HIV/AIDS and the Role of the Dentist

The good news is that transmission of HIV from a dentist to patient is very unlikely (Jaffe et al., 1994). In fact, patient-to-patient infection didn’t seem to occur in one dentist’s practice in spite of the fact that the dentist didn’t follow proper infection control practices – dental tools were not autoclaved after use and were treated with a disinfectant not recommended for disinfecting dental instruments. Also, dental lines were not flushed between patients, which can result in one patient’s tissue being expelled in the next patient’s mouth. Transmission from dentist-to-patient is known to have only occurred once - a Florida dentist infecting 6 patients. Patient-to-patient transmission is known to have occurred only once too.

Almost all AIDS patients will develop oral manifestations of the disease (Weinert et al., 1996), so the dentist definitely has a role in the management of HIV/AIDS patients. The frequency and type of oral lesion depends on the stage of the disease and degree of immunosuppression of the patient. During late stage infection more than 20% of patients experience at least one of the following oral conditions: aphthous ulcers, oral thrush, Kaposi’s sarcoma, oral hairy leukoplakia and linear gingival erythema. Left untreated these conditions can lead to the patient having difficulty talking, chewing and swallowing. Periodontal disease is also common.

HIV is infrequently transmitted orally because there are low numbers of CD4 cell targets and the presence of anti-HIV antibodies and anti-viral factors in the saliva as well as there being thick epithelial wall in the oral cavity (Shugars and Wahl, 1998). HIV recovery from the saliva is very poor.

Dental infection protocols are designed to reduce transmission of infection from any body fluid. In other words treat all patients as if all their body fluids are infectious. Dentists need to be able to recognise the oral features of HIV infection, manage their oral symptoms and understand the systemic effects of HIV, including their mental health and behaviour (Mulligan et al., 2006).

HIV/AIDS patients are likely to not disclose their HIV status to the dentist. One of the reasons for not disclosing is the attitude of the dentist. Some dentists stigmatise HIV/AIDS patients (Seacat et al, 2009). This means that dentists should always use Universal precautions and to display an empathetic attitude towards all patients. 46% of AIDS patients admit to not telling the dentist of their status at least once. Yet over 80% of HIV/AIDS patients would prefer their dentist did know their status (Charbonneau, 1999). The situation where it is most important to know a patient’s HIV status is perhaps after the dentist sustains a needle stick injury and the decision of whether to take antiviral prophylaxis needs to be made based on that patient’s HIV status.

Charbonneau A, Maheux B, Beland F (1999). Do people with HIV/AIDS disclose their HIV-positivity to dentists? AIDS Care. Abingdon vol 11, Iss. 1; pg. 61, 10 pgs

Jaffe HW, McCurdy JM, Kalish ML, Liberti T, Metellus G, Bowman BH, Richards SB, Neasman AR, Witte JJ (1994). Lack of HIV Transmission in the Practice of a Dentist with AIDS. Annals of Internal Medicine 855-859.

Mulligan R, Seirawan H, Galligan J, Lemme S (2006). The Effect of an HIV/AIDS Educational Program on the Knowledge, Attitudes, and Behaviors of Dental Professionals. Journal of Dental Education 70: 857 - 868.

Seacat JD, Litt MD, Daniels AS (2009). Dental Students Treating Patients Living with HIV/AIDS: The Influence of Attitudes and HIV Knowledge. Journal of Dental Education 73: 437 - 444.

Shugars DC, Wahl SM (1998). The Role of the Oral Environment in HIV-1 Transmission. Journal of the American Dental Association 129: 851 - 858.

Weinert M, Grimes RM, Lynch DP (1996).Oral Manifestations of HIV Infection. Annals of Internal Medicine 485-496.

Tooth Anatomy - First Maxillary Molars

The first maxillary molars (16 and 26 using the FDI terminology) have the largest occlusal table of all the teeth in the mouth and erupt at around 6 years of age - the first permanent molars to do so.

They have 4 cusps, the mesial-lingual being the largest, the distal-lingual is the smallest. The mesial and distal buccal cusps are about the same size. Sometimes a 5th cusp (cusp of Carabelli) can also be seen coming off the mesial lingual cusp. The cusps contain triangular ridges. There are also marginal ridges on the distal and mesial part of occlusal table and cuspal ridges.

