Introduction
The extensive usage of bisphosphonates (BP) to treat a variety of illnesses has heightened awareness of their potential link to jaw osteonecrosis. Bisphosphonates are extremely effective antiresorptive medications used to treat disorders such as cancer-related ailments, osteoporosis (a bone disease that occurs when bone mineral density declines), multiple myeloma (a plasma cell malignancy), Paget disease (a condition that prevents the growth of new bone tissue to replace the old bone tissue), osteosclerosis (it indicates thickening of trabecular bone), and fibrous dysplasia (it arises when a healthy bone is replaced by aberrant fibrous tissue) that have enhanced osteoclast (bone degrading) activity. However uncommon, avascular osteonecrosis of the jaw has just lately been identified as a side effect of bisphosphonate treatment. A bone that is exposed or that can be probed through a fistula in the craniofacial region as a result of current or previous treatment with bisphosphonates (BPs) and does not heal within eight weeks is known as bisphosphonate-related osteonecrosis of the jaw.
What Is Bisphosphonate?
A class of medications known as bisphosphonates act to stop the loss of bone density. These medications are the ones used to treat osteoporosis (a bone disease that occurs when bone mineral density declines) most frequently. They have two phosphonate groups, which is why they are known as bisphosphonates. In the current pharmacological arsenal, bisphosphonates are the main treatments for osteoclast-mediated bone loss caused by osteoporosis, Paget disease of the bones, cancers that have spread to the bones, multiple myeloma, and hypercalcemia of malignancy.
Due to their affinity for hydroxyapatite crystals, bisphosphonates have an extremely high affinity for bone minerals. Therefore, hydroxyapatite binding sites are necessary for bisphosphonate skeletal retention. As frequently the case in circumstances marked by increased skeletal turnover, bisphosphonates are preferentially absorbed into regions of active bone remodeling. Renal excretion quickly removes bisphosphonates from the bloodstream that are not kept in the skeleton. In addition to preventing calcification, bisphosphonates also prevent the breakdown of hydroxyapatite, effectively preventing bone resorption.
What Is Osteonecrosis?
A lack of blood supply leads to osteonecrosis, which is the death of bones. However, other big joints like the knee, elbow, wrist, and ankle can also be affected. It most frequently affects the hip and shoulder. When a bone dies because it lacks blood supply, it develops osteonecrosis. The bone may finally fall out over time. The joint deteriorates and develops severe arthritis if osteonecrosis is not treated. Osteonecrosis can be brought on by illness or severe trauma, such as a fracture or dislocation, that compromises the blood supply to the bone. Even without an illness or injury, osteonecrosis can happen. As it has no recognized etiology, this condition is idiopathic.
What Causes Bisphosphonates Related Osteonecrosis?
Bisphosphonates reduce bone resorption by inducing death in osteoclast cells, reducing the osteoclast's resorptive capacity, and preventing osteoclast development. They are highly voracious for bone minerals and concentrate mostly in the areas where osteoclasts are active. Without resorption and the creation of new bone, old bone endures past its prime, and its capillary network is not preserved, resulting in avascular necrosis of the jaw. Additionally, the toxicity of soft tissue and bone cells caused by high-potency bisphosphonates can cause necrosis, which is aggravated by infection. Delays in the mouth's mucosal opening's epithelial closure as a result of disrupted wound healing cause persistent infection and bone deterioration. The jaw experiences osteonecrosis because it remodels more quickly than other bones, rendering it more vulnerable to bisphosphonates' effects.
What Regions Are Most Prone to Bisphosphonates-Related Osteonecrosis?
Mandibular osteonecrosis is more common than maxillary osteonecrosis. Due to its higher bone turnover rate, which depends on osteoclast-related remodeling brought on by occlusion and pressure and tension forces from wearing dentures, it almost invariably starts in the alveolar bone. Nonhealing dentoalveolar sites, traumatic palatal and mandibular tori, and exposed areas of the mylohyoid ridge are the most often impacted locations.
The likelihood of bisphosphonates induced osteonecrosis of the jaw rises when:
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Intravenous bisphosphonates with higher nitrogen concentrations.
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Increased dosage and lengthened duration.
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Cancer patients who have bone metastases.
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Rapid bone turnover regions, such as the mandibular alveolar bone.
Which Are the Risk Factors Associated With Bisphosphonates Related Osteonecrosis?
Osteonecrosis of the jaw brought on by bisphosphonates is influenced by a number of factors, including:
1) The use of dentures, periodontal surgery, oral implant insertion, and other invasive oral procedures raises the risk of osteonecrosis and the rate of bone turnover.
2) Comorbidities include hypertension, hyperlipidemia, cancer, chemotherapy, low hemoglobin levels, diabetes mellitus, renal dialysis, and cancer.
3) Corticosteroids and H2 blockers promote bisphosphonates absorption. Antiangiogenic medicines, particularly Sunitinib and Bevacizumab.
4) It is unknown whether osteonecrosis occurs before or after the infection. However, bone resorption and necrosis have been linked to polymorphonuclear aggregates and bacterial microfilm in the surrounding tissue.
5) Increasing age, alcohol and cigarette use, and genetic predisposition are additional risk factors.
Which Are the Symptoms Associated With Bisphosphonates-Related Osteonecrosis?
The following symptoms may appear
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Pain.
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Swelling.
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Cellulitis (bacterial infection of the skin).
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Halitosis (bad breath).
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Trismus (difficulty in opening a mouth).
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Infection of the soft tissues is accompanied by inflammation, ulceration, and suppuration.
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Development of fistulas and intra and extraoral sinus tracts.
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A fracture that causes paresthesia or anesthesia.
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Chronic maxillary sinusitis.
Which Are the Treatment Modalities Associated With Bisphosphonates Related Osteonecrosis?
The following nonsurgical treatments are possible for bisphosphonates-related osteonecrosis:
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Antibacterial mouthwash.
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Systemic antibiotics.
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Topical or systemic antifungals.
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Treatment with bisphosphonates is stopped.
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Minimally invasive or no dental care (that is, root canal therapy instead of extraction).
Due to the compromised bone's capacity to repair, surgical intervention for bisphosphonate-related osteonecrosis of the jaw is occasionally used. As determined by the American Association of Oral and Maxillofacial Surgeons, patients with the stage III form of the illness undergo surgical debridement or resection (AAOMS).
Conclusion
Patients who have undergone oral and intravenous bisphosphonate medication for various bone-related disorders are at risk for developing bisphosphonate-related osteonecrosis of the jaw. Exposure to non-viable bone affecting the maxillofacial tissues is a symptom of bisphosphonate-related osteonecrosis of the jaw. It is believed that trauma to dentoalveolar tissues, which are affected by the effects of bisphosphonate therapy, results in osteonecrosis of the jaw that is associated with bisphosphonates. To know more about this condition, consult the doctor online.
