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DENTAL TRIBUNE Clinical 19 United Kingdom Edition · December 1–7, 2008 The effects of enlarged adenoids on a developing malocclusion By Dr Derek Mahony and Dr Kevin Williams Abstract This article reviews upper airway obstruction caused by hypertrophied adenoids and the possibilities of a subsequent malocclusion. Early diagnosis, and treatment, of pathological conditions that can lead to the obstruction of the upper airways is essential to anticipate and prevent alterations in dental arches, facial bones and muscle function. Correct nasal breathing facilitates normal growth and development of the craniofacial complex (Fig. 1). Important motor functions such as chewing and swallowing depend largely on normal craniofacial development. Any restriction to the upper airway passages can cause nasal obstruction possibly resulting in various dentofacial and skeletal alterations.1 Upper respiratory obstruction often leads to mouth breathing (Fig. 2). Habitual mouth breathing may result in muscular and postural anomalies, which may in turn cause dentoskeletal malocclusions 2 (Fig. 3). Hypertrophy of the adenoids, and palatine tonsils, are one of the most frequent causes of upper respiratory obstruction (Fig. 4). Philosophies regarding the treatment of adenoid hypertrophy range from dietary control and environmental modifi- cations to dentofacial orthopaedics, change of breathing exercises, and surgical procedures. Introduction The aims of this article are to highlight the skills and tools that assist the clinician in iden- tifying upper airway obstruction; to improve the diagnosis of adenoid hypertrophy; and to improve the classification and CHRONIC PERIODONTAL DISEASE? WHAT HAVE YOUR PATIENTS GOT TO LOSE? Fig. 1a treatment of associated malocclusions. The methodology used in this literature analysis consists of a thorough review of narrowly tailored research and Journal articles. The paradigm explored in each article involves upper airway obstruction, adenoid hypertrophy and malocclusion. The results and conclusions stemming DT page 20 PRESCRIBING INFORMATION. Please refer to full Summary of Product Characteristics before prescribing Periostat® 20mg Film-coated Tablets. Presentation: Film-coated tablets, each containing doxycycline hyclate equivalent to 20mg doxycycline in blister packs of 56 tablets. Indications: For patients with adult periodontitis. Periostat is indicated as an adjunct to supra-gingival and sub-gingival scaling and root planing, with oral hygiene instruction, carried out by a dental practitioner or hygienist as appropriate. Dosage and Administration: Adults and elderly – administered twice daily, at least one hour before meals or before bedtime. Swallow whole with at least 100ml of fluid, in an upright position. Take for periods of 3 months. Do not administer for more than 3 consecutive three month periods. Contra-indications: Infancy and childhood up to 12 years of age; hypersensitivity to any of the product excipients or to any of the tetracyclines; achlorhydria; pregnancy and lactation. Warnings & Precautions: To avoid oesophageal irritation and ulceration, adequate fluids should be taken with this medication in an upright sitting or standing position. Periostat therapy may result in overgrowth of nonsusceptible microorganisms including fungi. Periodic observation of the patient is essential and treatment stopped if overgrowth of resistant organisms appears. Use with caution in patients with a history of or predisposition to oral candidosis, hepatic impairment or to those receiving potentially hepatotoxic drugs and patients with myasthenia gravis who may be at risk of worsening of the condition. Avoid excessive sunlight or artificial UV light and discontinue therapy if phototoxicty occurs. Sunscreen should be considered. Treatment should cease at the first sign of skin erythema. In the event of the development of diarrhoea during treatment, the possibility of pseudomembranous colitis should be considered and appropriate therapy instituted. In the event of a severe acute hypersensitivity reaction (eg anaphylaxis) treatment with Periostat must be stopped at once and the usual emergency measures taken. Patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should not take this medicine. Interactions: Absorption of doxycycline from the gastro-intestinal tract may be inhibited by bi- or tri- valent ions such as aluminium, zinc, calcium, by magnesium or iron preparations, activated charcoal, cholestyramine, bismuth chelates and sucralfate. Such medicines or foodstuffs should be taken 2 