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Year : 2017  |  Volume : 7  |  Issue : 3  |  Page : 54-59

Oral Health Issues and Challenges in Parkinson’s Disease

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 Publication4-Jul-2017

Correspondence Address:
Ujwala R Newadkar
Department of Oral Medicine and Radiology, ACPM Dental College, Dhule - 424 003, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijnpnd.ijnpnd_22_17

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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 It is superseded only by Alzheimer’s disease as the most common neurodegenerative disorder.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 2023 Feb 1];7:54-9. Available from:

   Introduction Top

“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,[1] 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.[1]

   Epidemiology and Etiology Top

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.[1] PD has an annual incidence of about 0.2/1000 and a prevalence of 1.5/1000 in the United Kingdom.[2] Prevalence rates are similar throughout the world, though lower rates have been reported for China and West Africa.[3] 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.[4] Sex incidence is higher in men.[5] 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.[6] 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.[7],[8]

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.[9],[10]

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.[11],[12]

   Clinical Manifestations Top

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.[13] 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[14] [Table 1].
Table 1: Clinical manifestations of PD

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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.[15],[16]

   Diagnosis Top

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,[17] and a definite diagnosis of PD requires neuropathological confirmation.[18] 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].[19] 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].[15]
Table 2: Diagnostic criteria for Parkinson’s disease according to the revised 2015 MDS-UPDRS criteria

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Table 3: Differential diagnosis of Parkinsonism

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   Treatment Top

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.

Dopamine Agonists

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.[20] 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/Levodopa Formulations

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.

Levodopa Augmentation

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.[21]

Surgical Treatments

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].[22]
Table 4: Indications and contraindications for surgery in PD patients

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   Oral Health Considerations Top

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.[23] 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.[39] The rigidity, the reduced mobility, and the tremor complicate the formation and the placement of the food bolus, and the chewing process.[40],[41] Moreover, food retention and dysphagia are common. It has also been suggested that the rigidity and involuntary jaw movements may induce orofacial pain.[42] In PD, 30 to 80% of patients have drooling of saliva from the corners of the mouth,[43] 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.[44]
Table 5: Oral manifestations of PD

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   Dental Management of Patients with PD Top

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.[45] A recent preliminary study by South et al. demonstrated that chewing gum may modify certain swallowing parameters and reduce drooling in PD patients.[46] 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.[47]

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;[48],[49] thus, diathermy use is contraindicated in this population.

   Conclusion Top

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.

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Conflicts of interest

There are no conflicts of interest.

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  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]

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