|
| A) | There is a 9:1 male-to-female ratio. | ||
| B) | It has no influence upon the oral health. | ||
| C) | It usually occurs in the fourth and fifth decades of life. | ||
| D) | The primary form is associated with a diagnosed systemic connective tissue disease. |
Sjögren syndrome is a common autoimmune disease that occurs in two different forms. Primary Sjögren syndrome involves the lacrimal glands (keratoconjunctivitis sicca) and the salivary glands (xerostomia). The secondary form presents with these problems and a diagnosed systemic connective tissue disease such as rheumatoid arthritis or fibromyalgia. Sjögren syndrome develops slowly over many years, and diagnosis is made an average of 2.8 years after the onset of symptoms [3]. It is estimated that 4 million individuals in the United States have this disease, with an additional 2.5 million currently undiagnosed. There is a 9:1 female-to-male ratio [4]. While Sjögren syndrome can occur at any age, patients in their fourth and fifth decades of life are most frequently affected. The etiology of this autoimmune disorder is not well understood. Histopathologic examination reveals an infiltration of lymphocytes that causes chronic inflammation within the salivary glands and the lacrimal glands [5]. The secreting capacity of the salivary glands is diminished at rates that vary among patients. Similarly, the lymphocytic infiltration and subsequent proliferative epithelial response constricts the ducts. Decreased salivary production and flow results in xerostomia (dry mouth). The initiation of the syndrome is believed to be triggered by environmental factors, possibly viruses [4]. Because women are more likely to be affected, it is hypothesized that female sex hormones may influence the onset or presentation of the disease. The changes are irreversible, and with no current cure for Sjögren syndrome, patients are affected by numerous long-term problems of the oral and maxillofacial complex originating from xerostomia.
| A) | Difficulty speaking and swallowing | ||
| B) | A decreased incidence of dental caries due to a lower pH of the saliva | ||
| C) | Chronic problems with the oral mucosa, such as mucositis and glossitis | ||
| D) | An increased incidence of oral opportunistic infections, such as candidiasis |
Saliva plays a critical role in the health and maintenance of the oropharyngeal region. A sustained reduction of salivary production in patients afflicted with Sjögren syndrome increases the risk for dental caries and opportunistic infections, such as candidiasis, and causes problems with the oral mucosa such as mucositis and glossitis. Speaking, swallowing, and eating can become difficult tasks under these circumstances.
The adequate production of saliva is an essential component in the self-cleansing action of teeth, as cariogenic bacteria are less adherent to the surfaces of teeth when a salivary layer is present, which minimizes their physical retention. Saliva also has a buffering capacity that raises the oral pH and creates a less acidic oral environment. When salivary production decreases, its buffering ability is also diminished and the oral pH is lower. The acidic oral environment that develops is more favorable to the proliferation of cariogenic bacteria [6,7].
| A) | has both a discoid and a systemic form. | ||
| B) | has an occurrence with a 9:1 female-to-male ratio. | ||
| C) | can lead to renal failure and pulmonary and cardiovascular pathology. | ||
| D) | All of the above |
Lupus occurs in several forms, the two most common being discoid lupus erythematosus (DLE) and systemic lupus erythematosus (SLE). DLE affects the skin and mucosa, usually without systemic involvement. SLE can affect multiple organs and systems and is the more serious form of the disease. The underlying basis for lupus is the formation of autoantibodies, especially to DNA and other nuclear material. The precise antigenic stimulus that initiates the formation of these autoantibodies is unknown. The deposition of the antigen-antibody complex into varied tissues and the resultant inflammatory response is the pathophysiologic basis of SLE [13].
The lesions of DLE usually occur on the face, scalp, ears, and hands. These lesions can feature an erythematous area and scales that extend into hair follicles, causing follicular plugging. Although oral lesions are not a strict identifying feature of DLE, when they do occur the buccal mucosa and palate are areas of predilection. Oral lesions associated with DLE can feature irregular white borders and telangiectasia peripheral to a small atrophic area that contains white papules [14]. A biopsy may be required to differentiate the oral lesions of DLE from malignant lesions such as squamous cell carcinoma.
