|Year : 2017 | Volume
| Issue : 3 | Page : 54-59
Oral Health Issues and Challenges in Parkinson’s Disease
Ujwala R Newadkar1, Swapnil J Khairnar1, Arun S Dodamani2, Rohan Dilip Newadkar3
1 Department of Oral Medicine and Radiology, ACPM Dental College, Dhule, Maharashtra, India
2 Department of Public Health Dentistry, ACPM Dental College, Dhule, Maharashtra, India
3 Department of General Surgery, SBH Government Medical College, Dhule, Maharashtra, India
|Date of Web Publication||4-Jul-2017|
Ujwala R Newadkar
Department of Oral Medicine and Radiology, ACPM Dental College, Dhule - 424 003, Maharashtra
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Parkinson’s disease (PD) is a progressive neurodegenerative disorder with a slow onset, and compared with the familial forms of the disease, it is associated with advanced age (>55 years of age). It is characterized bycardinal features of bradykinesia, rigidity, tremor, and postural instability. It is superseded only by Alzheimer’s disease as the most common neurodegenerative disorder. PD patients may experience increased difficulties in oral health practices due to several factors: motor impairment, apathy, depression, and dementia. Patients with PD present several challenges to the dental healthcare team and to the patient related to both the illness and its treatment. Medications for neurodegenerative diseases can produce xerostomia, which will lead to dental caries. It can also produce the other problems like bruxism, dry throat, gingivitis, tongue edema, abnormal taste, glossitis, and orthostatic hypotension. Special care must be taken during treatment of such patients in the clinics. Our paper presents a brief comprehensive review on PD and its oral health consideration.
Keywords: Bradykinesia, neurodegenerative disorder, tremor, xerostomia
|How to cite this article:|
Newadkar UR, Khairnar SJ, Dodamani AS, Newadkar RD. Oral Health Issues and Challenges in Parkinson’s Disease. Int J Nutr Pharmacol Neurol Dis 2017;7:54-9
|How to cite this URL:|
Newadkar UR, Khairnar SJ, Dodamani AS, Newadkar RD. Oral Health Issues and Challenges in Parkinson’s Disease. Int J Nutr Pharmacol Neurol Dis [serial online] 2017 [cited 2017 Aug 17];7:54-9. Available from: http://www.ijnpnd.com/text.asp?2017/7/3/54/209422
| Introduction|| |
“For patients, Parkinson’s disease is not a time-neutral situation, it’s a ticking clock.”
-Michael Fox, 2002
Parkinson’s disease (PD) is a neurodegenerative disorder affecting adults in middle and late life. It is characterized by tremors, slowness of movements (bradykinesia), muscle rigidity, postural instability, and gait disturbances ultimately affecting their day-to-day life as described by James Parkinson in 1817, Nonmotor symptoms include change in speech, difficulty in swallowing, pain, confusion, depression, fatigue, and constipation; postural instability develops in later stages of the illness. PD is caused by depletion of neurotransmitters, dopamine, and norepinephrine in the basal ganglion. Dopamine depletion blocks autoinhibition of acetylcholine release through muscarinic auto receptors. PD demonstrated nonselective reductions of serotonin (5-HT) in brain tissues.
