Clínica de los Trastornos Temporomandibulares (TMD)

La molestia mas frecuente de los TMD es el dolor mandibular, facial o cefálico de intensidad moderada. La abertura limitada, una mandíbula que se atasca, adhiere o traba, son quejas funcionales habituales. Los sujetos se quejan con frecuencia de ruidos articulares, como un chasquido o chirrido cuando se abre o cierra la mandíbula. Los individuos tienen molestias percibidas de cefalea global y dolor de cuello u hombro que no se relacionan con la función mandibular. Algunos pacientes se presentan con quejas inexplicables de acufenos, plenitud ética, reducción auditiva y vértigo (Costen). Muchas veces se expresan molestias de aplicaciones dentales anormales, sensibilidad dental y dientes que no se unen de manera correcta.

Bruxismo

Es el rechinido de los dientes durante el sueño, se ha considerado un factor predisponente, precipitante de perpetuación. Tal anomalía puede generar activación excesiva de los músculos masticatorios y carga excesiva para la Articulación Temporomandibular (ATM), lo cual tal vez sea un factor en la recuperación  de algunos pacientes, mientras que en otros , el bruxismo no parece participar como factor. En estudios, el bruxismo no ha mostrado ser con claridad ser una causa de Trastornos Temporomandibulares (TMD). Algunos individuos que rechinan de manera intensa los dientes, no manifiestan síntomas o signos de TMD.

Transtornos Temporomandibulares

Son un conjunto de afecciones musculoesqueléticas que afectan la articulación temporomandibular,  los musculos masticatorios o ambos. Los transtornos temporomandibulares (TMD) comprenden muchos diagnosticos diversos con signos y sintomas similares que afectan al sistema masticatorio, los cuales pueden ser agudos, recurrentess 0 cronicos. Es infrecuente que los TMD pongan en peligro la vida, pero quiza tengan un efecto sobre la calidad de vida del individuo.

Los TMD aparecen de manera desproporcionada en mujeres en edad reproductiva en una proporción de 4:1 a 6:1. La prevalencia disminuye de manera notable tanto en varones como en mujeres después de los 55 años de edad.

Síndrome de Ernest

Conocido como inflamación del ligamento estilomandibular o Síndrome de Ernest.  Se trata de una “tendinitis de inserción”,  está estrechamente relacionada al Síndrome de Eagle y a otros dolores craneofaciales. La injuria del ligamento estilomandibular es un desorden frecuente en el dolor craneomandibular.

Etiología. Se debe al macrotrauma atribuible a golpes en la mandíbula, trauma craneal y síndrome de latigazo o “Whiplash” en accidentes de auto.  Las osteotomías quirúrgicas mandibulares en donde se produce distracción y movilidad pueden también inflamar este ligamento.

Los síntomas del Síndrome de Ernest son muy parecidos al Síndrome de Eagle. El dolor empieza debajo del pabellón auricular con síntomas adicionales ampliados a áreas vecinas; entre los más prevalentes se encuentran: dolor en la articulación temporomandibular, la zona temporal, la orbital, la garganta, los hombros, el cuerpo de la mandíbula, el proceso coronoides, la otalgia y la odontalgia en los molares inferiores. Un hallazgo clínico importante en pacientes con este síndrome es la reducción en los rangos de movimiento mandibular posteroanteriores y laterales. 

La resolución de esta sintomatología se logra con un abordaje no quirúrgico: una o varias infiltraciones de esteroides en la inserción mandibular del ligamento con resultados predecibles. Es importante de igual manera recomendar dieta blanda a los pacientes, calor húmedo al área infiltrada y analgésicos para el dolor post-infiltración. Si se llega a necesitar la intervención quirúrgica por sintomatología refractaria que no cede al abordaje conservador, la termólisis por radiofrecuencia se ha usado y brindado solución.   La termólisis por radiofrecuencia se ha usado para el tratamiento de algias craneocervicales de diferentes etiologías incluido el Síndrome de Ernest. Esta técnica genera denervación de las fibras nerviosas nociceptivas en la zona.

Sjögren’s syndrome (SS)

Sjögren’s syndrome (SS) is a chronic systemic autoimmune disease that initially presents in the head and neck region, affecting the lacrimal and salivary glands. Clinically, the patient will have objective findings of lacrimal and salivary dysfunction with subjective complaints of dry eyes and dry mouth.

Diagnosing SS is a challenge, as there are many conditions associated with dry eyes and dry mouth that can mimic the ocular and oral components. Documentation of objective tests of ocular and salivary dysfunction (Schirmer I test; ocular surface staining with a vital dye; labial salivary gland biopsy) is the most reliable for diagnosis of this syndrome.