As noted, SLE is more virulent than the discoid form of this disease. It primarily occurs in women of childbearing age, with a 9:1 female-to-male ratio [15]. Improved treatment modalities have increased the 10-year survival rate to greater than 85%, and the survival rate at five years is 95% [16,70]. Complications from infections, renal failure, and cardiovascular and pulmonary pathology are among the leading cause of death for these patients [17,18].
| A) | HIV/AIDS. | ||
| B) | cerebral palsy. | ||
| C) | Alzheimer disease. | ||
| D) | discoid lupus erythematosus. |
The lesions of DLE usually occur on the face, scalp, ears, and hands. These lesions can feature an erythematous area and scales that extend into hair follicles, causing follicular plugging. Although oral lesions are not a strict identifying feature of DLE, when they do occur the buccal mucosa and palate are areas of predilection. Oral lesions associated with DLE can feature irregular white borders and telangiectasia peripheral to a small atrophic area that contains white papules [14]. A biopsy may be required to differentiate the oral lesions of DLE from malignant lesions such as squamous cell carcinoma.
| A) | Down syndrome. | ||
| B) | Sjögren syndrome. | ||
| C) | Parkinson disease. | ||
| D) | systemic lupus erythematosus. |
A classic cutaneous manifestation of lupus, which occurs in approximately 30% to 40% of patients, is a butterfly-shaped (malar) rash that extends over the bridge of the nose and the cheeks. The degree of erythema accompanying this rash can range considerably. Oral lesions can be non-specific and can include ulcerations, petechiae, and erythematous lesions of varied morphology.
| A) | increased production of platelets. | ||
| B) | decreased production of leukocytes. | ||
| C) | increased hepatic function and liver enzymes. | ||
| D) | oral mucositis in more than 90% of the patients for whom it is prescribed. |
Immunosuppressive medications such as azathioprine and cyclophosphamide are used in patients with SLE to decrease the autoimmune response that causes organ and system damage. Azathioprine can cause bone marrow suppression and decrease production of platelets and granular and agranular leukocytes [20]. If a patient with SLE takes these medications, his or her physician must be consulted before any oral or periodontal surgical procedure is begun. Concerns about postsurgical hemostasis and infections should be discussed. The dosage of this medication may need to be adjusted pending the laboratory values as determined in the complete blood count. Hepatotoxicity is also a potential effect of azathioprine. Many medications utilized in dentistry are metabolized in the liver, and their metabolism may be diminished in patients taking azathioprine, with the potential for toxic accumulation [21]. Laboratory values for liver enzymes and a liver biopsy may be required if there is any concern about diminished hepatic function. Cyclophosphamide can also cause diminished production of platelets and leukocytes, with associated concerns about hemostasis and postsurgical infections. Mucositis may also occur in some patients for whom cyclophosphamide is prescribed [22].
| A) | oral candidiasis. | ||
| B) | necrotizing stomatitis. | ||
| C) | oral hairy leukoplakia. | ||
| D) | recurrent herpes labialis. |
Oral candidiasis is the most frequent opportunistic oral infection in patients with HIV/AIDS, with a very high occurrence in this population [23]. When C. albicans becomes an opportunistic oral pathogen, the extent and virulence of the infection increase as the CD4+ lymphocyte count decreases. Candidiasis can extend to the pharynx and esophagus and ultimately result in a fatal septic termination. Oral or intravenous antifungal medications such as fluconazole and itraconazole are used when advanced fungal infections occur. Caution must be exercised when other medications are prescribed, as antifungal medications can have numerous problematic drug-drug interactions. Invasive dental treatment should be avoided during an outbreak of oral candidiasis as surgical sites can become a means of systemic fungal dissemination.