| Epidemiology and Etiology|| |
The prevalence of this disease varies greatly throughout the world. It is estimated that 6.3 million people have Parkinson’s worldwide. Although India has low prevalence, but in Parsi community of Mumbai, its prevalence is 328.3 per 100,000. PD has an annual incidence of about 0.2/1000 and a prevalence of 1.5/1000 in the United Kingdom. Prevalence rates are similar throughout the world, though lower rates have been reported for China and West Africa. Although 10% of the patients are under 45 years at presentation, the incidence and prevalence both increase with age, the latter rising to over 1% in those over 60. Sex incidence is higher in men. Prevalence and incidence increase with age. The risk for PD increases with age, and mortality among elderly PD patients is two to five times that of age matched controls. The public health burden for PD is significant and growing as the population ages, with an annual estimated cost of 26 billion dollars in the United States.,
PD results from idiopathic degeneration of the dopaminergic cells in the pars compacta of the substantia nigra, leading to depletion of the neurotransmitter dopamine in the basal ganglia (caudate nucleus and putamen). The relative contributions of genetic versus environmental factors regarding the cause of PD have been hotly debated. Most agree that the pathogenesis is multifactorial, with environmental factors acting on genetically susceptible individuals. Degeneration of pigmented pars compacta neurons of the substantia nigra in the midbrain, resulting in lack of dopaminergic input to striatum; accumulation of eosinophilic intraneural inclusion granules (Lewy bodies). Cause of cell death is unknown, but it may result from generation of free radicals and oxidative stress.,
Rare genetic forms of Parkinsonism More Details exist; most common are mutations in synuclein or parkin genes. Early age of onset suggests a possible genetic cause of PD. The discovery in a small number of patients of genetic forms of PD demonstrated conclusively that PD can occur through inheritance, and several genes have been found to be associated with inherited PD: a-synuclein, parkin, pink1, and UCH-L1; clinical genetic testing is now available for the parkin and pink1 genes. Environmental toxins, particularly pesticides, likely play an important role in the risk for PD, and the protoxin n-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine has been shown to cause Parkinsonism in both humans and nonhumans.,
| Clinical Manifestations|| |
The four cardinal signs of PD are resting tremor (in hands, arms, legs, jaw, and face), rigidity or stiffness (limbs and trunk), bradykinesia (slowness of movement), and postural instability or impaired balance and coordination. Nonmotor symptoms include change in speech, difficulty in swallowing, pain, confusion, depression, fatigue, and constipation. As symptoms become more pronounced, patients may have difficulty in walking, talking, or completing other simple tasks. PD is divided into stages according to Hoehn and Yahr [Table 1].
Tremor (“pill rolling” of hands) at rest (4–6 Hz), worsens with stress. A faster (7–8 Hz) “action tremor” may also occur when the hands are held against gravity. Presentation with tremor confined to one limb or side of body is common. Other findings: rigidity (“cog wheeling”-increased ratchet-like resistance to passive limb movements), bradykinesia (slowness of voluntary movements), fixed expressionless face (facial masking) with reduced frequency of blinking, hypophonic voice, drooling, impaired rapid alternating movements, micrographia (small handwriting), reduced arm swing while walking, flexed “stooped” posture with walking, shuffling gait, difficulty initiating or stopping walking, en bloc turning (multiple small steps required to turn), retropulsion (tendency to fall backwards). Nonmotor aspects of PD include depression and anxiety, cognitive impairment, sleep disturbances, sensation of inner restlessness, loss of smell (anosmia), and disturbances of autonomic function. In advanced PD, intellectual and behavioral deterioration, aspiration pneumonia, and bedsores (due to immobility) are common.,
| Diagnosis|| |
Although the clinical diagnosis of PD is based on a combination of the four cardinal motor signs, other Parkinsonian disorders also express many of these signs, and a definite diagnosis of PD requires neuropathological confirmation. It has been estimated that >10% of PD cases can be diagnosed incorrectly by movement disorder specialists when clinical signs are the only basis for diagnosis [Table 2]. There are currently no laboratory tests with specificity for PD. Diagnosis based upon history and examination; neuroimaging, Electroencephalogram (EEG), and Cerebrospinal Fluid (CSF) studies usually normal for age. Clinical genetic markers are available for risk assessment where hereditary patterns of PD exist. Differential diagnosis of Parkinsonism includes various conditions [Table 3].
|Table 2: Diagnostic criteria for Parkinson’s disease according to the revised 2015 MDS-UPDRS criteria|
Click here to view
| Treatment|| |
Goals are to maintain function and avoid drug-induced complications. It is not always possible to exclude other causes of Parkinsonism prior to initiating treatment for PD. Bradykinesia, tremor, rigidity, and abnormal posture respond early in illness; cognitive symptoms, hypophonia, autonomic dysfunction, and balance difficulties respond poorly.
Initiation of Therapy
Dopaminomimetic therapy initiated when symptoms interfere with quality of life. In early PD, dopamine agonist monotherapy was well tolerated and reduces risk of later treatment-related complications such as motor fluctuations and dyskinesias (50% of patients treated over 5 years with levodopa). Motor fluctuations are the exaggerated ebb and flow of Parkinsonian signs between doses of medications. Levodopa, the metabolic precursor of dopamine, remains the most effective treatment for PD.
