The links between oral and systemic health

Jeffrey Astroth, DDS, MSPH
February 26, 2009

teethSome say the mouth is the body's mirror. And while associations between oral and systemic health can be made and research is on the rise, specific cause-and-effect relationships remain elusive. Life—and certainly health—are not so easily defined, packaged, and distributed.

Links have been made between oral health and cardiovascular disease, diabetes, respiratory disease, and osteoarthritis. But establishing cause and effect can be a complex and confusing process, confounded by a myriad of variables. Wherever the quest eventually leads, the basic oral health assessment is a good starting point. Remember that all clinical contacts should include protection for both your patient and yourself. This means using examination gloves, face mask, and a mirror or tongue depressor. These simple devices along with a good light source will facilitate a thorough examination.

Extraoral assessment

The examination should begin with an evaluation of the face and neck. Symmetry of the face is expected; asymmetry could be a sign of an intraoral infection or tumor manifested extraorally. Engage the patient in conversation to assess speech production and muscular function in the perioral structures. Palpate the neck for any masses or irregularities. To assess the temporomandibular joints, ask the patient to open and close his or her mandible. Pain, deviation to one side, and popping or clicking noises may all be signs and symptoms of degenerative joint disease.

A close look at the skin is particularly important during extraoral assessment. The skin should be free of ulcerated, cratered, crusted, or pigmented lesions (painful or not). Light-skinned individuals living in geographic areas of intense sun exposure and high altitude are particularly susceptible to basal cell carcinoma (BCC). The most common sites are the lower lip, top of the ear, and tip or side of the nose. Traditionally, these neoplasms have been considered slow-growing and noninvasive, but recent reports indicate that approximately 11% of BCCs are aggressive and feature deep-tissue invasion and metastasis.1 Evaluate the degree of skin hydration for clues to underlying dehydration, and investigate any bruises or discolorations by inquiring into the patient's medical and/or personal history. Last, the lips should be examined for lesions, palpated for lumps or bumps, and checked for signs of dehydration or infection.

Intraoral assessment

Inspect all aspects (dorsal, ventral, lateral) of the tongue. The tongue is normally pink to red with variable fissures on the dorsal surface. The lingual tonsils (often mistaken for neoplastic growths) are located on the posterior lateral border. The tongue, floor of the mouth, and mucosa of the cheek should appear intact, pinkish-red, and well hydrated. Ulcerated and/or discolored tissue (red or red-white) are a red flag for referral to an oral medicine or oral surgery service. Use two fingers to feel the floor of the mouth from within and outside the oral cavity, attempting to locate any mass or lump. 

Gingival tissues and the hard and soft palates should also be pink to reddish in color and firm in consistency.

The condition of the teeth may vary from absence of dental caries or filling material to serious disease and multiple missing teeth. Various restorations (e.g., crowns, veneers, bridges, partial or complete dentures, and dental implants) may be found. Most patients have a realistic grasp of their dental history and are able to provide accurate answers when questioned.

Benign soft- and hard-tissue lesions to look out for include Fordyce granules in the cheek, papillomas, fibromas, geographic tongue, trauma (e.g., burns, lacerations), and palatal and mandibular tori (i.e., outgrowths of normal bone).

Intraoral disease processes

The two most prevalent disease processes in the oral cavity are dental caries and periodontal disease. Both conditions may have profound links to severe systemic disease. Teeth may suffer dental caries so severe that the nerve has been compromised and bacteria have invaded the alveolar bone at the apex of the root(s). As these periapical abscesses expand, fluid pressure may bore through the bone and into soft tissues. From there, the infection spreads by separating fascial planes and creating, then occupying, anatomical “spaces” between fascial planes.

These so-called “space infections” constitute life-threatening episodes. An infection of the submandibular or sublingual space resulting from an abscessed lower tooth can distort the floor of the mouth and push the tongue posteriorly, causing an airway obstruction. A canine-space infection resulting from an abscessed upper canine or first bicuspid tooth has the potential for causing massive periorbital edema and obliterating the nasolabial fold. These infections may penetrate the valveless angular veins in the forehead and enter the cavernous sinus, causing thrombosis and death. Immediate surgical and antibiotic interventions (amoxicillin 500 mg daily for 10 days) are required.

decayed teethPeriodontal disease, or periodontitis (Figure 1), often begins as gingivitis but constitutes a far more serious condition. Rather than healthy, firm, pink gingival tissue, the clinician will usually notice red, edematous gingivae; exposed roots; deposits of dental plaque (oral biofilm); and calculus (tartar). These findings are accompanied by bleeding gums, purulent exudate, and halitosis. Periodontal disease is a chronic, progressive, inflammatory process. Its etiology has been traced to predominantly anaerobic gram-negative rods and spirochetes. The end point of this disease process is loss of alveolar bone, which anchors the teeth to the jaw. The result can be loose, diseased teeth that must be extracted. This inflammatory disease is a suspected source of antigens and virulence factors that circulate throughout the body.