| A) | HIV/AIDS. | ||
| B) | spinal cord injury. | ||
| C) | Sjögren syndrome. | ||
| D) | bone marrow transplant. |
Periodontal disease can manifest aggressively in patients with HIV/AIDS, especially those who are extremely immunocompromised. Most forms of periodontal disease progress slowly and asymptomatically. As the immunocompetence of patients with HIV/AIDS deteriorates, periodontal pathogens can accelerate the loss of soft tissue attachment and of the alveolar bone. Necrotizing gingivitis and periodontitis (previously called HIV-associated gingivitis and periodontitis) can be of such severity that loss of alveolar bone support requires the extraction of the involved teeth. Extension of the periodontal pathogens into the adjacent mucosa and bone can cause a necrotizing stomatitis, which can destroy these tissues and advance to a life-threatening infection [24]. It is critical for all HIV patients to maintain regular recall appointments during the entire course of their illness. Initial periodontal problems that can be treated conservatively with an early diagnosis will become increasingly difficult to treat and potentially refractory to periodontal treatment during the progression of the disease.
| A) | may develop hypotension. | ||
| B) | can develop hypoplasia of the gingival tissues. | ||
| C) | have a decreased susceptibility to opportunistic oral infections. | ||
| D) | can experience complications such as oral ulcers and xerostomia. |
Cyclosporine is a commonly used immunosuppressive agent prescribed for organ transplant patients. Systemically, it can induce changes in neural, renal, and hepatic function and can cause hypertension [26]. Potential oral effects include gingival hyperplasia, oral ulcers, xerostomia, and increased susceptibility to opportunistic oral infections. Gingival enlargement usually occurs within the first three months of cyclosporine administration and can be potentiated by the coadministration of medications such as the calcium channel blocker nifedipine, used to treat hypertension. The hyperplasia can involve the interdental papillae and the marginal and papillary tissues [27]. These tissue changes can complicate patients' ability to maintain ideal oral hygiene and increase the incidence of periodontal disease.
| A) | platelets. | ||
| B) | granular leukocytes. | ||
| C) | agranular leukocytes. | ||
| D) | All of the above |
Chemotherapy is used in conjunction with surgery and radiotherapy for varied systemic and organ-based malignancies. These medications have a low margin of safety and target rapidly dividing cells, which includes both the malignant cells and healthy cells of many tissues. The cells of the oral mucosa are rapidly dividing and may be damaged during chemotherapy. The resulting oral mucositis features painful mucosal ulcerations that can also serve as a means of systemic dissemination for oral pathogens. The alteration of the ability of the bone marrow to produce an adequate quality and quantity of platelets, erythrocytes, and granular and agranular leukocytes can make these patients prone to opportunistic infections and bleeding problems. Fortunately, these problems resolve after the cessation of chemotherapy.
| A) | Dopamine | ||
| B) | Epinephrine | ||
| C) | Acetylcholine | ||
| D) | Norepinephrine |
Parkinson disease is a progressive neurodegenerative condition that affects more than 1 million Americans [37]. The mean age at diagnosis is 60 years. In these patients, the neurons in the substantia nigra of the brain that store and release the neurotransmitter dopamine undergo a 60% to 70% depletion. The result is impaired motor function and poorly coordinated bodily movements [38]. The extent of impairment may be staged/measured using the Hoehn and Yahr scale, which describes five stages of Parkinson disease. The categories range from stage 1, which indicates mild tremors and minimal, unilateral functional impairment, to stage 5, which is characterized by incapacitating motor symptoms that require restriction to bed or dependence upon a wheelchair for ambulation [39]. However, this staging system has been criticized for its over-reliance on physical (rather than psychologic or behavioral) symptoms. The interference with normal motor function can have varied orofacial manifestations that progressively detract from optimal oral function.
| A) | Drooling | ||
| B) | Dysphagia (difficulty in swallowing) | ||
| C) | Problems with recurrent angular cheilitis | ||
| D) | All of the above |
Approximately half of patients with Parkinson disease have chronic problems with drooling [40]. Parkinson disease can affect the pharyngeal muscles and those of the tongue and the floor of the mouth, causing dysphagia (difficulty in swallowing). This condition combined with the head flexed in an anterior plane can make swallowing saliva difficult and drooling a chronic problem.