Compared to levodopa, they are longer acting and, thus, provide a more uniform stimulation of dopamine receptors. They are effective as monotherapeutic agents and as adjuncts to carbidopa/levodopatherapy. They can also be used in combination with anticholinergics andamantadine. Agonists are effective against bradykinesia and gait disturbancesbut less effective against tremor. Side effects include nausea, postural hypotension, psychiatric symptoms, daytime sedation, and occasional sleep attacks. Apomorphine, “rescue” drug, is a strong dopamine agonist. Levadopa-induced postural hypotension can be treated by fludrocortisone. Rivastigmine can be safely used for dementia associated with PD.
Carbidopa blocks peripheral levodopa decarboxylation into dopamine, and thus, symptoms of nausea and orthostasis often associated with the initiation of levodopa. Gradual dose escalation is recommended; initiation of dosing at meal times will reduce nausea.
Selegiline, rasagaline, and safinamide are selective and irreversible monoamine oxidase B inhibitors with a weak symptomatic effect when used as monotherapy or as an adjunct to carbidopa/levodopa. The catechol O-methyltransferase inhibitors entacapone and tolcapone offer yet another strategy to augment the effects of levodopa by blocking the enzymatic degradation of levodopa and dopamine.
In refractory cases, surgical treatment of PD should be considered. The use of ablation (e.g., pallidotomy or thalamotomy) has decreased greatly since the introduction of deep-brain stimulation. Symptoms not responding to levodopa are unlikely to benefit from surgery. The indications and contraindications for surgery are as given below [Table 4].
| Oral Health Considerations|| |
The neuromuscular (motor) and cognitive deficits associated with PD enhance the progression of dental disease, impair home care regimens, and encumber in-office dental treatment. The pathogenesis of these disturbances in PD may be multifactorial: some disorders occur due to general motor impairment and hypokinesia (dental and periodontal diseases due to difficulties in maintaining oral hygiene); others may be a manifestation of involuntary movements (facial dyskinesias/dystonia), due to medication (xerostomia), as a part of sensory dysfunction (taste impairment), or in relation to depressive symptoms (burning mouth syndrome and orofacial pain) [Table 5]. The jaw mobility and the speed of the jaw movements are reduced. The rigidity, the reduced mobility, and the tremor complicate the formation and the placement of the food bolus, and the chewing process., Moreover, food retention and dysphagia are common. It has also been suggested that the rigidity and involuntary jaw movements may induce orofacial pain. In PD, 30 to 80% of patients have drooling of saliva from the corners of the mouth, which is typically caused by a combination of pooling of saliva in the mouth as a result of dysphagia, decreased swallowing frequency, diminished closure of the lips, and antecollis.
| Dental Management of Patients with PD|| |
Patients with PD often must be treated in a relatively upright position, making complex dental procedures in the maxillary arch or posterior oral cavity a challenge. Resting tremors and drug-related dyskinesia can complicate procedures, and behavioral techniques to reduce anxiety as well as gentle cradling techniques can help. Dysphagia and impaired gag reflex increase the risk for aspiration of oral and irrigation fluids, and high-speed evacuation of fluids is important in reducing the risk for aspiration pneumonia. Some patients experience sialorrhea, making maintenance of a dry field difficult for some operative and surgical procedures. A recent preliminary study by South et al. demonstrated that chewing gum may modify certain swallowing parameters and reduce drooling in PD patients. Dental hygienists should be aware of PD patients’ vulnerability and special needs in order to implement strategies that may ensure a caring and effective treatment. It is preferable for dental hygienists to schedule the patient with PD 60 to 90 min after their medications have been taken, as medications tend to be most effective in that time period, rendering improved treatment conditions. Stress may exacerbate uncontrolled movements making any dental treatment more complicated.
Careful consideration and management include monitoring of blood pressure; correct positioning and repositioning during and after treatment; xerostomia and caries risk reduction through hygiene, sealants, and fluorides when indicated; impact of oromandibular dyskinesia on the design of dental prostheses; and periodic evaluation of the complete blood count to detect drug-related hematologic adverse effects. Several authors have reported severe neurological complications following diathermy use in Deep Brain Stimulation (DBS) implanted patients;, thus, diathermy use is contraindicated in this population.
| Conclusion|| |
Mastication and orofacial function are impaired in moderate and advanced PD. The physical disability of these patients compromises their daily activities, including food intake and oral hygiene. Due to poor oral hygiene, the extent of dental caries and edentulism increases; therefore, the number of these patients attending dental clinic is increasing. Both dentists and patients with PD may be reluctant to embark upon complex dental procedures. But prevention is the better element for maintenance of oral health in patients with PD. Comprehensive case history evaluation of such patients is mandatory so that oral healthcare professionals can coordinate with the healthcare team to provide effective and efficient management.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Rajeswari CL. Prosthodontic considerations in Parkinson’s disease. People J Sci Res 2010;3:45-7.
