|Year : 2014 | Volume
| Issue : 1 | Page : 34-38
Oral manifestations of parathyroid disorders and its dental management
Sanjeev Mittal1, Deepak Gupta2, Sahil Sekhri1, Shivali Goyal1
1 Department of Posthodontics, MM college of Dental Sciences and Research, Mullana, Ambala, Haryana, India
2 Department of Orthodontics, HS Judge Dental College, Panjab University, Chandigarh, India
|Date of Web Publication||6-May-2015|
Dr. Sanjeev Mittal
Department of Posthodontics, MM College of Dental Sciences and Research, Mullana, Ambala, Haryana
Source of Support: None, Conflict of Interest: None
Parathyroid hormone plays an important role in the metabolism of calcium and phosphorus, so, influence the mineralization of bone and teeth. Parathyroid disorder may lead to hyper or hyposecretion of hormone, which results in various oral manifestations. Common oral manifestations in patients with hyperparathyroidism (HPT) are brown tumor, loss of bone density, soft tissue calcification, and dental abnormalities. In hypoparathyroidism, the dental abnormalities are a delay or cessation of dental growth and development, paresthesia of the tongue or lips and alteration of the facial muscles. Dentist can easily diagnose the parathyroid disorders owing to their particular oral manifestations and radiographic finding. Dental management of patients with HPT involves a higher risk of bone fracture, whereas in hypoparathyroidism the caries control is the main concern. It is the important that the dentist be aware of the risks and difficulties that may arise during the dental management of these patients.
Keywords: Brown tumor, dental management, endocrine disorders, hyoparathyroidism, hyperparathyroidism, oral manifestations
|How to cite this article:|
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
|How to cite this URL:|
Mittal S, Gupta D, Sekhri S, Goyal S. Oral manifestations of parathyroid disorders and its dental management. J Dent Allied Sci [serial online] 2014 [cited 2020 Jul 4];3:34-8. Available from: http://www.jdas.in/text.asp?2014/3/1/34/156527
| Introduction|| |
The endocrine system is responsible for hormonal secretion and is closely related to the central nervous system, as it diversifies its functions through the hypothalamus and pituitary. It controls physiological processes and maintains homeostasis.  It is necessary to be aware of the most common oral manifestations associated with these disorders and difficulties that may arise during the dental management of these patients.
Parathyroid consists of four small glands (3 mm × 6 mm × 2 mm), which are paired and located behind the thyroid gland in the neck. Parathyroid glands produce and release parathyroid hormone (PTH), which is involved in regulating the metabolism of calcium and phosphorus. So, it plays an important role in tooth and bone mineralization, increases the bone resorption, stimulates formation of active metabolite of Vitamin D in the kidneys, which promotes the intestinal absorption of calcium and decreases renal reabsorption of phosphate.
Hyperparathyroidism (HPT) was first described by Von Recklinghausen in 1891. It results from excessive secretion of PTH with consequent osteoclastic resorption and hypercalcemia. It occurs in about 0.05-0.1% of the population and 2-3 times more prevalent in women than men. The female: Male ratio being 3:1. It usually affects middle-aged persons. Hypoparathyroidism is a rare disorder in which the body produces too little or no PTH. It can either be hereditary or acquired.
The oral health care professional should be familiar with the oral and systemic manifestation of parathyroid disease. Patient with a history of parathyroid disease should be carefully evaluated at the level of medical management, and consultation with the patient physician or endocrinologist is needed.
The aim of this article is to review the oral manifestations and dental management of patients with disorders of the parathyroid glands.
| Hyperparathyroidism|| |
Hyperparathyroidism is characterized by hypersecretion of PTH. HPT occurs in three categories: ,,,
Usually caused by a tumor (adenoma in 85% of all cases) or hyperplasia of the gland that produces an increase in PTH secretion resulting in hypercalcemia and hypophosphatemia.
When the parathyroid glands are stimulated to produce increased amounts of hormones to correct abnormally low serum calcium levels in different physiologic or pathologic conditions like renal failure, intestinal malabsorption syndrome, decrease of Vitamin D production, thus resulting in parathyroid hyperplasia.
When long-standing secondary hyperplasia becomes autonomous in spite of correction of the underlying stimulant (renal transplant). 