Saliva laden with the oral fungal organism C. albicans can inoculate the corners of the lips to cause angular cheilitis. This localized fungal infection can cause the lips and adjacent skin to remain cracked and inflamed for extended periods of time with subsequent pain during basic movements of the tissues. Antifungal preparations such as nystatin ointment may provide temporary relief, but angular cheilitis usually recurs in patients with Parkinson disease because its origin, chronic drooling, remains.
| A) | Selegiline | ||
| B) | Levodopa | ||
| C) | Entacapone | ||
| D) | Cyclosporine |
Pharmacologic management of Parkinson disease includes medications that replace the depleted dopamine, potentiate the action of dopamine that is produced, or increase dopamine availability as it crosses the blood-brain barrier. The medication levodopa is transformed into dopamine by the neurons of the substantia nigra. The benefit of this medication can decrease after prolonged administration, so its use is reserved for adjunctive treatment as the disease advances. A side effect of this medication is orthostatic hypotension; after dental treatment, patients should be raised incrementally from the reclined position to an upright position to minimize the chances of postprocedural syncope. Assistance to and from the chair may be necessary. Entacapone and carbidopa are utilized for patients with Parkinson disease to increase the bioavailability of levodopa, and both can also cause orthostatic hypotension. Selegiline is also prescribed with levodopa. Because selegiline is metabolized in the liver into l-methamphetamine and l-amphetamine, its combination with other sympathomimetic substances, such as epinephrine or levonordefrin, could cause an increase in blood pressure [41]. The patient's blood pressure should be recorded before any procedure, and vasoconstrictors should be used sparingly or avoided completely.
| A) | Periodontal disease is uncommon among these patients. | ||
| B) | Unique oral lesions are an identifying feature of this disease. | ||
| C) | Angle's Class II malocclusions are common among these patients. | ||
| D) | The muscles of mastication and swallowing are never affected by cerebral palsy. |
United Cerebral Palsy estimates that 764,000 individuals in the United States have cerebral palsy [42]. In 2006, the International Workshop on the Definition and Classification of Cerebral Palsy updated its definition of the condition, which is recognized as a group of activity-limiting disorders affecting the development of movement and posture [43]. Non-progressive disturbances that occur in the developing fetal or infant brain cause motor disorders; these can be accompanied by disorders that impair sensation, cognition, behavior, and communication [43]. Cerebral palsy is not associated with specific oral or maxillofacial lesions or abnormalities. However, several oral conditions occur within this patient population.
Periodontal disease is common in patients with cerebral palsy. The motor skills required for brushing and flossing are compromised to varying degrees, especially if cognitive and sensation disturbances accompany the motor problems, and optimal oral hygiene can be difficult to achieve and maintain. Caregivers may not be able to brush and floss the patient's teeth to a degree that allows for effective and consistent removal of bacterial plaque; the cumulative accretion of plaque may lead to gingivitis and ultimately periodontal disease. Some patients with cerebral palsy take medications to control seizures, such as phenytoin. Gingival hyperplasia has been identified as a side effect of this medication and may be exacerbated by plaque accumulation. When the surfaces of the teeth are covered by more gingival tissue, the ability to maintain plaque control becomes even more of a challenge. A gingivectomy can remove the hyperplastic tissue but recurrence with the continued use of phenytoin remains an issue.
Dental caries are more prevalent among patients with cerebral palsy as a result of the same factors that predispose patients to periodontal problems. Bacteria within accumulated plaque maintain prolonged contact with tooth surfaces and induce the development of dental caries. When the muscles of mastication and swallowing are compromised by cerebral palsy, the teeth have a prolonged exposure time to the bolus of food. This can result in an increased risk for caries. This problem is amplified when it is coupled with a patient's inability to maintain optimal oral hygiene. The irregular surfaces of unrestored carious lesions favor further accumulation of plaque and debris that perpetuate dental caries and periodontal issues.
