A Practical Approach to Special Care in Dentistry

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A Practical Approach to Special Care in Dentistry
Learn to treat dental patients with disabilities or who are medically compromised A Practical Approach to Special Care in Dentistry
A Practical Approach to Special Care in Dentistry

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Stage 2: Latency period/chronic infectionGenerally characterised by persistent generalised lymphadenopathyCan also be asymptomatic until the first opportunistic infections appear, such as oral candidiasisVery low viral load; if taking antiretroviral therapy, viral load may be undetectable with effectively no risk of viral transmission

Stage 3: AIDSCharacterised by the onset of conditions that have been called ‘AIDS‐defining’These include oesophageal candidiasis, systemic mycosis (histoplasmosis, coccidioidomycosis, cryptococcosis), cerebral toxoplasmosis, pneumonia by Pneumocystis carinii ( Figure 4.2.5), retinitis by Cytomegalovirus, encephalitis by HIV, tuberculosis and extrapulmonary infections by non‐tuberculosis Mycobacterium, cervical cancer, Kaposi sarcoma, lymphoma, progressive multifocal leucoencephalopathy and HIV wasting syndrome

Diagnosis

The initial diagnostic test is the enzyme‐linked immunosorbent assay (ELISA), which detects the viral protein p24, an HIV‐1 antigen; there can be a window of up to 6 months from exposure to the virus to when it becomes detectable

If the ELISA is positive, the HIV‐1/HIV‐2 antibody differentiation immunoassay confirmation test is applied (Western Blot, which was used prior to this test, could not differentiate between HIV‐1 and HIV‐2). If the result is negative or indeterminate, the nucleic acid test (NAT) may be employed to confirm that this is not an acute infection or a false positive Figure 4.2.5 Pneumonia by Pneumocystis carinii as an AIDS‐defining condition.

Rapid HIV antibody detection tests have been marketed and employ samples of oral mucosa exudate

The immunosuppression level is established based on the concentration of CD4+ T‐cells in peripheral blood and is the best predictor available for the onset of opportunistic infections, disease progression and survival (stage 1, ≥500 cells/μL; stage 2, 200–499 cells/μL; stage 3, <200 cells/μL)

Determining the viral load consists of quantifying the number of copies of HIV ribonucleic acid (HIV‐RNA) in peripheral blood, using the real‐time polymerase chain reaction (RT‐PCR); this test is applied as a predictor of disease progression and to select the antiretroviral regimen

A patient is considered to be in the AIDS stage when they have <200 CD4+ T‐cells/μL, their CD4+ T‐cell count is <14% of the total or they have an AIDS‐defining condition

Management

ART (antiretroviral therapy) is the combination of several antiretroviral agents, and should be commenced as soon as possible after diagnosis

Antiretrovirals seek to reduce the viral load (below 20–50 copies/mL is considered undetectable, depending on the test employed), increase the CD4+ T‐cell count, prevent opportunistic infections and reduce transmission to others

The most widely used families of antiretrovirals are:Nucleoside/nucleotide reverse transcriptase inhibitors (NRTI)Non‐nucleoside reverse transcriptase inhibitors (NNRTI)Protease inhibitors (PI)Entry or fusion inhibitorsIntegrase strand transfer inhibitors (INSTIs)

An initial HIV drug regimen typically includes 3 HIV medications from 2 or more different drug classes:Two NRTIs with an INSTI, NNRTI, or PIRitonavir (PI) or cobicistat as a booster (cytochrome P450 3A inhibitor)

The regime varies according to the patient's response and associated side‐effects

ART is associated with adverse effects that are not always predictable and include:Nausea and vomiting, diarrhoea, difficulty sleeping, dry mouth, headache, rash, dizziness, fatigue, and painThrombocytopenia caused by ritonavir

Prognosis

The main markers of disease progression are CD4+ T helper cell counts and the HIV replication rate (viral load)

The life expectancy of individuals with HIV infection who do not undergo ART is 2–3 years

About 85% of patients who undergo ART survive for more than 10 years

A World/Transcultural View

Africa remains the most affected region of the world due to HIV infection/AIDS, especially the sub‐Saharan region in which more than 30 million infected individuals live

The prevalence of HIV‐associated oral lesions remains significant in low‐income countries. Hairy leucoplakia is more common in Europe and America than in Africa and Asia. Paradoxically, the prevalence of salivary gland disease has decreased in the industrialised world and increased in low‐income countries

Dentists' willingness to provide dental treatment to patients with HIV varies depending on the dentists' origin and country in which they were trained

Recommended Reading

1 Diz Dios, P. and Scully, C. (2014). Antiretroviral therapy: effects on orofacial health and health care. Oral Dis. 20: 136–145.

2 Gay‐Escoda, C., Pérez‐Álvarez, D., Camps‐Font, O., and Figueiredo, R. (2016). Long‐term outcomes of oral rehabilitation with dental implants in HIV‐positive patients: a retrospective case series. Med. Oral Patol. Oral Cir. Bucal 21: e385–e391.

3 Ghosn, J., Taiwo, B., Seedat, S. et al. (2018). HIV. Lancet 392: 685–697.

4 Patton, L.L., Shugars, D.A., and Bonito, A.J. (2002). A systematic review of complication risks for HIV‐positive patients undergoing invasive dental procedures. J. Am. Dent. Assoc. 133: 195–203.

5 Porter, S.R., Luker, J., Scully, C., and Kumar, N. (1999). Oral lesions in UK patients with or liable to HIV disease‐ten years experience. Med. Oral 4: 455–469.

6 Robbins, M.R. (2017). Recent recommendations for management of Human Immunodeficiency Virus‐positive patients. Dent. Clin. North Am. 61: 365–387.

7 Santella, A.J. (2020). HIV testing in the dental setting: a global perspective of feasibility and acceptability. Oral Dis. 26: S34–S39.

4.3 Viral Hepatitis

Section I: Clinical Scenario and Dental Considerations

Clinical Scenario

A 74‐year‐old man attends to your clinic for an emergency appointment. He complains of a painful lump in the gum adjacent to the upper left first molar (#26) that presented 24 hours earlier and is getting worse.

Medical History

Moderate chronic hepatitis C (the patient declined treatment with direct‐acting antivirals [DAAs] due to a poor previous experience with interferon)

Thrombocytopenia (65 000 platelets/μL)

Arterial hypertension

Chronic obstructive pulmonary disease (exertional dyspnea)

Anxiety‐depression syndrome

Road traffic accident in 1988 resulting in a ruptured spleen and a mandibular fracture due to a work accident 40 years earlier – received blood transfusions

Splenectomy in 1988

Medications

Telmisartan

Alprazolam (recently commenced)

Beclomethasone

Dental History

It has been 40 years since the patient attended a dental clinic (only went at the time due to his mandibular fracture)

Admits being afraid of dentists due to a bad experience when he was a child

Does not brush his teeth regularly

Social History

Married and lives with his wife (drives his own vehicle)

Retired

Ex‐smoker (20 cigarettes/day until 4 years ago); alcohol – nil

Oral Examination

Poor oral hygiene

Missing teeth: #16, #17, #24 and #25

Periodontal abscess associated with tooth #26, which extends to the buccal sulcus

Caries in #26, #36, #47 and #48

Radiological Examination

Orthopantomogram undertaken ( Figure 4.3.1)

Generalised alveolar bone loss

Extensive, deep and unrestorable caries in #26

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