Post on 09-Feb-2022
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HIPAA Please do not photograph or record any of the minor patients in this
presentation.
All patients shown are treated by Dr. Ben Miraglia
Any reproduction and use of the patient case content is a violation of HIPAA
Children are struggling with symptoms…
ADHD
Bedwetting
Upper respiratory infections
Ear infections/tubes
Night terrors
Academic struggles
Hyperactivity
Aggressive behavior
Clenching/Grinding
Restless sleep/wakes
Asthma
Small/Delayed growth
Anxiety
Depression
Daytime sleepiness
Overweight
Obesity
Night sweats
GI distress/reflux
Emotional instability
Sensory issues
Snoring
Mouth breathing4
The most common orthodontic problem is a crowded malocclusion.
We are going to explore how common later.
1. Improper Arch Form
2. Improper Arch Width
1. Transverse Measurement
2. The Eyes
Causes of Crowded Malocclusion
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Improper Arch Width
2. Improper Arch Width
Transverse Measurement
The shortest distance between teeth 3 and 14.
Children who develop naturally without orthodontic intervention become adults who achieve a 35-39mm transverse measurement.
The Eyes
Venous Pooling - purple/blue discoloration under the eyes
CO2 is a vasodilator
Mouth breathing reduces blood CO2
Less CO2 means less vasodilation or more vasoconstriction
The inferior orbital vein is a superficial vessel, when it contricts we see…
VENOUS POOLING
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LET’S PUT SOME PIECES TOGETHER
Improper arch form and width are the result of underdevelopment of the maxilla and mandible.
I.E: An underdeveloped maxilla and mandible is the cause of malocclusion
An underdeveloped maxilla has an adverse effect on the position of the mandible. It traps the mandible in a retruded position.
Craniofacial Growth & Development Normal growth is wide, forward and downward
Abnormal growth is narrow, backward and downward
Abnormal growth is underdevelopment
Professionally known as Craniofacial Deficiency
Ideal Craniofacial Development – Age 5
1. A significant space between all primary teeth2. A full view of the lower teeth when closed3. Forward growing
% OF MM GROWTH ACHIEVED AGE MALE FEMALE AVERAGE
INCREASE
0-2 54% 54% 54%
2-4 73% 78% 21%
5
6
7
8
9
10
11
12
% OF MM GROWTH ACHIEVED AGE MALE FEMALE AVERAGE
INCREASE
0-2 54% 54% 54%
2-4 73% 78% 21%
5 76% 81% 3%
6 79% 84% 3%
7 81% 85% 2%
8 83% 87% 2%
9 84% 89% 2%
10 86% 91% 2%
11 88% 93% 2%
12 89% 94% 1%
Anthropology Research
Five researchers: Dr. James Sim Wallace
Dr. Westin A. Price
Dr. Robert Corruccini
Dr. Jerome Rose
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“An early SOFT DIET prevents the development of the
muscle fibers of the TONGUE resulting in a WEAKER
TONGUE which can not drive the primary dentition out
into a spaced relationship with fully developed ARCHES
which will lead to more crowding of the permanent
teeth.”
JAMES SIM WALLACE, DDS - 1900’s
WESTON A. PRICE, DDS BORN IN 1870
RESEARCH DONE DURING THE EARLY 1900’S
10 YEAR PERIOD OF TRAVEL
14 COUNTRIES
100’S OF CITIES
LOOKING FOR SECRETS OF HEALTHY PEOPLES
STUDIED ISOLATED, PRIMITIVE GROUPS LIVING ON INDIGENOUS FOODS
ESKIMOS, NATIVE AMERICANS, AFRICAN TRIBES, AUSTRALIAN ABORIGINALS, POLYNESIANS ETC.