An estimated 59% to 92% of patients with cerebral palsy have malocclusions, many of which are categorized as Angle's Class II ("buck teeth") classification [44]. Malocclusions decrease the efficiency of mastication and complicate oral hygiene, both of which can increase the risk of periodontal problems and caries. Further, protrusive teeth are more subject to traumatic dental injuries that require expensive endodontic and restorative procedures or extractions. Cerebral palsy is not an absolute contraindication to orthodontic correction for the varied malocclusions. However, an already challenging oral hygiene regimen will become even more difficult.
| A) | An increased risk of aspiration | ||
| B) | A reduction in the gag and cough reflexes | ||
| C) | Sustained pressure in weight-bearing areas while reclined that can cause decubitus ulcers | ||
| D) | All of the above |
The patient's physician should be consulted before any dental treatment is begun. Quadriplegic patients may have difficulty with adequate ventilation as well as an impaired gag and cough reflex and problems with the control of oral fluids that can accumulate during dental procedures [46]. Paraplegics usually do not have these difficulties but will require assistance upon transfer from the wheelchair to the dental chair. An accompanying caregiver may assist with the transfer in a manner that will not cause injury to the patient. Dental team members who wish to assist with chair transfers should obtain the proper training.
The sustained pressure on weight-bearing areas common among individuals who use wheelchairs or who are bedridden can cause localized ischemia and the development of decubitus (pressure) ulcers of the skin. If longer appointments are required, a change of the position of the legs can decrease the occurrence of this problem. If they develop, skin ulcerations of this nature can become infected locally and provide a portal of systemic dissemination for pathogenic organisms, potentially resulting in sepsis. Quadriplegic patients may require some of their dental or oral care treatment in a hospital setting.
| A) | The majority of strokes are hemorrhagic. | ||
| B) | It is the tenth leading cause of death in the United States. | ||
| C) | Clinical depression occurs in about 3% to 5% of stroke survivors. | ||
| D) | Residual oral problems include dysphagia and difficulty wearing prostheses. |
The American Heart Association estimates that every 40 seconds someone in the United States has a stroke [48]. As such, stroke is the fifth leading cause of death in the United States, after heart disease, cancer, accidents, and chronic lower respiratory diseases [49]. Strokes are the result of interruption of the blood supply to the brain via ischemic or hemorrhagic means. Ischemic strokes are more common and develop from the thrombosis of a cerebral vessel or from a distant embolus that has become lodged in a cerebral vessel. Hemorrhagic strokes involve bleeding within the brain; this type of stroke accounts for approximately 12% to 18% of all stroke cases [48,71].
The residual motor and sensory deficits associated with a stroke will depend upon the area of the brain in which the affected cerebral vessel was located. Strokes that involve the patient's dominant side can reduce the neuromuscular coordination that is essential for proper oral hygiene techniques. The hand of the unaffected, non-dominant side can be used in attempt to brush the teeth, and a flosser may be used to floss with only one hand. Physical therapy can help, but not all patients will regain use of the affected side. Stroke patients will depend upon healthcare professionals, while hospitalized, or home caregivers to provide basic oral hygiene procedures. Some stroke patients may require this assistance for the remainder of their lives. Because the oral hygiene of these patients can undergo demise after a stroke, it is essential that periodic dental examinations and prophylaxis appointments be maintained. Oral care should be deferred until the patient is stabilized and elective surgical procedures should be deferred for at least six months after the occurrence of a stroke [9]. The patient's physician should be consulted before any treatment is initiated.