Hobson P, Gallacher J, Meara J. Cross-sectional survey of Parkinson’s disease and Parkinsonism in a rural area of the United Kingdom. Mov Disord 2005;20:995-8.
Dotchin CL, Msuya O, Walkar RW. The challenge of Parkinson’s disease management in Africa. Age Ageing 2007;36:122-7.
Elbaz A, Moisan F. Update in the epidemiology of Parkinson’s disease. Curr Opin Neurol 2008;21:454-60.
Wirdefeldt K, Adami HO, Cole P, Trichopoulos D, Mandel J. Epidemiology and etiology of Parkinson’s disease: a review of the evidence. Eur J Epidemiol 2011;26(Suppl 1):S1-58.
Van Den Elden SK, Tanner CM, Bernstein AL, Fross RD, Leimpeter A, Bloch DA et al.
Incidence of Parkinson’s disease: variation by age, gender and race/ethnicity. Am J Epidemiol 2003;157:1015-22.
Rao SS, Hofmann LA, Shakil A. Parkinson’s disease: diagnosis and treatment. Am Fam Physician 2006;74:2046-54.
Simuni T. Diagnosis and management of Parkinson’s disease. Medscape Neurology. Available from: http://www.medscape.com
. [Last accessed on 2007 Aug 30].
McNaught KS, Olanow CW. Protein aggregation in the pathogenesis of familial and sporadic Parkinson’s disease. Neurobiol Aging 2006;27:530-45.
Jenner P, Olanow CW. The pathogenesis of cell death in Parkinson’s disease. Neurology 2006;66(10 Suppl 4):S24-36.
Lang AE, Lozano AM. Parkinson’s disease. Part 1. N Engl J Med 1998;339:1044-53.
Lang AE, Lozano AM. Parkinson’s disease. Part 2. N Engl J Med 1998;339:1130-43.
Lees AJ, Hardy J, Revesz T. Parkinson’s disease. Lancet 2009;373:2055-66.
Hoehn M, Yahr M. Parkinsonism: onset, progression and mortality. Neurology 1967;17950:427-42.
Allen CMC, Lueck CJ. Neurological disease. In: Haslett C, Chilvers ER, Boon NA, Colledge NR, editors. Davidson’s Principles and Practice of Medicine. 19th
ed. New Delhi: Churchill Livingstone; 2002. p. 1174-77.
Friedlander AH, Mahler M, Norman KM, Ettinger RL. Parkinson disease: systemic and orofacial manifestations, medical and dental management. J Am Dent Assoc 2009;140:658-69.
Tolosa E, Wenning G, Poewe W. The diagnosis of Parkinson’s disease. Lancet Neurol 2006;5:75-86.
Gelb DJ, Oliver E, Gilamn S. Diagnosis criteria for Parkinson disease. Arch Neurol 1999;56:33-39.
Hughes AJ, Daniel SE, Ben Shlomo Y, Lees AJ. The accuracy of diagnosis of Parkinsonian syndromes in a specialist movement disorder service. Brain 2002;125:861-70.
Savitt JM, Dawson VL, Dawson TM. Diagnosis and treatment of Parkinson disease: molecules to medicine. J Clin Invest 2006;116:1744-54.
Weintraub D, Comella CL, Horn S. Parkinson’s disease–Part 2: Treatment of motor symptoms. Am J Manag Care 2008;14:S49-58.
Olanow CW, Koller WC. An algorithm for the management of Parkinson’s disease: treatment guidelines. Neurology 1998;50:S1-7.
Hanaoka A, Kashihara K. Increased frequencies of caries, periodontal disease and tooth loss in patients with Parkinson’s disease. J Clin Neurosci 2009;16:1279-82.
Müller T, Palluch R, Ackowski JJ. Caries and periodontal disease in patients with Parkinson’s disease. Spec Care Dentist 2011;31:178-81.