Other soft-tissue conditions commonly encountered in the oral cavity include angular cheilitis at the commissures of the lips, usually in the elderly patient. This condition presents as cracked, weeping epithelium. Treatment consists of nystatin/triamcinolone (Mycolog II) cream or ketoconazole 2% cream to fight perioral yeast organisms.

Herpes simplex virus and recurrent intraoral herpes may cause painful ulcerated vesicles, but both conditions are self-limiting (7-14 days). OTC interventions include antiviral creams (docosanol [Abreva]) and lysine 1,000 mg t.i.d. for three to five days. Acyclovir 800 mg daily for three to five days is also helpful to accelerate healing.

Aphthous ulcers are painful, erythematous lesions with gray-yellow-white central pseudomembranes. Although these lesions are self-limiting, symptoms may be alleviated by OTC oral rinses, such as Rincinol, or prescribed medications, such as dexamethasone (Decadron) elixir one tablespoon four times daily (swish and spit), or lidocaine cream 4% (LMX 4%) applied t.i.d. to the affected area for five to seven days.

Xerostomia (dry mouth) can contribute to dental caries and uncomfortable or painful dentures. The most effective therapies are OTC enzyme products (e.g., mouthwash, toothpaste, chewing gum, oral moisturizer) from Biotene.

Oral candidiasis may present as areas of white, red, or white/red soft tissue. Causative yeast organisms are always present in the mouth but are usually kept in check. This condition may be prevalent in immunocompromised patients or on the palate beneath an ill-fitting denture. Treatment consists of such topical preparations as nystatin oral suspension or clotrimazole troches. Severe cases are usually treated with such systemic antifungals as fluconazole.

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

open mouthEvidence 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.

BON 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?”

Diabetes mellitus

Uncontrolled diabetes can reduce life expectancy by as much as 30% or more. The American Diabetes Association suggests that adult patients are within treatment goals when the hemoglobin A1c (HbA1c) is <7%. Many studies have been conducted to understand the relationship between glycemic control and periodontal disease. The question is, can a diabetic's condition be improved with healthy gums, or will it be worse with periodontal disease? A population study has shown that HbA1c >9% placed subjects at up to three times greater risk for progressive, severe alveolar bone loss (a measure of periodontal disease), and severe periodontal disease put subjects at risk for poor glycemic control.5,6 Other studies have shown that treating periodontal disease in diabetic patients with poor glycemic control significantly reduced HbA1c.7,8 The therapies included cleaning the tooth roots, antimicrobials (chlorhexidine 0.12% rinses), and doxycycline. These findings are of great clinical significance in view of the fact that periodontal disease is very amenable to treatment. They may also be expanded to attenuate some of the more severe complications of diabetes mellitus. One study has reported that patients with severe periodontal disease were at greater risk for stroke, transient ischemic attack, angina, and MI; an additional study suggested up to a 3.2-fold greater risk for ischemic heart disease and nephropathy than those without periodontal disease.9,10

Respiratory disease

Associations between periodontal disease and chronic obstructive pulmonary disease (COPD) have been investigated based on case reports of anaerobic periodontal pathogens in lung tissues. In one study of 46 cases of deadly anaerobic empyema, the most common microorganisms isolated were Fusobacterium nucleatum, Prevotella, Bacteroides, and Peptostreptococcus (all etiologic agents in chronic periodontal disease).11 These findings led to population-based studies that examined the risk of COPD in patients with periodontal disease. In one such study, adjusted for smoking status, risk of having COPD was 4.5 times greater in subjects with poor oral hygiene (high levels of oral biofilm and calculus) than for subjects with excellent oral hygiene.12 Another long-term study determined that alveolar bone loss at baseline was an independent predictor of COPD in men.13 Subjects with bone loss involving the mouth had a 60% increased risk of being a COPD patient (odds ratio 1.6). Perhaps the most compelling study of oral health and lung disease (pneumonia) was undertaken in nursing homes in Japan. This controlled study divided subjects into those who received weekly professional oral care and those with no professional care. Over the two-year follow-up, residents who attempted to maintain their own oral health were twice as likely to contract pneumonia and twice as likely to die.14

