W5: Management of Medically Compromised Patients Flashcards
- Pallor of oral mucosa
- Xerostomia
- Pigmentation of oral mucosa
- Parotid infections
- Dysgeusia
- Candidiasis
- Petechiae and ecchymosis of oral Mucosa
- Enamel hypoplasia
- Osteodystrophy- radiolucent jaw lesions
- Uremic stomatitis
CKD
CKD Mx
When should you do tx?
Kidney diseases, whether acute or acquired, imply a number of body dysfunctions such as prolonged bleeding, high blood pressure, infection tendency etc. which, in turn, pose a threat involving serious complications in cases of dental interventions in these patients…
With CKD of stage 4 or higher- contact GP- Control comorbidities- diabetes, hypertensions etc
- Deferral until CKD controlled
If dental tx is required:
- Blood pressure closely monitored
- If invasive treatment- pt should undergo prescreening for bleeding disorders
- Tendency to bleed.
- Consultation with GP if antibiotic prophylaxis is needed
- Peritoneal dialysis presents no additional problems in dental management.- Provide dental treatment on the day after hemodialysis. On the day of dialysis patients are fatigued and have tendency
PREGNANCY symptoms
- Pregnancy gingivitis- exaggerated inflammatory response to local irritants
- Pyogenic granuloma or “pregnancy tumor”- commonly on labial of interdental papilla
- Hyperplastic gingival changes – around second month
- Many women convinced that pregnancy causes tooth loss or calcium is withdrawn
- Gag-reflex- combination of morning sickness and hypersensitivity
Pregnancy trimesters- differentiate the experience:
First Trimester- fatigue, syncope and postural hypotension
- Second Trimester- sense of wellbeing and relatively few symptoms
- Third Trimester- increasing fatigue, discomfort, cardiovascular changes
- Supine hypotensive syndrome- abrupt fall in blood pressure, bradycardia, sweating, nausea, weakness and air hunger when in a supine position
HIV/AIDs manifestation to Mx
2.3. Angular Cheilitis
Angular cheilitis usually appears as fissures or linear ulcerations of the commissures and is frequently associated with small white unilateral or bilateral patches, as well as the presence of intraoral edema [15,16]. Overall, 20% of cases of this disease are caused by Candida spp., while 60% of cases are related to mixed C. albicans and Staphylococcus aureus infection [15]. Some local predisposing factors associated with this candidiasis presentation are narrow vertical oral dimensions, as well as aging-associated highly-stretchable skin. These conditions can lead to salivary contamination on the skin, triggering the disease. Angular cheilitis can appear with or without oral candidiasis (Figure 3) [16].
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Figure 3
Angular cheilitis.
Most forms of oral candidiasis are diagnosed through basic clinical characteristics. However, when a diagnosis is unclear, it can be confirmed through direct fungal culture or by a potassium hydroxide test. The goal of these diagnostic tools is to identify yeast or pseudohyphae. Generally, oral fungal cultures are reserved for patients who show no response to therapy or when antifungal resistance is suspected [16].
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3. Periodontal Disease
Periodontal diseases shows up in HIV-infected patients with a variable prevalence of 27% up to 76% when the patient has AIDS [6,12]. Periodontal disease encompasses a disease spectrum triggered by the complex interactions of mixed polymicrobial infections taking place in a dental biofilm while facing the host’s immune response, resulting in inflammation of the gums and surrounding tissues. In severe stages of periodontal disease, the destruction of teeth support structures (gum tissue, cementum, periodontal fibers, and alveolar bone) can be observed [12,17]. The mechanisms underlying the destructive process imply direct damage owing to the dental bacterial biofilm, as well as indirect damage, secondary to the bacterially-triggered host’s immune response [16,17]. The pathogens contributing to these inflammatory conditions are Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, Fusobacterium nucleatum, Campylobacter rectus, etc. However, in recent years, HIV-infected patients have been recognized to develop a much more severe and refractory periodontal disease, which has been attributed to the involvement of multiresistant pathogens, such as Pseudomonas aeruginosa, Acinetobacter baumannii, Escherichia coli, Klebsiella pneumoniae, Enterobacter faecalis, Clostridium clostridiiforme, as well as diverse Candida spp. [9,18,19,20,21,22,23,24,25]. The most relevant HIV/AIDS-related periodontal diseases are linear gingival erythema, chronic periodontitis, necrotizing gingivitis, and necrotizing ulcerative periodontitis [16,26].
