By Clayton A. Chan, D.D.S., M.I.C.C.M.O.
The following are excerpts, thoughts and lecture slides originated from Dr. James F. Garry a leading expert in the field of upper airway obstruction.
In 1829, Magendie was the first to refer to the nose as a part of the respiratory tract that helps warm and moisten inspirated air. ”The adenoidal face” was the first described by Tomes in the early 1872, who noted patients with V-shaped contracted maxillas and narrow long faces. Angle included airway obstruction as an important causative factor in the early childhood development of malocclusion in 1907.
• Dolicocephalic face • Narrow nasal oriface (disuse) • Open mouth habitus (chronic mouth breather) • Arched upper lip • Rolled dry lower lip • Deep labial mental fold • Steep mandibular plane angle • Chronic contracture of mentalis muscle
The first multi-disiplinary approach to treatment of malocclusion and upper airway obstruction was suggested by Ketchum in 1912. He proposed that patients should seek an opinion by both a rhinologist and an orthodontist to evaluate modern day science and therapeutic approaches. In 1935, McCoy related naso-respiratory function to craniofacial growth. He noted an increase in skeletal Class III prognathic malocclusion. Balyeat and Bowne in 1934, noted facial and dental deformities resulting from perennial nasal allergeis in childhood.
• Dolicocephalic face • Allergic shiners • Narrow nasal oriface (disuse) • Open mouth habitus (chronic mouth breather) • Arched upper lip • Steep mandibular plane angle • Micrognathia – Class II, 4 bicuspid extraction • Deep overbite
In 1939, Todd and Broadbent described the role of allergy in the etiology of orthodontic deformities. Numerous factors causing upper airway obstruction have been noted, such as inhalants, food allergens, developing chronic rhinitis, polypoid changes in the mucosa, and chronic nasal obstruction. The most common etiology of upper airway obstructions is respiratory tract allergies – pollents, animal dander, fungal spores, house dust, feathers, fabric dust, mites and detergents. Allergies to house dust can cause perinnial symptoms. Allergies to pollens can be seasonal.
Hypersensitivities can release chemical mediators such as histamines, kinins, slow reacting substance of anaphylaxis (SRA-A), and eosinophilic chemotractic factor (ECF) into microcirculation resulting in venous congestion. Allergic edema of the mucous membranes of the nasal and paranasal cavities results in “venous puddling”.
Veins of the maxilla, especially the dental arches and the adjacent structures anastomose freely with the veins of the nasal and paranasal cavities that empty into the pterygoid plexus. Edema of the allergic mucous membrane of the nose and sinuses interferes with venous drainage causing venous puddling in the dental alveoli and surrounding tissues within suing local tissue anoxia and acidosis. A common clinical sign is white stippling on crowns of developing permanent teeth.
Note: The allergic shiner in a 4 year old child with pronounced perennial rhinitis. The discoloration in the lower orbitopalpebral grooves is caused by venous stasis.
The allergic edematous mucous membranes of the nasal and paranasal cavities produce pressure on the marginal venous arcades, medial palpebral veins and inferior opthalmic veins. Pressure on the veins interfere with drainage backward and downward to the pterygoid plexus leading to venous stasis producing discoloration of the lower orbitopalpebral grooves.
Note: The allergic shiners in an 8 year old child with perennial allergic rhinitus and bronchial asthma since the age of 3. Note the infraorbital edema (bags) resulting from spasm of the unstriated Muscles of Muller. This child is a chronic mouth breather.
An additional factor in the production of edema and discoloration is allergic spasm of the Muscle of Muller. This is the only unstriated muscle of the eyelid musculature. Spasm of this muscle impedes venous return from the skin and subcutaneous tissues backward to the marginal arcades and palpebral veins. As a consequence edema is produced in the soft tissues below the eyelid.
Note: Both discoloration and edema in the lower orbitopalpebral grooves in a nine year child. The so-called “bags” are often indicative of allergy.
Recurrent bilateral seasonal interstitial inflammation of the tarsal conjunctivae is occasionally seen in children. It is characterized by flat-topped papules resembling cobblestones, and a thick mucinous discharge containing eosinophiles, symptoms of itching and redness of the eyes with lacrimation occur.
Arrows point to exudates in the limbus. Smears from the areas disclose clumps of eosinophiles.
Note: The muddy injected conjunctivae in a girl 14 years of age with perennial allergic rhinitis since they age of three.
Long silky eyelashes are often seen in allergic children. This 12 year old boy has had perennial rhinitus since infancy and bronchial asthma since the age of 3.
Airway obstruction in the child is usually a result of enlarged tonsils and/or adenoids, whereas airway obstruction in the adult is usually from responsive turbinates.
In the adult, turbinates are extremely responsive to allergens. As result vasomotor rhinitis is produced which must be distinguished from turbinate hypertrophy.
These problems will be exhibited in the interior of the allergic nose as: boggy, grayish-pink inferior turbinates with glistening mucoid secretions. Swollen mucous-covered turbinates often occlude the nostril. Marks pointed out that nasal septal deviations are not uncommon and occur in over one-third of children afflicted with persistent perennial allergic rhinitis. Additionally, the maxillary sinus polyps often accompany severe and chronic allergic rhinitis.
Dentist needs to recognize early signs of deformities that result from these airway obstructions. Chronic nasal blockage and the growth changes of the cranio-facial structures that are environmentally influenced are key underlying factors contributing to cranio-mandibular/temporomandibular joint dysfunction and cranio-cervical pain problems.
Every patient has a malocclusion to some degree. Teeth are not set in stone. There is a dynamic relationship between tooth position, arch shape and mandibular posture. When the pathologic position exceeds our accommodative capacity, patients begin to complain either of pain, discomfort, or esthetics.
*James F. Garry, D.D.S. -
I believe many that heard Jim Garry’s Lecture will remember GARRY’S DOGMATIC DICTUM - “ALL CHRONIC MOUTH BREATHERS, WITH A DENTITION, DEVELOP A MALOCCLUSION, Therefore …… It is essential that an upper airway evaluation be performed prior to initiating orthodontics, prosthodontics, periodontics, etc.”
He would end his lecture with these words,
“The most significant principle to understand is that teeth seek a neutral position within a system of forces acting on them. The force system changes constantly during growth, and teeth move in response to stimuli in their environment. Clinical observation can, with experience, enable a dentist to assess the force system in a child or adult and determine whether the position of the teeth may improve or deteriorate when balance between the dentition and force system has been established.”
“The most important thing you can put in your body is not food or water but it is OXYGEN! We must be chronic nose breathers not mouth breathers to maintain a stable occlusion.”
- Clayton A. Chan, DDS, Las Vegas, NV – Student of James F. Garry, DDS (September 8, 2004)
+ Dr. Clayton A. Chan is the honored recipient of Dr. James F. Garry life’s work, materials, slides and library which was awarded by Dr. Garry’s family to his closes and promising student and friend.
© 2009 Clayton A. Chan, DDS. All Rights Reserved.