Oral cancer

Most oral cancers are derived from squamous cells usually found in the area of the lower third molar or on the tongue (lateral and ventral border), floor of the mouth, or soft palate. Survival is only about 50% at five years; therefore early detection is essential for referral and treatment. Although white patches on the mucosa are always suspect, many oral cancers appear as a combination of white and red lesions, often ulcerated, with variable levels of discomfort. Ask the patient to remove his or her dentures to allow examination of the tissues beneath the prosthesis. Even ulcers you believe are due to denture-related irritation should be considered suspect until proven otherwise. All such lesions should be biopsied for diagnosis; the best survival rates are achieved with early surgical intervention. Cofactors in the development of oral cancer include male gender, age older than 40 years, and tobacco and ethyl alcohol use. These factors in concert can raise the risk to very significant levels.

Bisphosphonate-associated osteonecrosis of the jaw

Evidence has been presented, generally through case histories, regarding bisphosphonate-associated osteonecrosis (BON) of the jaw, a chronic, often painful condition that is resistant to treatment and resolution (Figure 2). The use of bisphosphonates to inhibit osteoclastic activity in patients with metastatic bone cancer and osteoporosis is a standard treatment approach. Such IV bisphosphonates as zoledronate (Zometa, Reclast) and pamidronate (Aredia) are commonly prescribed to prevent the spread of cancer cells and control hypercalcemias in malignancies. The cumulative incidence of BON is 0.8%-12% for patients on IV bisphosphonates. The jaw bones are more susceptible because of high bone turnover rates in the mandible (2.5-10 times those in the tibia). The long half-life of bisphosphonates and the disruption of vascular beds
appear to be contributing factors.

Continue Reading

Figure 2. Osteonecrosis of the jaw's maxillary archBON can occur spontaneously, or it can be triggered by oral surgery, periodontal surgery, or periodontal disease. Comorbid factors include chemotherapy, steroid therapy, periodontal disease, diabetes mellitus, smoking, and poor oral hygiene. Although lesions are more prevalent in the mandible, one third of BON cases occur in the maxilla. The intraoral presentation is characterized by denuded bone, lack of soft-tissue healing post surgery, and variable pain complaints. Many of the lesions do not heal even over time, and exposed, sometimes painful bone is simply tolerated in the oral cavity. Surgical intervention may not result in healing and is often contraindicated. The best therapy for BON is chlorhexidine 0.12% rinses with penicillin VK added for painful lesions. (Pain may be associated with bacterial infection, and penicillin VK remains the drug of choice for superficial oral infections.) Patients using IV bisphosphonates should avoid all elective dental surgeries.

For patients using oral bisphosphonates, the risk of BON is greatly reduced (on the order of 0.01%-0.1% incidence). Signs and symptoms, initiating events, and management are identical to those seen in patients receiving IV therapy. Patients who have taken oral bisphosphonates for up to three years appear to have no appreciable risk of developing BON. Those taking the agents for fewer than three years who have a concomitant history of corticosteroid use and those taking oral bisphosphonates for longer than three years are at risk of developing BON after dental surgery. Although the serum C-telopeptide test has been advocated to assess risk, there is no completely valid and reliable screening mechanism to predetermine a patient’s risk. The best course of action is to inform the patient of the problem, the risk, and the benefit of choosing alternatives to dental surgery whenever possible.

Cardiovascular disease

Possible connections between oral health and cardiovascular disease (CVD) focus on patients receiving warfarin (Coumadin) who require oral surgery and on those with chronic periodontal disease. It is a myth that patients taking Coumadin for atrial fibrillation, deep venous thrombosis, post cerebrovascular accident (CVA), or post MI are at very high risk for bleeding problems following oral surgery. If patients are consistently tested and remain in the therapeutic international normalized ratio range (2.0-3.0), routine oral surgery may be undertaken with no special precautions. In fact, patients who are taken off Coumadin prior to oral surgery may be placed at significant risk for embolic events or even death. Studies have shown there is no major difference in serious postoperative bleeding between patients who receive anticoagulants and those who do not. In most cases, no change in the strength of anticoagulation is required.

In patients with chronic periodontitis, the link to systemic disease is believed to be an extension of the continual bacterial challenge associated with the condition. Bacterial toxins and other pathogenic by-products elicit exaggerated host inflammatory responses, including localized periodontal infections. Over time, an associated low-grade, chronic inflammation in the host leads to pathologic processes in distant organs and body systems. A number of prospective, retrospective, and cross-sectional studies have attempted to quantify the relationship of periodontal disease or oral health status to CVD. Early results reported increased risks of 1.67-2.7 for MI and 3.0 for CVA in patients with periodontal disease.2-4 Only a handful of studies over the past 12 years has failed to show a significant association. Other studies have shown associations between periodontal disease and atherosclerotic plaques, C-reactive protein, and plasma fibrinogen, all known factors in CVD. The implications for the patient are obvious: Undiagnosed and untreated periodontal disease may constitute a significant CVD risk. A pertinent and poignant question clinicians should ask every patient is, “When did you last visit your dentist?”