3.1. Linear Gingival Erythema
This condition is considered a form of gingivitis, which is clinically composed of a 2–3 mm erythematous streak along the gingival frame. It is commonly accompanied by diffuse red lesions or petechiae-like wounds scattered towards the apex of gums as well as the alveolar mucous membrane (Figure 4a,b). It usually appears along the anterior teeth, though being capable of growing towards the molars, altogether with mucosal bleeding and scarce dental biofilm [4,23,26]. Among the representative features of this injury are clinical insertion loss and the absence of ulcers or pain. Multiple Candida spp. have been associated with triggering this condition [16,23,26].
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Figure 4
(a) Linear gingival erythema in the anterosuperior area (b) linear gingival erythema in the anteroinferior area.
3.2. Periodontitis
Periodontitis is characterized by microbial association within a dental biofilm, as well as host-mediated inflammation, which triggers the destruction of tissue supporting the teeth [27]. Its clinical manifestation includes gum inflammation, bleeding-prone mucous membranes, periodontal pouch formation, loss of clinical insertion, plaque, as well as supragingival and subgingival stone formation. In more severe cases, even dental displacement might develop, as well as pathological dental migration (Figure 5a,b) [27,28]. In HIV-positive patients, the dental biofilm usually has a relevant microbial heterogeneity, involving unusual bacteria within the oral cavity, such as P. aeruginosa, A. baumannii, E. coli, among others [18,20], as well as diverse Candida spp., encompassing C. albicans, C. glabrata, C. krusei, C. tropicalis, and C. dubliniensis. The presence of these microorganisms has been correlated to ART and a CD4+ T lymphocyte count of <200 cells/μL [9]. Some risk factors triggering periodontitis include passive tobacco consumption, diabetes, CD4+ T lymphocyte count <200 cells/μL, and xerostomia, among others [16,27].
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Figure 5
(a) Upper and lower arch chronic periodontitis (b) Anteroinferior sextant chronic periodontitis.
3.3. Necrotizing Gingivitis (NG)
This form of gingivitis is characterized by severe erythematous gingival tissue, covered by a necrotic white-colored pseudomembrane, which is composed of inflammatory cells, necrotic tissue, bacteria, fibrin, ulcers (with an interproximal crater aspect), bleeding-prone mucous membrane, foul-smelling breath, and pain [4,16,23,26,29]. Teeth located on the anterior sextant are the most common location of this disease. However, it can extend over to the posterior teeth [16,23,26,29]. Additional signs and symptoms might appear as well, such as malaise, lymphadenopathy, halitosis, and fever [30]. The predominant microorganisms of this condition are pleomorphic anaerobes, such as Prevotella intermedia, Fusobacterium nucleatum, plenty of spirochetes of the Borrelia genus, and gram-negative anaerobic bacteria as well. However, some clues lead to clinical findings representative of other species, including T. medium, T. maltophilum, T. amylovorum, T. oralis, T. macrodentium, Synergistetes cluster A, and Jonquetella anthropic [30].
3.4. Necrotizing Periodontitis (NP)
This ailment shares the same clinical manifestations as NG, together with acute and severe adjacent alveolar destruction, as well as spontaneous bleeding and deep, intense pain (Figure 6) [27]. The loss of the alveolar ridge is related to marginal necrosis, meaning that periodontal pouch formation is unlikely. On the other hand, exposed alveolar and interseptal bones are common [4,26]. Most NP cases are limited to a single or a number of teeth, although they can be generalized. Its aggressiveness is characteristic since it might present in up to a loss of 90% of insertion within 3 to 6 months. In HIV-positive patients, the dental biofilm is composed of microorganisms such as Enterococcus sp., Enterobacter sakazakii, Enterobacter cloacae, Serratia liquefaciens, Klebsiella oxytoca, and C. albicans. The identified risk factors for NUP are smoking, xerostomia, and a CD4+ T lymphocyte count of <200 cells/μL [23,26,31].
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Figure 6
Anterior sextant necrotizing ulcerative periodontitis.
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4. Xerostomia
Xerostomia is defined as the subjective feeling the patient senses within the oral cavity of poor salivation [32,33]. Its frequency is up to 39% in patients with a CD4+ T lymphocyte count of <200 cells/μL and 27% with a CD4+ T lymphocyte count of >200 cells/μL. Xerostomia is also associated with the consumption of some drugs, which include antidepressants, ART, anxiolytics, oral antidiabetic agents (mainly sulfonylureas), respiratory agents, quinine, antihypertensives (such as thiazides and calcium channel blockers), urinary anti-spasm agents, glucosamine, NSAIDs, opioids, ophthalmologic drugs, and magnesium hydroxide. Furthermore, another predisposing factor is head and neck radiotherapy [33]. This pathology is predominant in patients who have a CD4+ T lymphocyte count of <200 cells/μL and whom also have CD8+ T lymphocyte proliferation within the main salivary glands, resulting in its destruction [3,5,6,32].
