destruction of the structures involved. The femur, pelvis, and ribs are the most common sites for brown tumors.[9],[10] Elevated circulating levels of PTH produce increased bone resorption by osteoclasts, mainly in cortical bone, resulting in this bony HPT lesion. This could explain why the mandible, which is a cortical bone, is the most usually affected area in the maxillofacial region, but maxillary involvement is less prevalent. The simultaneous finding in both jaws is extremely rare. It is 3 times more frequently seen in females above 50 years of age unlike the present case who was a 40-year-old male. Brown tumors can impair the periodontal apparatus of the front teeth, causing considerable mobility in addition to bone resorption in the mandible's body. Previous literature has shown that the loss of the surrounding bone around the teeth is a radiologic feature in 6%–55% of cases.[3],[4] A soft to firm mass with varying extent of discomfort, facial anomalies, as well as decreased masticatory function may be present as in our case report. A well-defined unilocular or multilocular radiolucency characterizes a brown tumor. Their radiographic appearance, according to Ashrafi, was that of well-defined lytic lesions with no reactive bone growth, cortical expansion, or thinning. They are monocystic, with no internal septa or marginal scalloping, and they are monocystic. Acoording to literature, the mandibular lesions could be ill-defined as in the current situation to well defined osteolytic lesions.[5] Computed tomography revealed an expansile lytic lesion in the left posterior mandible, with thinning of the inner cortex along and thick sclerotic outer cortex, according to Nair PP's case report. The tumor also included several irregular bone septa with hyperdense foci, giving it a multilocular appearance.[11]

Brown tumor has no pathognomonic histologic changes, and identical changes can be seen in giant cell tumor, fibrous dysplasia, and reparative granuloma (RG). In young individuals, RG is found as a focal lesion. It mostly affects the mandible. However, the source is unknown, some researchers believe that these lesions are a result of trauma and that the absence of HPT distinguishes them from brown tumors.[12] Before considering removal of a brown tumor, HPT should be treated. Chronic renal failure should be treated with hemodialysis or, in the worst-case scenario, a kidney transplant in secondary and tertiary HPT. The autonomous PTGs should be removed during an initial HPT procedure.

  Conclusion Top

The Browns tumor of HPT is a rare entity that is reported in this case. This case highlights the importance of examining every osteolytic lesion in the maxillofacial region thoroughly. Furthermore, a thorough and comprehensive systematic examination should be carried out in all. To avoid late problems from HPT, patients should have regular checkups. The clinician should be aware of the clinical manifestations and radiographic appearances of these lesions so that the underlying diseases can be treated early and the overall prognosis can be improved.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Madkhali T, Alhefdhi A, Chen H, Elfenbein D. Primary hyperparathyroidism. Turk J Surg 2016;1:58-9.  Back to cited text no. 1
Kalinin AP, Pavlov AV, Alexandrov YK, Kotova IV, Patrunov YN, Pamputis SN. The parathyroid glands: Imaging and surgery. Sprin Sci Bus Med 2013;9:107-23.  Back to cited text no. 2
van der Plas W, Kruijff S, Sidhu SB, Delbridge LW, Sywak MS, Engelsman AF. Parathyroidectomy for patients with secondary hyperparathyroidism in a changing landscape for the management of end-stage renal disease. Surgery 2021;169:275-81.  Back to cited text no. 3
Wiederkehr M. Brown tumor complicating end-stage kidney disease. Clin Nephrol Case Stud 2020;8:72-9.  Back to cited text no. 4
Setiya SV, Sabhlok S, Shetty LS, Bharadwaj SR. Tertiary hyperparathyroidism inducing brown tumour: A rare case. J Craniofac Res 2016;1:56-9.  Back to cited text no. 5
Khalatbari MR, Moharamzad Y. Brown tumor of the spine in patients with primary hyperparathyroidism. Spine (Phila Pa 1976) 2014;39:E1073-9.  Back to cited text no. 6
Villa-Etchegoyen C, Lombarte M, Matamoros N, Belizán JM, Cormick G. Mechanisms involved in the relationship between low calcium intake and high blood pressure. Nutrients 2019;11:1112.  Back to cited text no. 7
Cormier C, Koumakis E. Bone and primary hyperparathyroidism. Joint Bone Spine 2022;89:105129.  Back to cited text no. 8
Kuperstein AS, Berardi TR, Mupparapu M. Systemic diseases and conditions affecting jaws. Dent Clin North Am 2016;60:235-64.  Back to cited text no. 9
Llach F, Velasquez Forero F. Secondary hyperparathyroidism in chronic renal failure: Pathogenic and clinical aspects. Am J Kidney Dis 2001;38:S20-33.  Back to cited text no. 10
Nair PP, Gharote HP, Thomas S, Guruprasad R, Singh N. Brown tumour of the jaw. BMJ Case Rep 2011;2011:bcr0720114465.  Back to cited text no. 11
James SL, Davies AM. Giant-cell tumours of bone of the hand and wrist: A review of imaging findings and differential diagnoses. Eur Radiol 2005;15:1855-66.  Back to cited text no. 12


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]


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