Underlying conditions such as diabetes, hypertension, and cardiovascular disease may have been instrumental in causing the stroke. Medications prescribed for these and other chronic conditions may affect the selection of local anesthetics, analgesics, and antibiotics that are used for dental treatment. In addition, anticoagulant medications such as warfarin, clopidogrel, or aspirin are usually prescribed to decrease the chance of another stroke. Anticoagulants' intended effects can be potentiated with the coadministration of many medications used in dentistry, including NSAIDs (e.g., ibuprofen, naproxen), penicillin, and amoxicillin [50]. Patients on anticoagulant therapy should not have any invasive procedure without collaboration with their physician. A temporary hold on anticoagulants may be necessary unless the risk of another stroke or other cardiovascular event precludes the temporary discontinuance. Patients should never discontinue anticoagulant therapy unless it is under the guidance of a physician. If use of anticoagulants must be continued, laboratory values such as INR and PT can provide the clinician with necessary information regarding the patient's ability to achieve hemostasis. Further considerations for patients on anticoagulant therapy will be discussed later in this course.
Dental treatment considerations vary considerably among stroke survivors according to the initial amount of cerebral damage and the level of long-term disability. Even patients for whom minimal damage has occurred and who appear to have minimal motor and sensory deficits should not undergo dental treatment until physician approval has been granted. Unfortunately, many stroke victims do retain long-term or permanent sensory, motor, and cognitive problems that impact oral health and function and the ability to undergo dental treatment.
Dysphagia can occur when strokes cause neural and muscular compromise to the floor of the mouth, the tongue, and the pharynx. Eating and drinking can become a challenge with this condition, and patients may select foods of softer consistency that facilitate swallowing but compromise proper nutrition. The same neural and muscular issues can make partial dentures difficult to wear and the use of complete dentures nearly impossible. Partial dentures are retained by teeth and only partially reliant upon a balance of muscular forces for their retention. A complete maxillary (upper) denture depends upon a functioning musculature, especially at the junction of the hard and soft palates, for its retention. A complete mandibular (lower) denture relies on a balance between the muscles of the cheeks, tongue, chin, and floor of the mouth for retention. When stroke-related involvement of one or more of these muscles occurs, the stability and retention of prostheses are compromised. Patients may also feel that it is difficult to re-establish the proper occlusal pattern needed for proper mastication. The use of implant-retained dentures or denture adhesives (zinc-free) may be of assistance. However, surgery for implant placement should only be done with physician approval.
Cognitive impairment may remain for the patient's lifetime. Matters related to treatment options and informed consent may be beyond the comprehension of some post-stroke patients and will be delegated to their legally appointed representative.
Because many stroke patients are also being treated for hypertension, the use of vasoconstrictors, such as epinephrine and levonordefrin, which are combined with most local anesthetics, should be kept to an absolute minimum or avoided. Appointments should be kept short and as stress-free as possible, with vital signs monitored throughout. Patients should be kept in a position that accommodates unilateral weakness or paralysis and protects them from the accumulation of fluids and debris in the mouth. Many stroke patients develop dysarthria, a condition in which the muscles used for proper speaking are weakened, resulting in slurred speech. Clinicians will need to spend more time to communicate effectively with patients when this occurs.
Approximately 30% of stroke survivors have depression [51,71]. This can decrease patients' desire for recovery and can result in an overall decline in oral hygiene. Some antidepressants used in the treatment of depression can cause xerostomia. As discussed, xerostomia decreases the cleansing action of saliva and increases the retention of plaque on teeth and within the gingival sulcus, resulting in an increased risk of caries and periodontal problems. Tricyclic antidepressants such as amitriptyline can potentiate the vasopressor effects of both epinephrine and levonordefrin [51]. The concurrent use of these agents can raise the blood pressure to levels that endanger stroke survivors, and their use should be avoided.