Sign and symptoms
In primary HPT, about 50% of patients have no symptoms and the problem is picked up as an incidental finding (via raised calcium or characteristic X-ray appearances [subperiosteal resorption of the phalanges of the index and middle fingers]). Many other patients only have nonspecific symptoms.  These are musculoskeletal problems (weakness, back pain, muscle soreness), gastrointestinal complaints, e.g., vomiting, nausea, constipation, loss of appetite.
One of the main clinical manifestations of HPT is bone disease. The ribs, clavicles, pelvic girdle and mandible are the bones most involved. A pathologic fracture may be the first symptom of the disease. Bone pain and joint stiffness may be present. Renal calculi are a common finding in this condition. Almost all patients with HPT have skeletal lesions in the advanced stages. The loss of calcium in this condition results in generalized osteoporosis.
Oral manifestation [Table 1]
In the oral cavity, the most common clinical manifestations of HPT is brown tumor; loss of bone density, mobile teeth, drifting of teeth, complaint of vague jaw bone pain, sensitive teeth in mastication and percussion, soft tissue calcifications and dental abnormalities such as development defects, alterations in dental eruption. ,,,,, Malocclusion due to drifting of teeth, with definite spacing of the teeth may be one of the first signs of the disease. Pseudocystic lesion can also be presents, radiolucent lesion at the apex of tooth misdiagnosed as periapical cyst or granuloma. , It does not have an appreciable effect on periodontal indices and radiographic bone height. 
|Table 1: Oral Manifestations of Patients With Parathyroid Gland Disorders|
Click here to view
Chronic renal failure and secondary HPT also manifest rarely, as maxillary hyperplasia and hyperostosis cranialis, gradual enlargement of the facial bones over a period. These facial enlargements cause a bizarre facial deformity and dental malocclusion. ,,, Primary HPT also rarely presents in the mandible as a large exophytic mass or painless swelling,  and also as a giant-cell epulis as an initial feature of primary HPT.  Primary HPT patients were more likely to have tori. 
Brown tumor lesions ,,, may be the earliest manifestation of this undiagnosed HPT in 6% of the cases. Brown tumor presents as osteolytic lesion (which may be associated with pain and swelling) that develops due to changes in bone metabolism caused by high serum concentration of PTH. It is an erosive bony lesions caused by rapid osteolysis and peritrabecular fibrosis resulting in a local destructive phenomenon.
Brown tumor presents itself as a friable red-brown mass. Its name is due to color that it takes from the hemorrhagic infiltrates and hemosiderin deposits that are often found inside. Bone lesion may produce significant cortical expansion. Mandible involvement is common, especially in the area of premolars and molars, and it is rare in the maxilla. It occurs mainly in secondary HPT patients with chronic renal failure or renal osteodystrophy,  but it has also been described as a rare manifestation of calcium malabsorption, some forms of osteomalacia and of primary HPT. ,
Radiographically, lesions are characterized by well-defined uni or multilocular radiolucent areas. The characteristic radiographic findings show a widespread loss of the lamina dura and changes in the pattern of the trabecular bone of the jaws. Long-standing lesion commonly produces a significant expansion of cortical bone, root resorption and displacement of roots.
Histologically, it is characterized by an abundant stroma, consisting of bundles of spindle or oval cells, and several multinucleated osteoclast-like giant cells. Calcified material can be found, as well as areas with extravasations of red blood cells and pigmentation by hemosiderin.
Differential diagnosis has to be made with other lesions,  such as an aneurismal bone cyst, cherubism, central giant cell granuloma.
Sagliker syndrome is known that skeletal changes due to secondary HPT can be severe in chronic kidney disease. Recently described Sagliker syndrome including an uglifying appearance to the face (unique facial bone changes), short stature, extremely severe maxillary and mandibulary changes, class II malocclusion of upper and lower jaws, teeth/dental abnormalities, fingertip changes, and knee and scapula deformities, hearing abnormalities, neurological and severe psychological problems. The medical history of these patients showed that they did not receive proper therapy. Changes, particularly in children and teenagers, become irreversible, which was disastrous for the patients both esthetically and psychologically. ,
Hyperparathyroidism-jaw tumor syndrome is a rare disease, other members of the family are also involved, and there is risk of malignant disease. The Patient presented with bilateral or recurrent mandibular radiolucencies diagnosed histopathologically as cemento-ossifying fibromas. It is due to mutation of gene. 