Osteoarthritis

Osteoarthritis (OA) afflicts millions of Americans and is the primary medical complaint of the elderly. Although a myriad of therapies have been advocated, no clear evidence exists to promote one safe, efficacious, long-lasting solution. Rather, most sufferers rely on systemic analgesics and/or anti-inflammatory preparations or topical analgesics. A large population-based study reported that subjects with OA reported fair to poor health three times more frequently than those without OA.15 Additionally, OA patients claimed significant limitation of normal activities, which is the foundation for the belief that many OA patients have reduced ability to perform adequate oral hygiene. By extension, these patients are at risk for poor oral health status and periodontal disease as well as for subsequent interactions with CVD, diabetes, and the respiratory system.

Clinician and patient responsibilities

Although researchers have not yet confirmed specific cause-and-effect relationships between oral health and systemic disease, studies are ongoing. In the meantime, it is imperative that clinicians educate their patients regarding the importance of oral health. Patients should be challenged to take ownership of their oral health, visit a dental provider regularly, and set treatment priorities for a healthy lifestyle.
Dr. Astroth is associate professor at the University of Colorado School of Dental Medicine and director of the Senior's Dental Clinic, both in Aurora.

References

1. Rishiraj B, Epstein JB. Basal cell carcinoma: what dentists need to know. J Am Dent Assoc. 1999;130:375-380.
2. Joshipura KJ, Rimm EB, Douglass CW, et al. Poor oral health and coronary heart disease. J Dent Res. 1996;75:1631-1636.
3. Genco R, Chadda S, Grossi S. Periodontal disease is a predictor of cardiovascular disease in a native American population (abstract). J Dent Res. 1997;76:408.
4. Beck JD, Garcia R, Heiss G, et al. Periodontal disease and cardiovascular disease. J Periodontol. 1996;67(10 Suppl):1123-1137.
5. Taylor GW, Burt BA, Becker MP, et al. Severe periodontitis and risk for poor glycemic control in patients with non-insulin dependent diabetes mellitus. J Periodontol. 1996;67(10 Suppl):1085-1093.
6. Taylor GW, Burt BA, Becker MP, et al. Non-insulin dependent diabetes mellitus and alveolar bone loss progression over 2 years. J Periodontol. 1998;69:76-83.
7. Westfelt E, Rylander H, Blohme G, et al. The effect of periodontal therapy in diabetics. Results after 5 years. J Clin Periodontol. 1996;23:92-100.
8. Grossi SG, Skrepcinski FB, DeCaro T, et al. Treatment of periodontal disease in diabetics reduces glycated hemoglobin. J Periodontol. 1997;68:713-719.
9. Thorstensson H, Kuylenstierna J, Hugoson A. Medical status and complications in relation to periodontal disease experience in insulin-dependent diabetics. J Clin Periodontol. 1996;23(3 Pt 1):194-202.
10. Saremi A, Nelson RG, Tulloch-Reid M, et al. Periodontal disease and mortality in type 2 diabetes. Diabetes Care. 2005;28:27-32.
11. Civen R, Jousimies-Somer H, Marina M, et al. A retrospective review of cases of anaerobic empyema and update of bacteriology. Clin Infect Dis. 1995;20 Suppl 2:S224-S229.
12. Scannapieco FA, Papandonatos GD, Dunford RG. Associations between oral conditions and respiratory disease in a national sample survey population. Ann Periodontol. 1998;3:251-256.
13. Hayes C, Sparrow D, Cohen M, et al. The association between alveolar bone loss and pulmonary function: the VA Dental Longitudinal Study. Ann Periodontol. 1998;3:257-261.
14. Yoneyama T, Yoshida M, Ohrui T, et al. Oral care reduces pneumonia in older patients in nursing homes. J Am Geriatr Soc. 2002;50:430-433.
15. Cook C, Pietrobon R, Hegedus E. Osteoarthritis and the impact on quality of life health indicators. Rheumatol Int. 2007;27:315-321.
From the March 2009 Issue of Clinical Advisor

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