SS may be the second most common autoimmune disease after rheumatoid arthritis, yet recent data suggests that there is an average delay in diagnosis of 6.5 years and many individuals remain undiagnosed. SS represents a spectrum of disease with great diversity in its initial presentation and clinical course, but with common underlying themes of lacrimal and salivary gland dysfunction associated with an autoimmune process. The diagnostic process is complicated by the lack of any single diagnostic test for SS. The three components, ocular, salivary, and systemic, are often assessed independently; and conditions that can mimic each component must be ruled out.

Reported ear, nose, and throat manifestations of SS include swallowing disorders, mucosal dryness, dysgeusia, anosmia, epistaxis, gastric reflux, major salivary gland swelling, and lymphoma.

PRIMARY HERPETIC GINGIVOSTOMATITIS

Human herpes virus (HHV-1) infections of the oral cavity
are very common. These are DNA viruses that spread
through direct contact. Primary infection most often occurs
in infancy or childhood. It typically follows viral entry into
the oral mucosa, and may be symptomatic, unnoticed,
unrecognized, or asymptomatic. Primary herpetic
gingivostomatitis occurs in individuals who lack primary
immunity 5–7 days following contact with a source. A
vesicular eruption can be preceded by a prodrome of local
tenderness. The vesicles are thin walled and short-lived,
leaving behind shallow, painful ulcers. A characteristic and
diagnostic feature of this infection is the involvement of
keratinized mucosa, especially the marginal gingiva
The lesions last 1–2 weeks and settle spontaneously
but, despite clinical resolution, viral shedding takes place
and these individuals can be a source of infection.
Differential diagnosis mainly consists of noninfective
conditions such as herpetiform apthous stomatitis,
erythema multiforme, and Stevens-Johnson syndrome.
Infective conditions include acute necrotizing
gingivostomatitis, herpes zoster, measles, and other rarer
viral infections.
Treatment is usually symptomatic to relieve the pain and
maintain oral hygiene. Paracetamol and ibuprofen are
effective in relieving pain and pyrexia. Local analgesics such
as benzydamine hydrochloride mouthwash or lidocaine
(lignocaine) ointment can be used, but their duration of
action is short-lived. Chlorhexidine mouthwash or gel helps
prevent bacterial superinfection of the ulcerated areas and is
therefore indicated. There is no evidence to support the use
of topical antiviral agents for the first attack of oral herpes
simplex. In severe cases, especially in adults or immuno -
compromised patients, systemic antivirals (acyclovir and
famciclovir) may reduce the duration of symptoms if taken
early in an attack and can be used in severe infections.
Owing to the high risk of infecting others, appropriate
advice on hand washing and limiting contact must be given.

MUMPS

Mumps caused by paramyxovirus is the most common viral
infection, usually involving the parotid gland. This is a RNA
virus transmitted by airborne droplets.

After an incubation period of 2–3 weeks,
low-grade fever, malaise, and anorexia
occur. This is then followed by parotitis, which is usually
bilateral. Enlargement of the gland can be differentiated
from cervical lymphadenopathy by outward displacement of
the lobule of the pinna.

Spontaneous resolution is the norm,
but this can take a few weeks. Mumps can be
associated with other serious complications such as
sensorineural hearing loss, aseptic meningitis, orchitis, and
pancreatitis.

The clinical presentation should suggest the
diagnosis. Serological tests to identify antibody to mumpsspecific
IgM will confirm a recent infection.

Treatment involves supportive care and recognizing the possible
complications, which often need medical input. Use of the
live attenuated MMR (mumps, measles, and rubella)
vaccine has led to a decrease in the incidence of this disease.

GABHS

GROUP A BETA HAEMOLYTIC
STREPTOCOCCI (GABHS).

GABHS are responsible for the majority of bacterial
pharyngitis. The profile of pharyngeal disease these
organisms can cause ranges from asymptomatic colonization
of the pharynx to a severe pharyngotonsillitis. The
symptoms and signs are as discussed above.

A scarlatiniform rash can accompany the
throat and systemic symptoms.
GABHS infections need systemic antibiotics as serious
complications can ensue from the infection.

These include
rheumatic fever, scarlet fever, toxic shock syndrome,
necrotizing fasciitis, and septicaemia.

Antibiotics do not
prevent poststreptococcal glomerulonephritis.

Scarlet fever is a very uncommon presentation these days,
and most cases are less severe than in the past. There are
characteristic findings in the oral cavity and oropharynx that
may be encountered in otolaryngological practice. These
include palatal petechiae and a strawberry tongue (white fur
on the surface through which red papillae appear) initially.
The white fur on the tongue later peels off leaving red papillae
(raspberry tongue).

The skin shows symmetrical, punctate,
diffuse, blanching rash in the neck, axillae, and groin, usually
on the second day of the infection.