Oral radiographs (intraoral and panoramic) of hyperparathyroid patient reveal. ,,,,
- HPT is the most common cause of generalized rarification of the jaws. The radiograph is typically described as loss of medullary trabecular pattern, jaw appears finely radiopaque described as clear "ground glass" appearance.
Differential diagnosed from fibrous dysplasia, Paget's disease, osteomalacia, and osteoporosis.
- Generalized loss or reduction of lamina dura.
- Loss of cortical bone thickness at the inferior border and angle of the mandible.
- Lytic bone cysts (brown tumors) may be seen in the jaws.
- Teeth appeared to be floating in air.
- Widening of periodontal ligament space around teeth correlated with serum PTH level.
- Dental pulp chamber was narrowed, calcified (pulp stone).
- Calcifications of soft tissues or salivary glands.
Serum parathyroid hormone (normal range 15-65 pg/ml) and calcium (normal range 9-11 mg/dl)
The gold standard of diagnosis is the parathyroid immunoassay. Once an elevated PTH has been confirmed, goal of diagnosis is to determine whether the HPT is primary or secondary in origin by obtaining a serum calcium level). Very high serum calcium level due indicate primary HPT. Whereas, low or normal calcium level may indicate secondary HPT.
Tertiary HPT has a high PTH and high serum calcium. It is differentiated from primary HPT by a history of chronic kidney failure and secondary HPT.
Serum phosphate (normal range: 2.4-5 mg/dl)
In primary HPT, serum phosphate levels are abnormally low as a result of decreased renal tubular phosphate reabsorption. However, this is only present in about 50% of cases, as dietary intake also influences phosphate level. This contrasts with secondary HPT, in which serum phosphate levels are generally elevated because of renal disease.
Alkaline phosphatase (normal range 500-750 IU/L)
Alkaline phosphatase levels are usually elevated in HPT. In primary hyperthyroidism, levels may remain within the normal range, however, this is "inappropriately normal" given the increased levels of plasma calcium.
Dental management of the patient with hyperparathyroidism
The clinical management of these patients does not require any special consideration. We should know that there is a higher risk of bone fracture, so we must take precaution in surgical treatments. It is important to recognize the presence of the brown tumor and to perform a correct differential diagnosis so as not to conduct an inadequate treatment.
The treatment of HPT is the first step in the management of the brown tumor, as spontaneous regression of the lesion often occurs. However, several cases of brown tumor that did not disappear or even grew after normalization of PTH level have been reported. In these cases, brown tumor resection should be the preferred treatment. ,,,,
Jaw enlargement is treated by recontouring of the maxilla and mandible. A three-dimensional reconstruction of the computed tomography (CT) scan was helpful in evaluating the facial deformities and in treatment planning. 
A thorough clinical and radiographic examination is essential before providing endodontic treatment. The sequence of diagnostic procedures must begin with a well-organized review of the medical history. There are a number of systemic diseases that can cause bone lesions throughout the body. In some instances, these lesions appear in the periapical region of teeth and can lead to a misdiagnosis of a lesion of endodontic origin. ,, The finding of periapical radiolucency on a radiograph should not automatically lead to access opening and root canal therapy by the dentist.
| Role of Dentist|| |
The dentist plays important role in the detection of HPT. Occasionally, the first sign of the disease may be a cyst in the jaw. The disease should be considered by the dentist whenever single or multiple radiolucencies are observed on radiography of the jaw.
Oral manifestations and dental radiographs of jaws are of value in early detection of secondary HPT due to renal osteodystrophy.
| Hypoparathyroidism|| |
Hypoparathyroidism is a metabolic disorder characterized by low serum calcium and high serum phosphorus concentrations due to a deficiency or absence of PTH secretion.
It may also develop as an isolated entity of unknown etiology (idiopathic), or in combination with other disorders such as autoimmune diseases or developmental defects. 
In primary hypoparathyroidism, parathyroid gland is either not present or atrophied or do not function normally or damage to parathyroid gland after surgical excision (acquired hypoparathyroidism). As a consequence, the concentration of PTH in the serum is often low.