THE PEOPLE HE OBSERVED… DISPLAYED PHYSICAL EXCELLENCE
HAD PERFECT JAWS AND TEETH
EMOTIONAL STABILITY
NO ALLERGIES
COMMONALITIES BREASTFEEDING FOLLOWED BY A GRITTY, HARD DIET AT AN EARLY
AGE
NATURAL FOODS FROM SEA, PLANT AND MEAT
MOSTLY A RAW DIET WITH LITTLE COOKING OF THE FOOD
MEATS ARE DRIED AND CURED, SOME SALT
NO SUGAR, NO PRESERVATIVES, NO CHEMICALS,
NO CANNED OR PROCESSED FOODS
CHANGES OCCUR ONCE ISOLATION IS BROKEN
ESKIMOS DISPLAYED PERFECT OCCLUSION WITH EXCELLENT MAXILLARY
WIDTH
AFTER CONTACT WITH INDUSTRIALIZED SOCIETIES – A SHIFT TO SOFT FOODS AND REFINED SUGARS
MALOCCLUSION RATES ROSE TO OVER…
50% IN THE FIRST GENERATION!
Dr. Robert S. Corruccini ANTHROPOLOGIST
30+ YEARS OF RESEARCH
7 BOOKS
HUNDRES OF JOURNAL ARTICLES
FOSSIL STUDIES
POPULATION STUDIES
ANIMAL TESTING
POPULATION STUDIES DR. CORRUCCINI TRAVELED THE WORLD
STUDIED ISOLATED RURAL PEOPLES
BREASTFEEDING
ALL HAD A HARD DIET
LITTLE TO NO INCIDENCE OF MALOCCLUSION OR OTHER DEGENERATIVE DISEASES
LITTLE TO NO VARIATION
ALSO STUDIED SEVERAL POPULATIONS AS THEY BECAME EXPOSED TO WESTERN CULTURES
ANIMAL STUDIES DECADES WORTH OF HARD-SOFT DIET STUDIES
RESULTS ALWAYS THE SAME:
SOFT-DIET ANIMALS
SMALLER BODY MASS
LESS DENSE BONE
SMALLER, WEAKER ORAL MUSCULATURE
NARROWER MAXILLA
SMALLER MANDIBLE
THINNER ALVEOLUS
SMALLER CONDYLES
BROKEN ISOLATION MALOCCLUSION SHOWS UP IN THE FIRST
GENERATION AFTER EXPOSURE TO PREPARED, PROCESSED AND PRESERVED FOODS
50%
MALOCCLUSION RATES RISE DRAMATICALLY INTO THE SECOND GENERATION
70%
AND THIRD GENERATION
85%
AND FOURTH GENERATION
>90%
VARIATION ALSO INCREASES
CONCLUSIONS BREASTFEEDING RESULTS IN PROPER TRAINING AND
DEVELOPMENT OF THE TONGUE
THEN THE EARLY HARD DIET CONTINUES THE PROCESS
WHEN THE TONGUE POSTURES, SWALLOWS AND SPEAKS PROPERLY, WE GET IDEAL GROWTH
MOST MALOCCLUSIONS ARE ACQUIRED, NOT INHERITED
MALOCCLUSION IS A DISEASE OF WESTERN SOCIETY
DR. CORRUCCINI “DIETARY CONSISTENCY AND TOUGHNESS PROMOTE PROPER
BONE GROWTH AND PROPER PERMANENT TOOTH ERUPTION, BRINGING ABOUT IDEAL OCCLUSION; WHEN NONRESISTANT PROCESSED FOODS BECOME UBIQUITOUS AFTER INDUSTRIALIZATION, AND THE ERUPTION AND CUSPAL COORDINATION OF TEETH LOSE THE CRITICAL PATHFINDER INFLUENCE OF VIGOROUS MASTICATORY PRESSURES, MALOCCLUSION SHOWS A RAPID RISE.” from: How Anthropology Informs the Orthodontic Diagnosis of Malocclusion’s Causes
Dr. Jerome Rose
“95% of all malocclusions are acquired. Genetics play a role in only 5% of malocclusions. This is indisputable.”
