What is osteonecrosis in the jaws?

The osteonecrosis of the jaws It is a rare clinical entity, which is associated with an alteration of the blood supply or an inhibition of bone formation and an increase in the death of osteocytes.

Formerly it was thought that osteonecrosis was related to diseases such as systemic lupus erythematosus, a type of anemia or Caisson’s disease. But nowadays recent scientific publications have shown that patients taking bisphosphonates also had osteonecrosis.

Bisphosphonates are a group of drugs that are widely used in a large number of metabolic bone diseases, some of them very common in the elderly population, such as osteoporosis.

The etiology of osteonecrosis of the jaws is not known, but a series of factors that may be related to the disease have been described. In a percentage of more than 95% of patients with osteonecrosis of the jaws, there is a neoplasm as the underlying disease. High-dose bisphosphonates inhibit cell proliferation and low bone turnover. The action of bisphosphonates works by inhibiting the activity of bone remodeling cells. Bisphosphonates not only act at the bone level but also in other cells, such as in soft tissues. It is possible that osteonecrosis of the jaws is a multifactorial disease, that is, in which multiple factors intervene for its appearance.

Osteonecrosis of the jaws is classified into three main stages:

  • Stage I. At this stage, there is the presence of exposed or necrotic bone in patients with no symptoms without evidence of infection.
  • Stage II. The presence of exposed or necrotic bone in patients causes pain and signs of infection.
  • Stage III. There is exposed or necrotic bone in patients with pain, infection, and signs such as fracture, fistula, or osteolysis.

What are the treatments and solutions for osteonecrosis of the jaw?

Osteonecrosis of the jaws is treated according to the stage to which it belongs.

In stage number one, there is a necrotic bone exposure but no infection. The treatment is based on the millimetric quantification of the size of the exposure, the suspension of the bisphosphonate, the regimen of a chlorhexidine mouthwash for two weeks and controls at 15 days and one month.

If the stage is number two, the guidelines are the same and the oral administration of antibiotics is added for 15 days along with oral anti-inflammatories.

In the third and final stage, the therapy applied is the same as in stage two, but also, bone sequestration is eliminated under local anesthesia and, if necessary, the teeth involved. Finally, the same controls are followed as in the other stages.

Conclusion

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