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CASE REPORT
Year :   |  Volume :   |  Issue :   |  Page :  

Role of oral physician in diagnosis of occult disease of primary hyperparathyroidism


1 Department of Oral Medicine and Radiology, Dr. D. Y. Patil Vidyapeeth, Pune, Maharashtra, India
2 Dental Practitioner, Healthy Smiles Dental Care, Pune, Maharashtra, India

Date of Submission03-Jun-2021
Date of Decision19-Jun-2021
Date of Acceptance26-Dec-2021
Date of Web Publication03-Nov-2022

Correspondence Address:
Shraddha C Jugade,
Assistant Professor, Department of Oral medicine and Radiology, Dr. D.Y.Patil Dental College & Hospital, Dr. D.Y.Patil Vidyapeeth, Pimpri, Pune, Maharashtra
India
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ccd.ccd_432_21

   Abstract 


Parathyroid hormone (PTH) plays a key role in the regulation of calcium homeostasis. It is secreted by a pair of parathyroid glands located behind the thyroid gland. Primary hyperparathyroidism is the disorder which is seen in 0.2%–0.3% of the population. It is the third most common endocrine disorder after Diabetes Mellitus and Thyroid disorders. There are several systemic manifestations of the disease including skeletal, Renal, abdominal, neurological ones. The following case report discusses some of the classic oral manifestations of the disease and signifies the role of an Oral physician in the diagnosis of underlying systemic disorder.

Keywords: Oral manifestations, parathyroid hormone, primary hyperparathyroidism



How to cite this URL:
Jugade SC, Bhalchim S, Karkhanis A. Role of oral physician in diagnosis of occult disease of primary hyperparathyroidism. Contemp Clin Dent [Epub ahead of print] [cited 2022 Nov 30]. Available from: https://www.contempclindent.org/preprintarticle.asp?id=360369




   Introduction Top


Primary Hyperparathyroidism is an endocrine disorder caused by the excessive secretion of the parathyroid hormone, which is an integral component in the maintenance of normal calcium homeostasis.[1],[2] Presence of excess PTH creates an imbalance between osteoblastic deposition and osteoclastic resorption causing an increased bone modeling.[3] PHPTH is most commonly caused by parathyroid adenoma, hyperplasia, carcinoma, multiple endocrine neoplasias, and other rare syndromic states.[2],[4] PHPTH has profound impact in the jaw bones demineralization of cortices of inferior border of mandible, Inferior alveolar nerve canal, walls of maxillary sinus, presence of radiolucencies in the bone, alteration in the bony trabeculae, presence of brown tumors.

The aim of the article is to emphasize upon definitive oral manifestations of PHPTH, which in conjunction with certain systemic findings and biochemical analysis aids the clinician to ascertain the diagnosis of a systemic disorder unknown to the patient and modify the dental management accordingly.


   Case Report Top


A 35-year-old female patient reported to the hospital with the chief complaint of painless swelling in the lower front region and lower left back region of the jaw for 3 months. She also complained of generalized joint pain, abdominal pain, and lethargy. The swelling was abrupt in onset, gradually increased in size and attained the present day size. Clinical examination revealed two well-defined, bony hard, nontender swellings in mandibular anterior and left posterior regions with the obliteration of labial and buccal vestibule. The mucosa over the swellings was completely normal. On examination of the teeth, it was found that there was presence of extrinsic stains on all the mandibular teeth along with mild recession. The teeth associated with the swellings; 31, 32, 33, and 46.47 were vital in nature [Figure 1]. The provisional diagnosis of the above was stated as benign tumor of the oral cavity.
Figure 1: Intraoral swelling on the labial aspect of 31, 32 and on the buccal aspect of 36, 37

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Intraoral periapical of the concerned regions revealed loss of lamina dura in all the teeth covered along with ill-defined areas of radiolucency [Figure 2]a and [Figure 2]b.
Figure 2: (a and b) Intraoral periapical showing non traceable lamina dura and an ill-defined radiolucent lesion (c) orthopantomogram showing well-defined radioloucent osteolytic lesion with generalized loss of lamina dura. (d and e) Cone beam computed tomography showing osteolytic areas in the mandible causing perforation (f and g) hand wrist and foot radiograph showing osteolytic lesion

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Orthopantomograph showed generalised loss of lamina dura, well defined, noncorticated radiolucent osteolytic lesion in mandibular left posterior region, reduced thickness and density of cortication at the periphery of the mandible, inconspicuous outlines of inferior alveolar nerve canal [Figure 2]c.

Cone Beam Computed Tomography: Axial and Coronal sections showed multiple osteolytic, hypodense areas in the mandible [Figure 2]d and [Figure 2]e.

Skeletal radiographs showed osteolytic lesions in the proximal phalanyx below the interphalangeal joint and metacarpophalangeal joint [Figure 2]f and [Figure 2]g.

The patient was subjected further to certain blood investigations as shown above [Table 1].
Table 1: Blood Investigation Reports

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Based upon clinical, radiographical, and biochemical analysis, the diagnosis was stated as “Hyperparathyroidism” with the following differential diagnosis:

  1. Paget's Disease: It is seen in patients above the age of 60 years with generalized radiopacity, expansion of jaws with no loss of lamina dura
  2. Osteomalacia
  3. Osteoporosis

    Both show a generalized radiolucency of jaw bone with thinning (no loss) of lamina dura. Serum 25(OH) D levels are reduced in patients with osteomalacia which were found to be normal in the above patient.
  4. Langerhans cell disease: Presents as solitary or multiple, “scooped out” lesions in the jaw bones, periosteal reaction and localized loss of lamina dura.