Regarding physical examination, it might be identified as a saliva-scarce mouth floor, together with erythematous dry oral mucosal membranes and tongue, which might come along with fissures (Figure 7) [32]. This ailment might develop together with a swallowing and/or speaking impairment and a low spicy, sour, and crunchy flavor threshold. Additionally, patients complaining of taste distortion or trouble using dentures are common. Salivation impairment has been considered a risk factor for developing caries, as well as increasing the risk of oral infection, such as candidiasis and periodontal disease [33,34]. It might also favor mucositis, tongue fissures, dysgeusia, speech difficulties, halitosis, oral irritation, chewing and swallowing trouble, and even weight loss and cachexia [33,34,35].
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Figure 7
Tongue xerostomia and bilateral angular cheilitis.
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5. Kaposi’s Sarcoma
Kaposi’s sarcoma is the most common oral HIV-associated neoplasia, appearing in up to 6% of patients, and has been notably decreasing due to the use of ART [36,37]. This endothelial angioproliferative neoplasia is caused by human herpesvirus 8, which is transmitted during anal intercourse or through blood and saliva [4,16,37].
Its pathological features might oscillate according to the location of the lesions (ganglia, mucous membranes, or skin) as well as its morphological stage (patch, plaque, and nodule), progressing from papules, which convalesce into red-purplish plaques, which might ulcer and cause nearby tissue destruction [38,39]. The early lesions are usually flat, red, and asymptomatic. However, together with its evolution, the lesion usually develops a darker color with convergent wounds (Figure 8a) [4,16,37]. In advanced stages, the lesion might appear as multiple firm purple nodules, which might disturb normal mouth function and cause symptoms owing to trauma or infection. The ulceration and local destruction of this entity lead to the extraction of some dental organs in some cases (Figure 8b). It predominantly appears on the hard palate, major salivary glands, and jawbone [39]. Having a viral HIV load greater than 5000 copies/mL is an associated risk factor. The presumptive diagnosis of this neoplasia is made according to clinical characteristics. However, a definite diagnosis requires histopathological analysis after performing a biopsy [4,16,37].
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Figure 8
(a) Kaposi’s sarcoma in the soft palate and retromolar area; (b) Kaposi’s sarcoma of the gingiva, hard, and soft palate.
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6. Recurrent Aphthous Ulcers
Recurrent aphthous ulcers are the most common oral non-traumatic wounds. Their frequency ranges from 5% (without ART) up to 10% (patients on ART). The presence of these lesions is associated with a CD4+ T lymphocyte count of <200 cells/μL [7,40]. Their cause is yet unidentified. However, some theories have linked these lesions to an immune complex vasculitis or even to ART (Zalcitabine and abacavir) [37,40]. This ailment can be classified into minor aphthous ulcers and major aphthous ulcers:
6.1. Minor Aphthous Ulcers
These kinds of ulcers tend to appear most frequently. They usually show up as a simple yet painful erythematous halo, coated with a yellow-grayish pseudomembrane, with a diameter ranging from 2 to 5 mm (Figure 9). Its most common location is on a non-keratinized oral mucous membrane, typically lingering from seven to ten days, healing later without any scarring [4,16,41].
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Figure 9
Minor aphthous ulcer in the lower vestibule mucosa.
6.2. Major Aphthous Ulcers
These kinds of ulcers are generally observed in severely immunosuppressed AIDS patients (T CD4+ ≤100 cells/μL). These injuries appear as craters with elevated borders, covered with a white-yellowish pseudomembrane, measuring between 1 and 5 cm in diameter (Figure 10) [16,41]. These ulcers generally appear on the lateral border of the tongue, soft palate, mouth floor, oral mucous membranes, and oropharynx (including both keratinized and non-keratinized mucosal surfaces). Ulcers of this kind are remarkably painful, particularly while consuming salty, spicy, sour, and hard or rough foods and beverages. They may last up to weeks, causing dysphagia, trouble speaking and chewing, developing an induration on their borders, and leaving retractile fibrous scars after healing [4,16,41].
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Figure 10
Major aphthous ulcers on the lateral borders of the tongue and coated tongue.
