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© Borgis - New Medicine 4/2020, s. 135-142 | DOI: 10.25121/NewMed.2020.24.4.135
*Magdalena Sobecka-Frankiewicz1, Ireneusz Nawrot2, Laretta Grabowska-Derlatka3, Agnieszka Mielczarek1
Oral changes in secondary to chronic kidney disease hyperparathyroidism
Zmiany w jamie ustnej wywołane wtórną nadczynnością przytarczyc w przebiegu przewlekłej choroby nerek
1Department of Conservative Dentistry and Endodontics, Medical University of Warsaw, Poland
Head of Department: Professor Agnieszka Mielczarek, MD, PhD
2Department of General, Vascular and Transplantation Surgery, Medical University of Warsaw, Poland
Head of Department: prof. Sławomir Nazarewski MD, PhD
32nd Department of Radiology, Medical University of Warsaw, Poland
Head of Department: prof. Olgierd Rowiński MD, PhD
Streszczenie
Najczęstszą przyczyną wtórnej nadczynności przytarczyc jest przewlekła choroba nerek. Zaburzenie równowagi pomiędzy wapniem, fosforem i witaminą D3 w przebiegu wtórnej nadczynności przytarczyc może wpływać na stan zdrowia jamy ustnej. Zmiany te objawiają się w kościach szczęk jako utrata gęstości kości, ogniska demineralizacji, a nawet jako duże guzy zniekształcające okolicę twarzoczaszki – guzy brunatne, włókniaki kostniejące i torbiele kostne. Obserwuje się również zwiększone występowanie próchnicy, chorób przyzębia i infekcji grzybiczych. Wtórna nadczynność przytarczyc w młodym wieku może powodować zaburzenia rozwoju zębów i nieprawidłowości zębowe. Leczenie stomatologiczne u pacjenta z wtórną nadczynnością przytarczyc może być wyzwaniem dla lekarza stomatologa, dlatego konieczna jest ścisła współpraca z lekarzem prowadzącym, a także jak najszybsze wprowadzenie profilaktyki stomatologicznej. Dodatkowo, ze względu na występowanie charakterystycznych zmian w jamie ustnej, stomatolog może odegrać istotną rolę w pierwotnym wykrywaniu wtórnej nadczynności przytarczyc.
Summary
The most common cause of secondary hyperparathyroidism is a chronic kidney disease. The imbalance between calcium, phosphorus and vitamin D3 in the course of secondary hyperparathyroidism may affect an oral health. The changes are presented in jaw bones as a loss of bone density, focuses of demineralization or even large tumors deforming facial region – brown tumors, ossifying fibromas and aneurismal bone cysts. There is also a higher frequency of dental caries, periodontal disease and fungal infections. Secondary hyperparathyroidism in the young age may cause teeth development disorders and dental abnormalities. Dental treatment in patient with secondary hyperparathyroidism can be a challenge for a dentist, so the strict cooperation with an attending physician is needed, as well as to introduce dental prophylactic procedures as soon as possible. In addition, due to the occurrence of characteristic changes in the oral cavity, the dentist may play an important role in the primary detection of secondary hyperparathyroidism.
Introduction
Hyperparathyroidism occurs in about 0.05 to 0.10% of the population. Mostly affects women (3 times more often than men), mainly in middle age (30-60 years) (1-3). Hyperparathyroidism is a condition connected with an overproduction of parathyroid hormone that increases calcium concentration in the blood by potentiating its absorption from bones and kidneys. Secondary hyperparathyroidism is an over-secretion of parathyroid hormone caused by a decreased level of blood calcium. The most common cause is a chronic renal insufficiency, which is estimated at 8-16% of the population (4, 5). Other causes may relate to other kidney diseases, malabsorption syndrome, and reduced vitamin D3 production (2, 3). The basis for secondary hyperparathyroidism is the insufficient conversion of vitamin D3 to its active form the lack of second hydroxylation of cholecalciferol in renal tubules by 1-alpha-hydroxylase (OH) D3 and inadequate removal of phosphates by inefficient kidneys, what as a consequence decreases the serum calcium level. Compensatory the parathyroid size and hormone secretion is increased and hyperparathyroidism occurs (6). Parathyroid hormone works primarily on the bones and kidneys, where it causes increased calcium absorption and additionally in kidneys reduces the phosphorus absorption and increases production of the active form of vitamin D3 (1, 7, 8). In the case of secondary hyperparathyroidism caused by chronic kidney disease, the onset of the disorder is associated with changes in calcium, vitamin D and phosphate levels what affects the bones and soft tissues. Therefore, are often defined as the CKD-MBD syndrome (chronic kidney disease – mineral and bone disorder syndrome) (9). Another syndrome, described in secondary hyperparathyroidism, is the Sagliker syndrome, noticed for the first time in severe chronic kidney disease. Its frequency among people with chronic kidney disease is about 0.5%. Its occurrence is associated with the destructive effect of hyperparathyroidism at a young age. This syndrome includes: facial deformity, short stature, jaw bone lesions, teeth malocclusion – 2nd class, dental abnormalities, fingertip changes, scapula and collarbone deformities and hearing, neurological and psychological disorders. There is also a higher rate of early mortality (10-15).