In pseudohypoparathyroidism (PHP), parathyroid gland function is normal, but kidneys fail to respond to PTH due to deficient receptor. As a result, the parathyroid glands secrete the hormone in excess, and serum-PTH is increased.
Sign and symptoms
There is wide variation in the severity of symptoms. Hypoparathyroidism can cause hypocalcemia with consequent circumoral numbness, paresthesias of distal extremities (finger and toes), muscle pain, abdominal pain or muscle cramping which can progress to spasm or tetany. Laryngospasm or bronchospasm and seizures may also occur.
Disorders of ectodermal tissues are also common in these patients. These disorders include alopecia, loss of axillary and pubic hair, coarsening of body hair, scaling of the skin, deformities of the nails. 
Increased neuromuscular irritability (due to hypocalcemia) may be demonstrated by eliciting a Chvostek or Trousseau sign. In positive Chvostek's sign tapping, the facial nerve at its point of origin (anterior to ear tragus) will cause spasm of facial musculature particularly of the lip and the alae of the nose. In Tousseau's sign Carpal, spasm occurs after inflation of the blood pressure cuff.
In PHP certain skeletal and development, abnormalities are generally present, e.g., a round face, short stature, obese, ectopic soft tissue ossification, cataract and short hands and feet due to irregular shortening of the small tubular bones. There is a considerable reduction in the length of the 3 rd and 4 th fingers and toes. In addition, memory loss and mental deficiency are usually seen. These specific pattern of physical findings called as Albright hereditary osteodystrophy (because kidney responds as if PTH are absent). 
The two most frequent dental abnormalities are enamel hypoplasia (enamel is thin), delayed eruption, and there may be multiple unerupted teeth.
Teeth appear dull white in color with hypoplastic pitting. Crowns are small (microdontia) and the roots are often short with blunt ends. In some teeth, roots are malformed, resulting from nontreated hypocalcemia during the developmental phase of the dentition. A delay or cessation of dental growth and development, a full complement of teeth is not always developed, premolars being the teeth most usually missing (hypodontia). The teeth may show ankylosis, the jaws are generally short and wide with high arch palate. Severe dental caries is usually noted in the deciduous and permanent teeth, the teeth are lost early due to caries.
There may be chronic candidiasis of the oral mucosa and nail, paresthesia of the tongue or lips, and facial twitching can occur. ,,,,
Radiographically there is thickening of the lamina dura, widened root canal, and poorly calcified dentine with multiple resorptions in the cementum. The pulp chambers are large, often nearly occluded by calcified deposits (dental pulp calcifications).
In primary hypoparathyroidism, serum calcium and PTH are low, serum phosphate level is high and alkaline phosphatase is normal.
In PHP serum calcium is low, PTH is high or normal.
The main treatments available for these patients is Vitamin D or its analogs, calcium salts and drugs that increase renal tubular resorption of calcium, to obtain adequate, but low, normal serum calcium levels. 
Dental management of the patient with hypoparathyroidism
These patients have more susceptibility to caries because of dental anomalies. Dental management will be the prevention of caries with periodic check-up, advice regarding diet and oral hygiene instructions. Before performing the dental treatment, serum calcium levels should be determined. They must be above 8 mg/100 ml to prevent cardiac arrhythmias, seizures, laryngospasms or bronchospasms.
Due to enamel hypoplasia there is an increase chance of dental caries. As pulp chamber are large caries, easily involve the pulp causing pulpitis, requiring endodontic treatment. Pulp calcification and malformed root cause difficulty in endodontic treatment. Ankylosis causes difficulty in extraction. Delayed eruption and hypodontia cause malposition and has to be treated by orthodontics.
| Role of Dentist|| |
Dental aspects of hypoparathyroid disease often have been overlooked. Dental disturbances were most severe and frequent in the pseudohypoparathyroid group. Hypoparathyroid conditions are easily accessible to treatment, but often undiagnosed for years. Therefore, the dental observation of severe disturbances in tooth formation and eruption pattern may be of crucial importance and should lead to further medical investigation.
| References|| |
Lorenzo-Calabria J, Grau D, Silvestre FJ, Hernández-Mijares A. Management of patients with adrenocortical insufficiency in the dental clinic. Med Oral 2003;8:207-14.