| A) | ibuprofen. | ||
| B) | rifampicin. | ||
| C) | raloxifene. | ||
| D) | azathioprine. |
Underlying conditions such as diabetes, hypertension, and cardiovascular disease may have been instrumental in causing the stroke. Medications prescribed for these and other chronic conditions may affect the selection of local anesthetics, analgesics, and antibiotics that are used for dental treatment. In addition, anticoagulant medications such as warfarin, clopidogrel, or aspirin are usually prescribed to decrease the chance of another stroke. Anticoagulants' intended effects can be potentiated with the coadministration of many medications used in dentistry, including NSAIDs (e.g., ibuprofen, naproxen), penicillin, and amoxicillin [50]. Patients on anticoagulant therapy should not have any invasive procedure without collaboration with their physician. A temporary hold on anticoagulants may be necessary unless the risk of another stroke or other cardiovascular event precludes the temporary discontinuance. Patients should never discontinue anticoagulant therapy unless it is under the guidance of a physician. If use of anticoagulants must be continued, laboratory values such as INR and PT can provide the clinician with necessary information regarding the patient's ability to achieve hemostasis. Further considerations for patients on anticoagulant therapy will be discussed later in this course.
| A) | It must always be held before oral surgery. | ||
| B) | It inhibits the formation of thromboxane A2. | ||
| C) | It inhibits the synthesis of vitamin K-dependent coagulation proteins. | ||
| D) | Medications, such as the nonsteroidal anti-inflammatory drugs, have no effect on warfarin. |
Many stroke patients are initiated on anticoagulant therapy as a secondary prevention measure. Anticoagulant medications influence the synthesis of clotting factors. Antiplatelet therapy is used to decrease the risk of adverse cardiovascular events in patients with arterial or venous thrombosis, ischemic heart disease, coronary artery stents, or a history of an ischemic cerebrovascular accident [52]. Aspirin and clopidogrel, used individually or in combination, are among the most common of these agents. Aspirin inhibits the formation of thromboxane A2, a platelet product necessary for platelet adhesion. This inhibitory effect lasts for the 7- to 10-day lifespan of the platelet; the production of new platelets overcomes the inhibitory effects [53]. Clopidogrel inhibits the activation of platelets and ultimately the fibrinogen binding that is required for platelet adhesion.
Among the coumarin derivative class of anticoagulant medications, warfarin is the most commonly prescribed. Warfarin inhibits the synthesis of Factors VII, IX, and X and prothrombin, all of which are vitamin K-dependent coagulation proteins. The efficacy of warfarin therapy is monitored using the INR, the values of which reflect the therapeutic range of anticoagulant therapy. This ratio is determined by dividing the PT of the patient by the mean normal PT of the laboratory. The latter is determined by using the International Sensitivity Index [54]. A value of 1.0 reflects normal PT, while higher values indicate an extended PT. The goals of anticoagulant therapy are determined by the nature and extent of the medical problem involved. Prescribed and over-the-counter medications used in the treatment of oral conditions must not potentiate the intended therapeutic range of anticoagulant therapy, as internal bleeding can result. When procedures such as periodontal surgery or root planing and curettage are planned, verifying the patient's ability to attain and maintain hemostasis is essential. When extensive treatment such as multiple or full-mouth extractions is planned, postoperative bleeding can be significant and the procedure may need to be performed in a hospital setting. Patients who use either clopidogrel or aspirin for antiplatelet therapy have a lower risk of postoperative bleeding compared to those on combination therapy. As discussed, patients must be advised never to discontinue their anticoagulant or antiplatelet therapy unless it is approved by their physician.
NSAIDs, some antibiotics, and certain antifungal medications can increase the risk of postoperative bleeding when they are combined with anticoagulant or antiplatelet medications. Whenever possible, alternative medications should be utilized. The duration of anticoagulant and antiplatelet therapy is usually for the lifetime of the patient. Dental clinicians must be cognizant of the patient's current regimen and note any difficulties in internal or occult bleeding that would indicate potential problems in the achievement of postoperative hemostasis. Recent INR value and PT and consultation with the patient's physician can provide guidance for the course of dental treatment that is the safest for the patient.