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7. Oral Hairy Leukoplakia
Oral hairy leukoplakia has a lower prevalence among HIV-positive patients without ART (10%) compared to patients on ART (18%); its appearance is common during the fourth decade of life (52.1%), especially in the male population (about 79.8%) [7,42]. This lesion is caused by Epstein-Barr virus infection, though it is also associated with fungal microbes, usually Candida spp. [43] It often appears as a well-limited white lesion of variable appearance, transitioning from a flat lesion to growing papillary processes, similar to hair. Unlike candidiasis, it cannot be scraped off from mucosal surfaces. It commonly appears on the lateral borders of the tongue (bi or unilateral). However, it might extend to the tongue’s dorsum and mouth floor. On some occasions, it can appear on the oropharyngeal mucosa [4,26,42,43,44] (Figure 11a,b). This entity is associated with a low CD4+ T lymphocyte count, tobacco use, as well as topical and systemic steroid use [4,42,43,44].
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Figure 11
(a) Oral hairy leukoplakia on the underside of the tongue; (b) Oral hairy leukoplakia on the lateral border of the tongue.
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8. Oral Hyperpigmentation
Oral hyperpigmentation appears in up to 37% of patients who have a CD4+ T lymphocyte count of <100 cells/μL. The causes of this condition remain unknown, though it has been associated with ART, particularly zidovudine, a thymidine analog reverse transcriptase inhibitor. Other drugs, such as clofazimine and ketoconazole, have also been associated, among others [16,45]. Oral hyperpigmentation manifests as black or maroon papules, associated with intraleukocytic melanin or pigments within the basal cell membrane or lamina propria, with premature melanosomes. It can show up anywhere on oral mucosal membranes [16,46] (Figure 12a,b). According to reports, HIV-positive patients are more frequently related to illicit drug use compared to the general population (28% vs. 16%, respectively) [47]. Methamphetamine use has been linked to developing dental disease, which might be relevant. These patients can show up with precarious oral hygiene, xerostomia, hypochromic lip lesions, lateral sides of cheeks and palate, accompanied by rampant caries (so-called oral “meth sores”), aside from grinding-related excessive dental wasting (Figure 13) [47].
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Figure 12
(a) Oral hyperpigmentation on the palate due to the use of the antiretroviral drug zidovudine; (b) Oral hyperpigmentation on the cheeks due to the use of the antiretroviral drug zidovudine.
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Figure 13
Hyperpigmentation in the lip mucosa, with severe dental destruction “methamphetamine mouth”.
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9. Oral Herpes Virus
Oral wounds associated with Human Herpes Simplex Type 1 Virus (HSV-1) appear commonly. They affect up to 20% of HIV-positive patients [3,4]. Recurrent intraoral outbreaks due to HSV-1 infection begin as multiple fragile grouped papules and vesicles with a diameter shorter than 3 mm. These lesions fragment themselves to generate tiny and painful ulcers. Most of the lesions appear on keratinized or partially keratinized mucosal membranes (lips, hard palate, and gums). These wounds are self-limited, disappearing within seven to thirty days, although leaving a scar; they are linked to a CD4+ T lymphocyte count <100 cells/μL [4,44,48].
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10. Oral Warts
The prevalence of oral mucous membranes and skin warts caused by multiple subtypes of human papillomavirus (HPV) is about 4.6%. This value has been increasing within the ART era [7,46]. As a consequence, studies have suggested that drugs or combinations of ART drugs might be a risk factor for HPV oral infection development [46]. These wounds show up as papules or solid elevated nodules, with a cauliflower or wheat spike appearance, flat or with a pedicle [46] (Figure 14a,b).
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Figure 14
(a) Hyperplastic HPV lesion in the mucosa of the base of the lingual frenulum and sublingual caruncle; (b) wart due to HPV on the lower lip, with multiple umbilicated papules due to molluscum contagiosum and oily scaling lesions due to perioral seborrheic dermatitis.
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11. Caries
Dental caries is considered the most common oral disease in HIV-positive patients, with a prevalence reported between 54% and 83% [3,49,50]. It is a multifactorial disease triggered by the interactions of dental biofilm, skin surface, sugary diets, and the host’s vulnerability [2]. Bacteria on the biofilm involved in caries onset and progression, mainly Streptococcus mutans and Lactobacillus, respectively, metabolize sugars, thereby producing acid substances which that decompose enamel and dentin [10].