Magalhães DP, Osterne RL, Alves AP, Santos PS, Lima RB, Sousa FB. Multiple brown tumours of tertiary hyperparathyroidism in a renal transplant recipient: A case report. Med Oral Patol Oral Cir Bucal 2010;15:e10-3.
Triantafillidou K, Zouloumis L, Karakinaris G, Kalimeras E, Iordanidis F. Brown tumors of the jaws associated with primary or secondary hyperparathyroidism. A clinical study and review of the literature. Am J Otolaryngol 2006;27:281-6.
Hougardy DM, Peterson GM, Bleasel MD, Randall CT. Is enough attention being given to the adverse effects of corticosteroid therapy? J Clin Pharm Ther 2000;25:227-34.
Sutbeyaz Y, Yoruk O, Bilen H, Gursan N. Primary hyperparathyroidism presenting as a palatal and mandibular brown tumor. J Craniofac Surg 2009;20:2101-4.
Carl W. Chronic renal disease and hyperparathyroidism: Dental manifestations and management. Compendium 1987;8:697-9, 702, 704.
Silverman S Jr, Ware WH, Gillooly C Jr. Dental aspects of hyperparathyroidism. Oral Surg Oral Med Oral Pathol 1968;26:184-9.
Bissada NF, el-Mostehy MR. Hyperparathyroidism. Pathogenesis, diagnosis and oro-dental manifestations. Egypt Dent J 1968;14:226-34.
Silverman S Jr, Gordan G, Grant T, Steinbach H, Eisenberg E, Manson R. The dental structures in primary hyperparathyroidism. Studies in forty-two consecutive patients. Oral Surg Oral Med Oral Pathol 1962;15:426-36.
Bridge AJ. Primary hyperparathyroidism presenting as a dental problem. Br Dent J 1968;124:172-6.
Venkatesh KV, Nandini VV. Periapical radiolucency not requiring endodontic therapy: An unusual case. Indian J Dent Res 2009;20:126-8.
Loushine RJ, Weller RN, Kimbrough WF, Liewehr FR. Secondary hyperparathyroidism: A case report. J Endod 2003;29:272-4.
Frankenthal S, Nakhoul F, Machtei EE, Green J, Ardekian L, Laufer D, et al.
The effect of secondary hyperparathyroidism and hemodialysis therapy on alveolar bone and periodontium. J Clin Periodontol 2002;29:479-83.
Michiwaki Y, Michi K, Yamaguchi A. Marked enlargement of the jaws in secondary hyperparathyroidism - A case report. Int J Oral Maxillofac Surg 1996;25:54-6.
Bakathir AA, Margasahayam MV, Al-Ismaily MI. Maxillary hyperplasia and hyperostosis cranialis: A rare manifestation of renal osteodystrophy in a patient with hyperparathyroidism secondary to chronic renal failure. Saudi Med J 2008;29:1815-8.
Vigneswaran N. Oral and maxillofacial pathology case of the month. Renal-osteodystrophy induced macrognathia. Tex Dent J 2001;118:570-1, 582.
Antonelli JR, Hottel TL. Oral manifestations of renal osteodystrophy: Case report and review of the literature. Spec Care Dentist 2003;23:28-34.
Dinkar AD, Sahai S, Sharma M. Primary hyperparathyroidism presenting as an exophytic mandibular mass. Dentomaxillofac Radiol 2007;36:360-3.
Parbatani R, Tinsley GF, Danford MH. Primary hyperparathyroidism presenting as a giant-cell epulis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1998;85:282-4.
Padbury AD Jr, Tözüm TF, Taba M Jr, Ealba EL, West BT, Burney RE, et al.
The impact of primary hyperparathyroidism on the oral cavity. J Clin Endocrinol Metab 2006;91:3439-45.
Prado FO, Rosales AC, Rodrigues CI, Coletta RD, Lopes MA. Brown tumor of the mandible associated with secondary hyperparathyroidism: A case report and review of the literature. Gen Dent 2006;54:341-3.
Nair PP, Gharote HP, Thomas S, Guruprasad R, Singh N. Brown tumour of the jaw. BMJ Case Rep 2011;pii: bcr0720114465.
Rai S, Bhadada SK, Rattan V, Bhansali A, Rao DS, Shah V. Oro-mandibular manifestations of primary hyperparathyroidism. Indian J Dent Res 2012;23:384-7.
