Alveolar Bone is a bone of the jaw containing the tooth sockets on bones that help in holding the teeth. The alveolar process comprises of the region of the compact bone attached to cementum of the roots by periodontal ligaments (D’Astous, 2015). As is the case with other bone in the human body, alveolar bone is also modified all through one’s life, however, due to impacts of various external factors, it might suffer the process of the bone formation or even bone resorption. According to Kakade et al., (2015), the periodontium supports teeth during their function, and it often depends on stimulation that it tends to receive the role for the preservation of its structure. Based on this, it is evident that a permanent balanced condition often exists between the external forces and the periodontal structures.
The alveolar bone tends to undergo a constant physiologic remodelling as a response to the external forces such as occlusal forces. The bone is thus removed from an area where it might not be needed and then added to regions where it is demanded, but secondary hyperparathyroidism prevents this process from occurring affecting the alveolar bone (Nikodimopoulou & Liakos, 2011). Secondary hyperparathyroidism has been shown to cause increased risks of the alveolar bones as a result of the excessive secretion of the parathyroid hormone. A patient with kidney illness which is the causal factor of secondary hyperparathyroidism might develop bone diseases resulting to alveolar bone pain, weakness and even fracture that often results for the malfunction of the kidney to sustain normal calcium and the phosphate levels.
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However, in cases of a severe secondary hyperparathyroidism, bone pain or even deformity might occur, substantially affecting periodontium and alveolar bone. According to Kakade et al., (2015), periodontal diseases often are caused by bacteria from a dental plague such as secondary hyperparathyroidism. In cases of bacterial infection, the primary barrier is always the gum, but the infection tends to gradually progress to alveolar bone and the periodontal ligament that entails the gradual alveolar bone loss in the teeth causing them to loosen or even fall off.
According to Kakade et al., (2015), patients diagnosed with chronic kidney disease which is the leading cause of secondary hyperparathyroidism shows the broader range of oral signs affecting both soft and hard tissues including jaw bones’ radiographic change, calculus accumulation on the teeth and periodontitis. The overall dialysis’ period might impact the pervasiveness of oral abnormality resulting in deterioration of periodontium and alveolar bone health (Nikodimopoulou & Liakos, 2011). The bone disorder is caused by a potential distorted blood level of phosphorus and calcium in response to the lack of vitamin D activation by the kidney promotes secondary hyperparathyroidism’s development. It further, contributes to the loss of alveolar bone through changing remodelling of the normal skeletal and supporting growth of intraosseous lesions such as a brown tumour.
Due to the lack of the vitamin D deficiency that causes secondary hyperparathyroidism, symptoms are often from vitamin deficiency such as muscle weakness, increased the possibility of bone fractures in addition to the lack of bone mineralization. Secondary hyperparathyroidism can easily be treated medically instead of surgically. Therefore, the treatment should focus on the condition that needs to be addressed rather than directly focusing on secondary hyperparathyroidism itself through managing vitamin D deficit or even kidney illness’s treatment. Failure of patient’s response to this level of medical treatment, a practitioner might use calcimimetics such as Cinacalcet.
References
D’Astous, J. (2015). Periodontology: An overview of alveolar bone expansion. The Canadian Veterinary Journal , 56 (3), 295.
Kakade, S. P., Gogri, A. A., Umarji, H. R., & Kadam, S. G. (2015). Oral manifestations of secondary hyperparathyroidism: A case report. Contemporary clinical dentistry , 6 (4), 552.
Nikodimopoulou, M., & Liakos, S. (2011). Secondary hyperparathyroidism and target organs in chronic kidney disease. Hippokratia , 15 (Suppl 1), 33.