Kalf JG, Bloem BR, Munneke M. Diurnal and nocturnal drooling in Parkinson’s disease. J Neurol 2012;259:119-23.
Chou KL, Evatt M, Hinson V, Kompoliti K. Sialorrhea in Parkinson’s disease: a review. Mov Disord 2007;22:2306-13.
Clifford T, Finnerty J. The dental awareness and needs of a Parkinson’s disease population. Gerodontology 1995;12:99-103.
Cersósimo MG, Tumilasci OR, Raina GB, Benarroch EE, Cardoso EM, Micheli F et al.
Hyposialorrhea as an early manifestation of Parkinson disease. Auton Neurosci 2009;150:150-51.
Ha AD, Jankovic J. Pain in Parkinson’s disease. Mov Disord 2012;27:485-91.
Clifford TJ, Warsi MJ, Burnett CA, Lamey PJ. Burning mouth in Parkinson’s disease sufferers. Gerodontology 1998;15:73-8.
Coon EA, Laughlin RS. Burning mouth syndrome in Parkinson’s disease: dopamine as cure or cause?. J Headache Pain 2012;13:255-7.
Bakke M, Larsen SL, Lautrup C, Karlsborg M. Orofacial function and oral health in patients with Parkinson’s disease. Eur J Oral Sci 2011;119:27-32.
Wali GM. Asymmetrical awake bruxism associated with multiple systematrophy. Mov Disord 2004;19:352-5.
Abe S, Gagnon JF, Montplaisir JY, Postuma RB, Rompre PH, Huynh NT et al.
Sleep bruxism and oromandibular myoclonus in rapid eye movement sleep behavior disorder: a preliminary report. Sleep Med 2013;14:1024-30.
Sienkiewicz-Jarosz H, Scinska A, Kuran W, Ryglewicz D, Rogowski A, Wrobel E et al.
Taste responses in patients with Parkinson’s disease. J Neurol Neurosurg Psychiatry 2005;76:40-6.
Shah M, Deeb J, Fernando M, Noyce A, Visentin E, Findley LJ et al.
Abnormality of taste and smell in Parkinson’s disease. Parkinsonism Relat Disord 2009;15:232-7.
Kashihara K, Hanaoka A, Imamura T. Frequency and characteristics of taste impairment in patients with Parkinson’s disease: results of a clinical interview. Intern Med 2011;50:2311-5.
Dorsey ER, Constantinescu R, Thompson JP, Biglan KM, Holloway RG, Kieburtz K et al.
Projected number of people with Parkinson disease in the most populous nations, 2005 through 2030. Neurology 2007;68:384-6.
Scott S, Caird FI, Williams BO. Communication in Parkinson’s Disease. Rockville, MD: Aspen Systems Corporation; 1985.
Dougall A, Fiske J. Access to special care dentistry, Part 9. Special care dentistry services for older people. Br Dent J 2008;205:421-34.
Apel C, Forlenza OV, de Paula VJ, Talib LL, Denecke B, Eduardo CP et al.
The neuroprotective effect of dental pulp cells in models of Alzheimer’s and Parkinson’s disease. J Neural Transm 2009;116:71-8.
Boucherie C, Hermans E. Adult stem cell therapies for neurological disorders: benefits beyond neuronal replacement. J Neurosci Res 2009;87:1509-21.
Huang GT, Gronthos S, Shi S. Mesenchymal stem cells derived from dental tissues vs. those from other sources: their biology and role in regenerative medicine. J Dent Res 2009;88:792-806.
Kieser J, Jones G, Borlase G. Dental treatment of patients with neurodegenerative disease. N Z Dent J 1999;95:130-4.
South AR, Somers SM, Jog MS. Gum chewing improves swallow frequency and latency in Parkinson patients: a preliminary study. Neurology 2010;74:1198-202.
De Bowes SL, Tolle SL, Bruhn AM. Parkinson’s disease: considerations for dental hygienists. Int J Dent Hyg 2013;11:15-21.
Nutt JG, Anderson VC, Peacock JH, Hammerstad JP, Burchiel KJ. DBS and diathermy interaction induces severe CNS damage. Neurology 2001;56:1384-86.
Roark C, Whicher S, Abosch A. Reversible neurological symptoms caused by diathermy in a patient with deep brain stimulators: case report. Neurosurgery 2008;62:E256.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]