Due to the influence of calcium, phosphorus and vitamin D3 on oral health, their imbalance in the course of secondary hyperparathyroidism can be important in functioning masticatory system. In addition, the impact of hyperparathyroidism on the dysfunction of internal organs may also be presented as changes in the oral cavity.
Symptomatology
The earliest symptoms in the oral cavity are jaw bone lesions. In most cases the changes are painless and accidentally found on extra- and intraoral radiographs, although sometimes patients report vague discomfort in the mandibular area, rarely in the maxilla (2, 16, 17) (fig. 1-4).
Fig. 1. CT exam, transverse projection. Bone changes – osteosclerosis present in cranial basis area
Fig. 2. CT exam, transverse projection of maxilla. Osteosclerosis and erosions (arrow)
Fig. 3. CT exam, coronal projection of maxilla. Bone changes – osteosclerosis
Fig. 4. CT exam, sagital projection of maxilla. Bone changes: osteosclerosis and erosions (arrows)
There is a generalized loss of bone density that results in blurring of the characteristic trabecular pattern with an appearance of ground glass (18-21). In about 10% of patients with hyperparathyroidism there is also a loss of lamina dura of the jaw bone. Rarely, jaw hyperplasia and jaw and facial bones enlargement may occur (1, 9, 16, 22).
Changes in the bones have a direct effect on the teeth, causing gradual loosening, displacement, and eventually tooth loss (1, 2, 23, 24). Malocclusion and chewing difficulties appear due to teeth’s hypersensitivity to occlusal forces and percussion. The influence of secondary hyperparathyroidism on the dentition is also seen in the x-rays as a narrowing and calcifications in the pulp chambers as well as denticuli inside it. There is also seen enlargement of the periodontal ligament around the roots what visibly correlates with parathyroid hormone levels (2-4, 22, 25, 26). Hyperparathyroidism is also a favorable factor of occurrence, especially multiple, of internal and external resorptions of the teeth (27, 28).
Hyperparathyroidism may be manifested by changes in the development of the dentition, such as alterations in dental eruption or dental abnormalities. Studies show that modifications of calcium, phosphorus, and parathyroid hormone levels can contribute to the defects in the formation of the teeth and alveolar processes (2, 29).
High levels of parathyroid hormone can affect periodontal tissues and may worsen the course of periodontal disease by increasing the production of pro-inflammatory cytokines (30-32). However, some studies indicate for the lack of significant effects of secondary hyperparathyroidism on periodontal disease indicators and radiologically evaluated alveolar bone level (30, 33).
Secondary hyperparathyroidism is associated with a presence of single or multiple focuses of bone osteolysis. They are most commonly found as brown tumors, in advanced form called osteitis fibrosa cystica or von Racklinghausen’s bone disease (21, 26, 34). These lesions usually appear as a late manifestation of the disease. Brown tumor is a focal, sinus-like bone destruction with the presence of caverns filled with connective tissue. Coalescence of bone lesions with bone marrow cavities causes bleeding and thus their brown coloration by blood hemosiderin (19, 21, 35, 36). Histologically, the brown tumor may be indistinguishable from the peripheral gigantocellularis granuloma (19, 37). It may achieve extreme sizes that may be mimicking the brown tumor is found in 1.5-1.7% of patients with secondary hyperparathyroidism (1, 4, 7), but also, even more likely (4.5%), may affect patients with primary hyperparathyroidism (7, 38, 39). In most cases, equalizing of parathyroid hormone levels cause spontaneous withdrawal of the tumor (36, 37, 40), but in some cases, despite the hormonal regulation, there is still need for surgical resection of the lesion (2, 22). Corticosteroids are also used to reduce the tumor mass before its resection (7).

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otrzymano: 2020-11-06
zaakceptowano do druku: 2020-11-27

Adres do korespondencji:
*Magdalena Sobecka-Frankiewicz
Zakład Stomatologii Zachowawczej Warszawski Uniwersytet Medyczny
ul. Binieckiego 6, 02-097 Warszawa
tel.: +48 (22) 116-64-46
magsobecka@gmail.com

New Medicine 4/2020
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