There is a buccal groove that runs from the central pit to the buccal aspect above the height of contour. The lingual groove (also called the disto-lingual groove) runs from the distal pit adjacent and distally to the oblique ridge and down the lingual aspect of the tooth - crossing the height of contour. The oblique ridge crosses the occlusal width of the tooth from the mesial-lingual cusp to the buccal-distal cusp.

The occlusal table has a rhomboidal shape.

There are 3 roots. The lingual root is the largest, followed by mesial-buccal and the smallest is the distal-buccal.

Video explanation of maxillary molar anatomy from the Michigan School of Dentistry.

Infection spread via tissue spaces

Infection can spread via the blood, lymph and the tissue spaces. In dentistry, the most relevant tissue spaces are the:

• pterygomandibular space
• lateral pharyngeal space
• retropharyngeal space
• infratemporal fossa
• buccal space
• vestibular space
• sublingual space
• submandibular space
• submental space

Many of these spaces run into each other, allowing infection to spread from one space to another. For example, an infection from a wisdom tooth can spread to the pterygomandibular space and from there it can travel to the lateral pharyngeal space, then to the retropharyngeal space and even to the mediastinum.

Infection can also spread to the pterygomandibular space and lateral pharyngeal space from the infratemporal fossa.

Infection spread from maxillary teeth

Infections from the maxillary teeth can spread to the maxillary sinus, the canine fossa, palatal space, infratemporal fossa, buccal space and vestibular space. Infection will spread to the buccal space if the infection's path is outside the attachment of the buccinator muscle, but will spread to the vestibular space if the infection's path is inside the attachment of the buccinator muscle.

Infection can spread to the cavernous sinus from the infratemporal fossa and from the canine fossa. Infection in the cavernous sinus can lead to cavernous sinus thrombosis, which is potentially fatal.

Infection spread from mandibular teeth

Infections from mandibular teeth can spread to the vestibular and buccal space in the same way as from the maxillary teeth. Infection can also spread to the pterygomandibular space, sublingual space, submandibular space and submental space. The sublingual, submental and submandibular spaces can be referred collectively as the submandibular spaces.

Sometimes when an infection spreads to the submandibular spaces a life threatening condition called Ludwig's angina occurs. Angina is latin for strangle therefore this angina is referring to the sensation of being strangled caused by the swelling of the neck region. Tracheotomy is sometimes necessary to maintain the airway.

Pain as a Motivational Tool

Dr Feinstone motivates patient to comply promptly.

Drilling Technique

Dr Feinstone demonstrates a cavity preparation on the mandibular first molar.

Got to have a sense of purpose

From the movie The Dentist starring Corbin Bernsen as Dr Alan Feinstone.

Enamel Hypoplasia

The cell responsible for enamel formation is the ameloblast. If the ameloblast is exposed to a stress when it is in its secretory phase it will stop secreting enamel matrix properly and the result will be an enamel hypoplasia. This enamel hypoplasia will then be a feature of the tooth for long after the person it was attached to is dead and buried, unless it is worn away. The permanency of enamel hypoplasias coupled with the fact that teeth are so durable over time makes hypoplasias a very useful indicator of physiological stress.

Enamel hypoplasias can be seen as: no enamel at all, grooves, horizontal lines and pits. Ameloblasts lay down enamel matrix in increments. These increments are separated by striae of Retzius, which under light microscope are seen as perikymata at the crown’s lateral surfaces. Each increment indicates a constant period of growth in an individual of between 6-12 days. This period of growth in an individual can be determined by counting the number of daily growth striations (seen as cross striations) within each increment.

Linear enamel hypoplasias (LEH) are seen as enlargements of the width of the striae. This enlargement is the result of enamel matrix not being secreted by the ameloblast during periods of stress. An LEH is seen as a groove; one side of the groove is called the occlusal wall (closer to the occlusal surface of the tooth) and represents the period of disrupted enamel formation and the other side of the groove is called the cervical wall (closer to the cervical part of the tooth) and represents the period of return to normal enamel formation. The duration of the disruption of enamel formation can be found by multiplying the number of perikymata in the occlusal wall by the daily growth striations within those perikymata. For example if three perikymata are seen in the occlusal wall and each perikymata consists of 8 daily growth increments, then the duration of disruption is approximately 24 days.