The patient was referred to the endocrinologist who subjected the patient to ultrasonography (USG) and Biopsy of the parathyroid gland. USG revealed a hypoechogenic structure close to the thyroid gland. Biopsy was suggestive of a parathyroid adenoma. Final diagnosis of the above case was given as “PHPTH.” Patient was prescribed sodium alendronate 35 mg OD, cinacelet 30 mg OD, calcitriol 0.25 mg OD. The parathyroid levels did not reduce considerably within 3 months. The patient underwent the surgical procedure of Minimally invasive Parathyroidectomy followed by an uneventful recovery. The timeline of the above Case Report is as follows: [Table 2].
Table 2: Timeline of the Case report

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   Discussion Top


It dates back to 1705 where Courtial, a French surgeon gave the complete description of a patient with HPTH. Von Recklinghausen reported three patients with Osteitis fibrosa cystica (OFC).[5]

The pathophysiology of PHPTH has been described above[6],[7] [Figure 3].
Figure 3: Pathophysiology of primary hyperparathyroidism

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The classic description of clinical manifestations of PHPTH is 'Stones, Bones, Groans, Psychic Moans, Fatigue overtones.[8],[9] In India, females are affected greater than Males with a ratio of 1.7:1 with a majority of cases <40 years of age.[9]

An array of oral manifestations can be found in patients with PHPTH which include loss of lamina dura, bony pathologies in jaw bones, cortical destruction, changes in trabecular pattern, root resorption, tooth displacement.[10]

OFC is an extensive osteoclastic activity causing resorption in the bone manifesting as a radiolucency. “Brown tumors” are nonneoplastic lesions that replace bone marrow with fibrous tissue and contain multinucleated giant cells, spindle cell stroma, extravasated blood cells and hemosiderin deposition thus imparting brown color. The dentist should consider the risk of bone fractures while performing the surgical procedures.[7]

Earliest change includes subperiosteal resorption at phalanges, OFCs at multiple sites such as Skull, radius, Phalanges, femur reducing patients' bone mineral density and making them prone to fracture. Renal complications such as Nephrolithiasis and Nephrocalcinosis, Psychiatric symptoms, Cardiac symptoms such as coronary artery disease, conduction abnormalities.[1],[10]

PHPTH is a challenging disease to treat. Cinacelet, a calcimimetic agent lowers the serum calcium and PTH levels. Bisphosphonates and Estrogen therapy act as antiresorptive drugs and increase the bone mineral density.

The above case was approached in a streamlined manner with the involvement of Oral Physician, Endocrinologist, General Surgeon leading to an accurate diagnosis and treatment plan. The limitation of the above case was that the “Single photon emission computerized tomography” images could not be obtained as the patient did not undergo the investigation due to certain financial problems.

The patient solely came with the purpose of treating the oral lesions, completely unaware about the underlying systemic disease. Therefore, the statement, “Mouth is the mirror of the body” is justified from the above case.

Early and apt diagnosis by the dentist along with interdisciplinary approach limited the progression of the disease and saved the patient from further systemic complications. This emphasizes upon the role of oral physician in diagnosing an occult systemic disease.

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 initial s will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
White SC, Pharoah MJ. Oral Radiology – Principles and Interpretation. 7th ed. Missouri: Elsevier Publishers; 2014. p. 453-6.  Back to cited text no. 1
    
2.
Mackenzie-Feder J, Sirrs S, Anderson D, Sharif J, Khan A. Primary hyperparathyroidism: An overview. Int J Endocrinol 2011;2011:251410.  Back to cited text no. 2
    
3.
Fraser WD. Hyperparathyroidism. Lancet 2009;374:145-58.  Back to cited text no. 3
    
4.
Mittal S, Gupta D, Sekhri S, Goyal S. Oral manifestations of parathyroid disorders and its dental management. J Dent Allied Sci 2014;3:34-8.  Back to cited text no. 4
  [Full text]  
5.
Dorairajan N, Pradeep PV. Vignette hyperparathyroidism: Glimpse into its history. Int Surg 2014;99:528-33.  Back to cited text no. 5
    
6.
Khan A, Bilezikian J. Primary hyperparathyroidism: Pathophysiology and impact on bone. CMAJ 2000;163:184-7.  Back to cited text no. 6
    
7.
Neville BW, Damm DD, Allen CM, Chi A. Oral and Maxillofacial Pathology. First South Asia Edition. New Delhi: Elsevier Publishers; 2015.  Back to cited text no. 7
    
8.
Saleem M, Iftikhar H. Stones, bones, groans, and psychic moans: Primary hyperparathyroidism presenting as surgical emergency. Cureus 2019;11:e4989.  Back to cited text no. 8
    
9.
Pradeep PV, Jayashree B, Mishra A, Mishra SK. Systematic review of primary hyperparathyroidism in India: The past, present, and the future trends. Int J Endocrinol 2011;2011:7.  Back to cited text no. 9
    
10.
Percivale A, Gnerre P, Damonte G, Buscaglia S, Monachesi M, Parodi L, et al. Primary hyperparathyroidism: Epidemiology, clinical features, diagnostic tools and current management. Ital J Med 2015;9:330.  Back to cited text no. 10
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1], [Table 2]



 

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