A neurodegenerative disorder that affects predominately dopamine-producing (“dopaminergic”) neurons in the substantia nigra, a specific area of the midbrain.76 Damaged neurons in the substantia nigra display a primary diagnostic marker of Parkinson’s disease called Lewy body.77-79 This decreases the availability of dopamine, a chemical that is partially responsible for transmitting messages which control movement and coordination in the midbrain and emotions in the forebrain.78-80 Parkinson’s disease clinical signs and symptoms are diverse. In most cases, they begin subtly and progress gradually over time. Providers may initially notice a patient’s body is stiff and unsteady or their face lacks expression and animation.79 As the disease progresses, providers may observe individuals with Parkinson’s disease begin to exhibit the clinical signs and symptoms summarized in Figure 18.
Epidemiology and Etiology
Parkinson’s disease is the second most common adult-onset neurodegenerative disease lagging only behind Alzheimer’s disease.82 Worldwide, it is estimated that four to six million individuals have this disorder.77 In the United States it is estimated that one million individuals have Parkinson’s disease.76 The cause remains largely unknown.76 There is ongoing debate about the etiology of Parkinson’s disease and whether the disease is from genetic factors, environment toxins or injury, an illness, or some other event. Many experts think it is combination of factors. Scientific advances point towards genetic mutations as the most likely etiology of the disease.83-85 Environmental factors such as long-term pesticide exposure, have also been shown to play a causative role in developing Parkinson’s disease. However, there is no evidence to substantiate that environmental factors can singlehandedly cause the disease. Other factors that contribute to developing Parkinson’s disease include head trauma involving loss of consciousness, gender, and increasing age.76,82,86 Protective factors have also been identified. They include caffeine, uric acid, anti-inflammatory drugs, smoking, vitamin D, exercise, and low cholesterol levels.76 Figure 19 provides additional statistics about this disease.
Patient Management and Oral Health Considerations for Parkinson’s Disease
Patients diagnosed with Parkinson’s disease have altered face and tongue muscle function.88 Apathy, depression, forgetfulness, and the physical effects of rigidly and tremors can make oral self-care challenging for them. Patients experience oral motor and sensorimotor impairment, salivary dysfunction, dysphagia, burning mouth pain, loss of taste, and olfactory dysfunction.89-91 Factors such as medications, dry mouth, nutritional deficiencies, and functional deficiencies contribute to developing these problems.89,92 Dental providers must be attentive to these impairments because they may lead to inadequate oral self-care, poor oral health, decreased quality of life, and increased risk for developing oral infections such as caries, periodontal involvement, tooth mobility, and tooth loss.89,93-98 Dental providers must be attentive to salivary dysfunction (conditions of sialorrhea in conjunction with xerostomia) because this can increase problems with dysphagia and result in choking, sudden coughing, and “silent aspiration” pneumonia.89 They must also be attentive to the medications patients are taking and the length of time the patient has been taking each medication. Patients who have been taking levodopa for several years may begin to develop dyskinesia which can affect the jaw and create difficulty in safely accessing the patient’s mouth.90 Patients diagnosed with Parkinson’s disease may be unable to verbalize dental pain.27