Breastfeeding Trends in the USA The current rate is 70%
Drops to 50% at 6 months – partial/pumping
Bottle feeding/jar or blended food is different(soft)
Results:
Tongue is not trained properly – poor function
Tongue musculature is weaker – poor growth
Child misses the optimal growth and development of the maxilla and mandible during the first 2 years of life
Craniofacial Deficiency Next question…
WHAT ARE THE RESULTS OF HAVING AN UNDERDEVELOPED MAXILLA AND MANDIBLE?
WE NEED TO LOOK AT OUR ANATOMY FOR THE ANSWERS.
Airway Anatomy
Our airway anatomy is directly related to our craniofacial growth and development
The more ideal the craniofacial growth and development, the larger the airway space
Craniofacial deficiency includes airway compromise/deficiency
Airway compromise/deficiency results in compensation
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DR. EGIL HARVOLD
• Director – Center for Craniofacial Anomalies –UCSF
• Research – Primate Center – UC – Davis• Rhesus monkeys • Blocked monkey’s noses with cotton rolls• Conducted airway studies• Nasal obstruction > mouth breathing >
lower tongue posture > malocclusion
Dr. Sten Linder-Aronson Dr. Sten Linder-Aronson – children
Research focus was the difference between nasal breathing kids and mouth breathing kids
Same results – mouth breathers develop differently
MOUTH BREATHING + POOR TONGUE POSITION/FUNCTION = HIGH RATES OF MALOCCLUSION
FUNCTIONS OF THE NASAL CAVITY FILTER
HUMIDIFY
WARM
ACCELERATE
One Purpose:
Prepare the air for the lungs
PROPER NASAL BREATHING LIPS TOGETHER AND AT REST
TONGUE AT THE ROOF OF THE MOUTH
INVISIBLE
SILENT
NO MOVEMENT OF LIPS AND CHEEKS DURING SUBCONSCIOUS SWALLOW
END RESULT: NON-RESISTANT AIRFLOW
NASAL BREATHING DIAPHRAGMATIC BREATHING FILLS THE LUNGS WITH IDEAL AIR
LEADS TO OPTIMAL CO2, O2, NO BALANCE
END RESULT: A PROPERLY OXYGENATED, WELL BALANCED, HEALTHY CHILD
MOUTH BREATHERS INCREASE IN UPPER RESPIRATORY INFECTIONS
INCREASE IN ENT INFECTIONS
INCREASE IN ASTHMA
WHY?
MOUTH BREATHING COMPENSATION
OVERBREATHING, AKA HYPERVENTIALTING
DECREASED CO2 – CHEST BREATHING
DOES NOT FILL THE LUNGS WITH IDEAL AIR
IMBALANCE IN CO2, O2, NO
END RESULT: A POORLY OXYGENATED, IMBALANCED, AND UNHEALTHY CHILD
MOUTH BREATHING
VENOUS POOLING
CO2 HAS A VASODILATORY EFFECT
MOUTH BREATHING REDUCES BLOOD CO2
INFERIOR ORBITAL VEIN CONSTRICTS
THE RESULT IS VENOUS POOLING
ALSO
NASAL BREATHING RELEASES NITRIC OXIDE FROM THE PARANASAL SINUSES
MOUTH BREATHERS REDUCE BLOOD NO
INFERIOR ORBITAL VEIN CONSTRICTS
THE RESULT IS VENOUS POOLING and…
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MOUTH BREATHERS INCREASE IN UPPER RESPIRATORY INFECTIONS
INCREASE IN ENT INFECTIONS
INCREASE IN ASTHMA
WHY?
The decrease in NO
NO is antibacterial, antiviral and antifungal
Connecting the Dots…
“Mouth breathing has been linked to oral conditions such as craniofacial deformity, malocclusion and obstructive sleep apnea.”
García Triana, B., Hibatulla Ali, A., & Grau León, I. (2016). Mouth breathing and its relationship to some oral and medical conditions: physiopathological mechanisms involved. Revista Habanera De Ciencias MéDicas, 15(2).