This rash resolves over 3 weeks and skin
peeling occurs over the extremities.
Several clinical scoring systems have been developed to
help diagnose GABHS infection to start prompt antibiotic
treatment. None have demonstrated high diagnostic efficacy.
The streptococcal rapid antigen test is a rapid immuno assay
that looks for specific group A streptococcal carbohydrate
antigen from a throat swab, with the results being available in
a few minutes. This has been demon strated to have a high
specificity and negative predictive value.

The antibiotic of choice is penicillin, with erythromycin for
individuals allergic to penicillin. Analgesia and supportive
care are essential.

However, aspirin should be avoided in
children under 16 years due to the risk of Reye’s syndrome.

ORAL CANDIDIASIS

Oral candidiasis is caused by Candida species, a saprophytic
yeast that is a commensal in the oral cavity. Candida
albicans is the most common agent, with others such as C.
krusie and C.tropicalis also being implicated. The presence
of oral candidosis should prompt a search for local or
systemic predisposing factors.
Clinical presentation of oral candidiasis can take distinct
forms:

Local factors

1 Diet rich in carbohydrates
2 Tobacco smoking
3 Denture hygiene and wearing
4 Xerostomia
5 Topical steroid use (most commonly steroid inhalers
in asthmatics)

Systemic factors

1 Physiological factors: infancy, old age, pregnancy
2 Drug therapy: antibiotics
3 Endocrine disease
a Diabetes mellitus
b Autoimmune polyendocrinopathy
4 Immunosuppression:
a Primary immune deficiency
b Steroids, cancer chemotherapy
c Radiation therapy
d HIV infection
e Leukemia

• Pseudomembranous oral candidiasis (thrush). Patches of
curd-like white pseudomembrane occur on the cheek,
gums, and the palatal mucosa. These are easily removed
and reveal an erythematous base. It may involve the
tongue in immunocompromised patients.

• Acute erythematous oral candidiasis usually occurs
following antibiotic treatment and in immunosupression,
marked by erythema on the dorsum of the tongue.

• Chronic erythematous stomatitis (denture stomatitis) is
characterized by redness in the denture bearing area in
the palate. Soreness is not a prominent
feature.

• Chronic hyperplastic oral candidiasis (candidal
leukoplakia) presents with white plaques on the cheek or
tongue that are not easily removed, with little or no
symptoms. It is nearly always seen in smokers and
regression may follow smoking cessation. An incisional
biopsy is indicated to determine the presence of dysplasia.
This lesion can be classed as a premalignant one.

• Median rhomboid glossitis shows an erythematous area
devoid of papilla of the tongue in the midline just anterior
to the circumvallate papillae.

• Angular stomatitis presents as erythema and fissuring of
the angles of the mouth. These lesions may also be
caused by a staphylococcal infection or may also be an
indicator of underlying vitamin deficiency, anaemia, or
even diabetes, hence appropriate screening is warranted.

The varied presentation of oral candidiasis permits many
differentials. All keratotic lesions can be ruled out easily as
they do not rub off on examination. Chemical burns,
superficial bacterial infections, lichen planus, white sponge
nevus syndrome, and necrotic ulcers from systemic disease
should be considered.
As a first-line drug, topical miconozole or nystatin is
recommended; if a response does not occur with one of
them, the other can be tried. Oral imidazoles (fluconazole
and itraconazole) are licensed for use in oral candidiasis
where first-line measures have been unsuccessful.
Identification and removal of predisposing factors is
essential. Avoiding sleeping with dentures in place, tobacco
cessation and rinsing of the mouth following steroid inhaler
use are examples of simple advice that may be given when
indicated. In the absence of obvious predisposing factors,
screening for systemic risk factors may be warranted.
Recurrent infections in the immunocompromised patient
may warrant prophylaxis.

RECURRENT HERPETIC INFECTIONS (COLD SORES)

During the primary infection, the virus also gains entry into
the neurones and becomes latent in the trigeminal, vagal,
and sympathetic ganglia. At times when the host immunity
is compromised or following certain triggers like stress,
illness, and sunlight, viral reactivation may occur. Generally
this results in a clinical picture of recurrent herpes labialis
with the vermillion of the lip and adjacent skin
characteristically involved. The prodrome is characterized
by tingling, itching, or pain, followed by vesicular eruption.
These crust over 48 hours and heal without scarring over a
week. However, reactivation may also involve oral mucosa
(recurrent intraoral herpes) with vesicles developing which
burst to leave a cluster of oral ulcers. Their
distribution tends to be localized and unilateral.
While there is no consensus on the use of topical
antivirals, best evidence suggests that topical penciclovir 1%
or acyclovir 5% must be started as soon as symptoms begin,
to be of any benefit. Oral antivirals may be of benefit in
severe cases. Prevention is possible in the presence of welldefined
triggers, e.g sunscreens when sunlight can trigger an
episode. For most patients there is no role for prophylactic
antivirals to prevent cold sores.