Andreades D, Belazi M, Antoniades D. Diagnosis of a maxillary brown tumor associated with hyperparathyroidism secondary to chronic renal failure - A case report. Oral Health Prev Dent 2004;2:143-7.
Angadi PV, Rekha K, Shetty SR. "An exophytic mandibular brown tumor": An unusual presentation of primary hyperparathyroidism. Oral Maxillofac Surg 2010;14:67-9.
Vardhan BG, Saraswathy K, Koteeswaran D. Primary hyperparathyroidism presenting as multiple giant cell lesions. Quintessence Int 2007;38:e342-7.
Sagliker Y, Acharya V, Ling Z, Golea O, Sabry A, Eyupoglu K, et al.
International study on Sagliker syndrome and uglifying human face appearance in severe and late secondary hyperparathyroidism in chronic kidney disease patients. J Ren Nutr 2008;18:114-7.
Uzel A, Uzel I, Sagliker Y, Yildiz I, Halvaci I, Paylar N, et al.
Cephalometric evaluation of patients with Sagliker syndrome: Uglifying human face appearance in severe and late secondary hyperparathyroidism in chronic renal failure patients. J Ren Nutr 2006;16:229-32.
Aldred MJ, Talacko AA, Savarirayan R, Murdolo V, Mills AE, Radden BG, et al.
Dental findings in a family with hyperparathyroidism-jaw tumor syndrome and a novel HRPT2 gene mutation. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006;101:212-8.
Asaumi J, Aiga H, Hisatomi M, Shigehara H, Kishi K. Advanced imaging in renal osteodystrophy of the oral and maxillofacial region. Dentomaxillofac Radiol 2001;30:59-62.
Scutellari PN, Orzincolo C, Bedani PL, Romano C. Radiographic manifestations in teeth and jaws in chronic kidney insufficiency. Radiol Med 1996;92:415-20.
Ganibegovic M. Dental radiographic changes in chronic renal disease. Med Arh 2000;54:115-8.
Houston JB, Dolan KD, Appleby RC, DeCounter L, Callaghan NR. Radiography of secondary hyperparathyroidism. A case of hyperparathyroidism resulting from chronic glomerulonephritis. Oral Surg Oral Med Oral Pathol 1968;26:746-50.
Fernández-Sanromán J, Antón-Badiola IM, Costas-López A. Brown tumor of the mandible as first manifestation of primary hyperparathyroidism: Diagnosis and treatment. Med Oral Patol Oral Cir Bucal 2005;10:169-72.
Martínez-Gavidia EM, Bagán JV, Milián-Masanet MA, Lloria de Miguel E, Pérez-Vallés A. Highly aggressive brown tumour of the maxilla as first manifestation of primary hyperparathyroidism. Int J Oral Maxillofac Surg 2000;29:447-9.
Yamazaki H, Ota Y, Aoki T, Karakida K. Brown tumor of the maxilla and mandible: Progressive mandibular brown tumor after removal of parathyroid adenoma. J Oral Maxillofac Surg 2003;61:719-22.
Kelly A, Pomarico L, de Souza IP. Cessation of dental development in a child with idiopathic hypoparathyroidism: A 5-year follow-up. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2009;107:673-7.
Sarkar S, Mondal M, Das K, Shrimal A. Mucocutaneous manifestations of acquired hypoparathyroidism: An observational study. Indian J Endocrinol Metab 2012;16:819-20.
Wilson LC, Trembath RC. Albright's hereditary osteodystrophy. J Med Genet 1994;31:779-84.
Takeuchi H, Hioki H, Ishikura Y, Tomizawa M, Noda T, Fukushima M. Dental findings in a case of idiopathic hypoparathyroidism. Shoni Shikagaku Zasshi 1989;27:678-91.
Hansted C, Holst G. Changes in dental tissue in hypoparathyroidism. Acta Odontol Scand 1952;10:71-4.
Goepferd SJ, Flaitz CM. Enamel hypoplasia associated with congenital hypoparathyroidism. Pediatr Dent 1981;3:196-200.
Jensen SB, Illum F, Dupont E. Nature and frequency of dental changes in idiopathic hypoparathyroidism and pseudohypoparathyroidism. Scand J Dent Res 1981;89:26-37.
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