Recuperado de
Connecting the Dots… “A narrow maxilla with high arched palate characterizes a phenotype of patients
with obstructive sleep apnea. This is associated with increased nasal airflow resistance and posterior displacement of the tongue.”
Johal A, Conaghan C. Maxillary morphology in obstructive sleep apnea: a cephalometric and model study. Angle Orthod. 2004;74:648-656.
Abdullantif J, Certal V, Zaghi S, et al. Maxillary expansion and maxillomandibular expansion for adult OSA: a systematic review and meta-analysis. J Craniomaxillofac Surg. 2016;44:574-578
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Connecting the Dots… “Snoring is associated with straight profiles, V-shaped palatal morphology,
increased neck circumference, decreased upper arch length, and decreased inter-first upper premolar distance.”
Al-Madani GH, Banabihl SM, El-Sakhawy MM. Prevalence of snoring and facial profile type, malocclusion class and dental arch morphology among snorer and nonsnorer university population. J Orthodont Sci 2015;4:108-12.
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CONNECTING THE DOTS… “Patients with OSA had significantly narrower maxillary and mandibular arch
widths when compared to control groups. These findings support the notion that a narrow maxilla or mandible may lead to airway obstruction because of
inadequate space for the tongue. Thus when the space in the oral cavity is inadequate, it is possible that a normal sized tongue can gravitate to the back of
the oro-pharynx.”
Banabilh SM, Suzina AH, et al. Dental arch morphology in south-east Asian adults with obstructive sleep apnoea: geometric morphometrics. Journal of Oral Rehabilitation 2009;36:184-
192.
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Connecting the Dots… In 98% of patients with OSAS, the condition is due to abnormal
anatomical features of the soft tissues and/or the structures of the maxillomandibular skeleton that cause a “disproportionate anatomy” of the airway,4,5 and in only 2% of adult patients is the condition due
to a space-occupying lesion, such as adenoidal, tonsillar or uvula hypertrophy, in which case resection would be curative.
Barceló X, Mirapeix RM, Bugés J, Cobos A, Domingo C. Oropharyngeal Examination to Predict Sleep Apnea Severity. Arch Otolaryngol Head Neck Surg. 2011;137(10):990–996. doi:10.1001/archoto.2011.176
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SLEEP DISORDERED BREATHING (SDB)
Karen Bonuck, PhD.
Published research in 2012 that followed 11,000 kids for 6 years
Objective
Examine statistical effects of SDB symptom trajectories from 6 months to 7 years on subsequent behavior.
Results of Dr. Bonucks Research “A STRONG AND PERSISTENT ASSOCIATION BETWEEN
SLEEP DISORDERED BREATHING AND DIMINISHED IQ”
SLEEP DISORDERED BREATHING INCREASED THE RISK OF ADD/ADHD BY 50%
SLEEP DISORDERED BREATHING KIDS WERE 40-100%MORE LIKELY TO HAVE NEURO-BEHAVIORAL ISSUES
SDB/OSA ASSOCIATED WITH
INCREASED FACE HEIGHT
DECREASED NOSE PROMINENCE
DECREASED NOSE WIDTH
RETROGNATHIC MANDIBLE
THIS IS THE FACE OF SDB/OSA
SDB/OSA ASSOCIATED WITH NARROW ARCHES
HIGH VAULT
ELONGATED SOFT PALATE
RETROGNATHIC MAXILLA
RETRUDED MANDIBLE
THIS IS THE ORAL CAVITY OF SDB/OSA
SLEEP DISORDERED BREATHING• Mouth breathing - Snoring - UARS - OSA
• Increased nasal airflow resistance
• Sympathetic Nervous System activation
• Altered biochemistry and physiology during sleep
• End result: sleep fragmentation or disruption of the reparative sleep
cycle delivers an unhealthy child who will grow up to be an unhealthy
adult
DR. JERALD SIMMONS
Jerald H. Simmons, M.D. is Triple
Board-Certified in Neurology,
Epilepsy and Sleep Medicine. A
graduate of Ohio State University, he
did his Neurology residency at
Washington University, Sleep
Medicine Fellowship at Stanford
University and Epilepsy Fellowship at
University of California. He began his
professional career as Assistant
Professor of Neurology at UCLA
while co-directing the UCLA Sleep
Disorders Center and directing the
Clinical Neuro-physiology lab at Olive
View UCLA Medical Center.