| A) | An overdeveloped maxillary arch | ||
| B) | Shorter and smaller clinical crowns | ||
| C) | A lower occurrence and severity of periodontal disease | ||
| D) | Molar roots that are longer and more divergent than normal |
The presence of an underdeveloped maxillary arch is typical among patients with Down syndrome. This coupled with a mandibular arch of normal dimensions establishes a Class III jaw relationship (mandibular prognathism or underbite) [57]. Abnormal morphology of the teeth, such as shorter and smaller clinical crowns, coupled with a Class III malocclusion can cause compromised occlusal function and difficulties with the proper mastication of food. The delayed eruption sequence of teeth and a higher incidence of congenitally missing teeth among these patients can further prevent the development of a stable occlusion [58]. The occurrence and severity of periodontal disease are both more prevalent among individuals with Down syndrome. The aforementioned problems with congenitally missing or late erupting teeth can cause teeth to drift and incline in a fashion that does not facilitate optimal oral hygiene. Deficiencies in the immune system among these individuals will diminish the response against pathogenic bacteria. Leukocytes such as granulocytes and lymphocytes are the primary cells involved with defense against bacterial infections [59,60]. Nearly half of patients with Down syndrome have chemotactic defects in their neutrophils that prevent the proper migration of these leukocytes towards the pathogenic bacteria [61]. The function of T-lymphocytes is also compromised among many patients with Down syndrome. A combination of decreases in both mitotic activity and the response to an antigenic challenge and an increase in the production of immature T-lymphocytes diminishes the appropriate immune response to periodontal pathogens [62].
| A) | have oral lesions that are unique to this disease. | ||
| B) | will be more cooperative during dental treatment as this disease progresses. | ||
| C) | generally do not require obtaining consent for treatment from a caregiver. | ||
| D) | may take medications such as donepezil to decrease the degradation of acetylcholine. |
There are no oral lesions that are unique to Alzheimer disease. The dental considerations for these patients involve proactive and preventive care in the early stages of the disease while patients are most cooperative and are able to provide a reasonable level of basic oral hygiene by themselves. The ability of the patient to cooperate during dental treatment will decrease during the later stages of this disease. Thus, addressing dental problems as soon as possible after a diagnosis of Alzheimer disease has been confirmed as essential.
The interaction of medications prescribed for Alzheimer disease and systemic illnesses with those utilized for dental treatment are an additional concern. Patients with Alzheimer disease for whom periodontal problems have been controlled and carious lesions have been restored will require recall appointments, the frequency of which is determined by the patient's or caregiver's ability to maintain adequate home care. As this disease progresses, patients may forget to brush and floss their teeth on a regular basis (or forget what a toothbrush is) and may not be cooperative when a caregiver attempts to provide this service. This can potentiate existing periodontal problems or cause new problems to develop. Similarly, new and recurrent carious lesions can develop when the ability to maintain oral hygiene declines.
Because cognitive ability can vary considerably among patients with Alzheimer disease, even in the initial stages, it may be necessary to obtain consent for treatment from an accompanying caregiver or family member. Some patients with Alzheimer disease will not seek routine dental care, and advanced periodontal problems and multiple carious lesions can develop. An attempt to resolve these periodontal issues and to restore the carious lesions is the ideal treatment plan. However, maintenance of these teeth will become more difficult as the disease progresses. The patient, caregiver, and allied healthcare team must discuss optimal treatment options. Patients who did not practice good oral care prior to the diagnosis of Alzheimer disease are unlikely to improve these skills. Extractions of periodontally involved teeth and those with extensive carious lesions can be a practical option for these patients. As the patient's ability to cooperate during dental treatments declines, procedures that require longer appointments and are more complex must be done as early in the disease progression as possible. If partial or complete dentures are made, the patient's name should be incorporated into the acrylic of each prosthesis. This identifying feature will facilitate the return to the appropriate patient if the prosthesis is misplaced. Partial dentures should have a simplified design to facilitate their insertion and removal, and caregivers should be taught these techniques and appropriate home care.