Caries can affect one or multiple dental surfaces; however, studies on the clinical characteristics and behavioral patterns of dental caries among HIV patients are scarce. Rezaei-Soufi et al. showed in their study a significant difference in the number of carious surfaces, including roots and crowns, in HIV-positive patients compared to HIV-negative patients. However, the prevalence of root caries is not significantly different between the two groups [51]. Additionally, it has been suggested that the severity of dental caries increases significantly with age and the duration of ART [51]. Within recent years, it has been suggested that C. albicans might increase caries development in patients who have HIV/AIDS, considering its capability to produce lactic acid through carbohydrate fermentation and hydroxyapatite dental structure degeneration processes, which is complicated with greater severity and the progression of caries development [10,11].
On the other hand, saliva has an essential role in preventing dental caries development due to its antibacterial and antifungal properties. It also possesses pH-buffering features within the oral cavity through bicarbonate and phosphate. As well, it provides necessary calcium and phosphate substrates to maintain dental enamel integrity. Lastly, saliva is also capable of producing antibodies [34]. HIV infiltration, CD8+ T lymphocyte proliferation within salivary glands, as well as antiretrovirals decrease the quality and quantity of salivary flow and modifies the normal oral cavity microbiome [8]; for this reason, these are considered the main risk factors for dental caries development in HIV-positive patients. Adding to the already mentioned predisposing conditions, suboptimal oral hygiene, tobacco use, drugs, periodontal disease, and a carbohydrate-rich diet are relevant factors leading to substantial dental caries development in this population (Figure 15a,b) [34,50].
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Figure 15
Multiple dental caries. (a) Front view, softened tissue in cervical and interproximal areas; (b) Lateral View, softened tissue in cervical areas.
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12. Conclusions
Due to the advent of antiretrovirals, lifespan prolongation has been achieved for people living with HIV. The presence of oral disease can have a relevant negative impact on the quality of life of these patients. As previously mentioned, oral health is strongly associated with physical and mental health; therefore, the integral care of these patients must include the observation, detection, and treatment of oral pathologies, which can be complex and diverse; and that, on many occasions, could represent a challenge for the clinician, due to the development of more than a single disease in individual patients. None of the lesions described is exclusive to HIV/AIDS patients; however, all of them present higher prevalence, severity, and progression in comparison to HIV-negative patients, especially in low CD4+ T lymphocyte counts and, in some cases, associated with the use of ART. Three groups of oral disease manifestation have been defined and linked to HIV/AIDS, according to their severity and clinical presentation:
(a) Group 1: these oral lesions are strongly associated with HIV/AIDS and are composed of seven kinds of lesions: oral candidiasis, hairy leukoplakia, Kaposi’s sarcoma, linear gingival erythema, necrotizing ulcerative gingivitis, necrotizing ulcerative periodontitis, and non-Hodgkin’s lymphoma;
(b) Group 2: this group includes atypical ulcers, salivary glands diseases, viral infection, such as cytomegalovirus, herpes simplex virus, papillomavirus, and herpes zoster virus; and
(c) Group 3: this group includes lesions rarer than those on groups 1 and 2, such as squamous cell carcinoma and diffuse osteomyelitis [37]. Given the aforementioned statement, it is relevant to remove barriers within oral healthcare for people living with HIV/AIDS, considering optimal and integral care as a goal.
- Mucositis
- Herpes simplex infections
- Herpes zoster
- Candidiasis
- Apthous ulcers
- Unusual alveolar bone loss
- Kaposi sarcoma
- Hairy leukoplakia
Transplant Patients oral findings
Organ and Bone Marrow Transplant
- What should be done prior transplant and when?
- How long should elective dental procedures be delayed??
- Always_____
Appropriate Dental Treatment
Examination and history
Radiographs
Those with poor prognosis – periodontally involved, those with periapical radiolucency, grossly carious should be removed at least 10 days prior to transplant
Bone Marrow/Stem Cell Transplant
Monitor oral infection on the tongue and oral mucosa, Dry mouth, Plaque control
- Tooth demineralization, Dental caries, Infection,
- DO to consult with oncologist prior to any oral health procedures – including prophylaxis
- Delay elective dental procedures for at least 1 year
RBC Do S/S
- Oral tissues may show petechiae, ecchymoses, jaundice, pallor, and ulcers.
- Spontaneous gingival bleeding and petechiae usually are found in patients
+ Management?
bleeding disorder
Mx:
- Patients who are about to undergo major oral surgery and are receiving warfarin therapy should have
input from their GP regarding the INR level that would be indicated.
- An INR above 3.0 may need to be adjusted by the GP. It will take 3 to 5 days for any effective reduction
of the INR to occur.
- Aspirin and NSAIDs must be avoided.
cancer treatment:
S/S + Mangament
When should tx be completed proliferation therapy?
MRONJ management