BRUXISM
“Nocturnal bruxism is a compensatory mechanism of the upper airway to help overcome upper airway obstruction by activation of the clenching muscles which results in bringing the mandible, and therefore the tongue, forward. This study suggests such a compensatory mechanism is the etiological force behind nocturnal bruxism in many patients.”
Simmons JH, Prehn RS. Airway Protection: The Missing Link between Nocturnal Bruxism and Obstructive Sleep Apnea.
BRUXISM Airway protection mechanism
Triggered by upper airway resistance/obstruction
As airflow resistance increases, first response – mouth opens
Airflow Resistance rarely decreases from mouth breathing
Masseter muscle activity follows
Other muscles of mastication join until there is jaw movement
As the jaw moves, the tongue is repositioned, the airflow resistance decreases, the muscle activity decreases and the jaw stops moving, until the resistance builds again
Vicious cycle during sleep
Not dependent on O2 drop
Ankyloglossis
AKA – tongue-tie
Abnormal shortness of the lingual frenum causing limited movement of the tongue
TONGUE TIE RELATED TO DEVELOPMENT
“Restricted tongue mobility was associated with narrowing of the maxillary arch and elongation of the soft palate. These findings suggest that variations in tongue mobility may affect maxillofacial development.”
Yoon AJ, Zaghi S, Ha S, Law CS, Guilleminault C, Liu SY. Ankyloglosis as a risk factor for maxillary hypoplasia and soft palate elongation: A functional-morphological study. Orthod Craniofac Res.
2017;00:1-8.
ONE STEP FURTHER…
“Soft palate length is significantly greater in OSA patients and it is well established that increased soft palate length is a prominent risk factor for upper airway collapsibility.”
Shigeta Y, Ogawa T, Tomoko I, Clark GT, Enciso R. Soft palate length and upper airway relationship in OSA and non-OSA subjects. Sleep Breath. 2010;14:353-358.
Sforza E, Bacon W, Weiss T, Thibault A,Petiau C, Krieger J. Upper airway collapsibility and cephalometric variables in patients with obstructive sleep apnea. Am J Respir Crit Care Med. 2000;161:347-352.
TIE it all together… “Children with untreated short frenulum developed abnormal tongue
function early in life with secondary impact on orofacial growth and sleep disordered breathing(SDB).”
“Short lingual frenulum may lead to abnormal orofacial growth early in life, a risk factor for development of SDB.”
Huang YS, Quo S, Berkowski JA, Guilleminault C (2015) Short Lingual Frenulum and Obstructive Sleep Apnea in Children. Int J Pediatr Res 1:003
Irene Marchesan, PhD SLP Research Associate at CEFAC, Department of Orofacial Myofunctional Therapy. She is world-renowned in this field having authored over 300 articles and books and presided over 400 thesis defenses. She has over 30 years of experience in research and clinical practice in Brazil. As a professor, she has lectured around the world. She is currently President of the Brazilian Speech Pathology Society.
Lingual Frenum Assessment
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Summary
The early soft diet results in muscle weakness and dysfunction
The soft tissue weakness and dysfunction results in underdevelopment
Craniofacial deficiency includes airway deficiency/compromise
Airway compromise leads to sleep disordered breathing
SDB results in sleep fragmentation
Ultimately compensatory breathing and sleep fragmentation deliver unhealthy children who struggle with a long symptom list
An unhealthy child grows up to be an unhealthy adult
Better to treat the craniofacial deficiency early