to 3 hours following ingestion of Periostat. Didanosine and quinapril tablets may decrease the absorption of doxycycline and should therefore be taken at least 2 hours after doxycycline. Doxycycline may potentiate the hypoglycaemic effect of sulphonylurea oral antidiabetic agents. May depress plasma prothrombin activity thereby potentiating the effect of anticoagulants of the dicoumarol type. Avoid concomitant administration of doxycycline and isotretinoin, as there is the possibility of potentiation between the drugs to cause reversible pressure increase in the intracranial cavity (pseudotumour cerebri). As bacteriostatic drugs may interfere with the bacteriocidal action of penicillin and betalactam antibiotics, it is advisable that Periostat and betalactam antibiotics should not be used in combination. Rifampicin, barbiturates, carbamazepine, diphenylhydantoin, primidone, phenytoin, and chronic alcohol abuse, may accelerate the decomposition of doxycycline due to enzyme induction in the liver thereby decreasing its half-life. Sub-therapeutic doxycycline concentrations may result. Doxycycline used concurrently with cyclosporine has been reported to decrease the half-life of doxycycline. Tetracyclines and methoxyflurane used in combination have been reported to result in fatal renal toxicity. Tetracyclines used concurrently with oral contraceptives have in a few cases resulted in either breakthrough bleeding or pregnancy. Side-effects: Refer to SPC for full list. The most commonly reported adverse events in Phase III clinical trials were headache and common cold. The following adverse reactions have been observed in patients receiving tetracyclines: Gastro-intestinal: anorexia, nausea, vomiting, diarrhoea, glossitis, dysphagia, enterocolitis and inflammatory lesions with monilial overgrowth in the ano-genital region, oesophagitis and esophageal ulceration. Hepatoxicity has been reported rarely. Skin: maculopapular and erythematous rashes, StevensJohnson syndrome, skin photosensitivity. Exfoliative dermatitis has been reported but is uncommon. Renal: an apparently dose related increase in blood urea. Blood: thrombocytopenia, neutropenia, haemolytic anaemia, eosiniphilia and porphyria. Hypersensitivity reactions: exacerbation of systemic lupus erythematosus, anaphylaxis, anaphylactoid purpura, pericarditis, urticaria and angioneurotic oedema. Musculoskeletal: Arthralgia. Other: bulging fontanelles in infants and benign intracranial hypertension in adults. Treatment should cease if evidence of raised intracranial pressure develops. Brown-black microscopic discolouration of thyroid tissue has been reported with long term use of tetracyclines. Adverse reactions typical of the tetracycline class of drugs are less likely to occur during medication with Periostat, due to the reduced dosage and the relatively low serum levels involved. Legal Category: POM. Packs: PVC Aclar/aluminium foil blisters containing 14 tablets. Carton pack size 56 tablets. Basic NHS price: 56 tablets – £16.50. Marketing Authorisation number: PL 16853/0078. PA 943/12/1. Full prescribing information is available from: Alliance Pharmaceuticals Ltd, Avonbridge House, Bath Road, Chippenham, Wiltshire, SN15 2BB UK. Alliance Pharmaceuticals Ireland, United Drug House, Magna Drive, Magna Business Park, Citywest Road, Dublin 24 Ireland. Date of preparation/last revised: November 2006. J Clin. Periodontol, 2004; 31: 697-707. References: 1. Preshaw P.M. 2. Data on file – Alliance Pharmaceuticals Ltd. Adverse Event Reporting. Adverse events should be reported. Reporting forms and information can be found at www.yellowcard.gov.uk. Adverse events should also be reported to Pharmacovigilance at Alliance Pharmaceuticals, tel: 01249 466966, email: [email protected]. Fig. 1b AF/815/09.08/0.001 Sept 2008 © Alliance Pharmaceuticals Ltd. Periostat, Alliance and associated devices are registered trademarks of Alliance Pharmaceuticals Ltd. PS20 is a registered trademark of CollaGenex Pharmaceuticals, Inc under licence by Alliance Pharmaceuticals Ltd. Fig. 2 Periostat® contains 20mg doxycycline, a sub-antimicrobial dose. Periostat®, taken twice daily as support to SRP, inhibits the collagenases that attack and weaken tooth attachment structures and thus halts and can even reverse the disease process.1,2 What is more, being systemic, Periostat® treats the whole mouth in one go. Distributed in the UK by: Oraldent Ltd Unit 11 Harvard Industrial Estate Kimbolton Cambridgeshire PE28 0NJ Tel: 01480 862080 Email: [email protected] www.oraldent.co.uk doxycycline film-coated tablets Helping win the battle against gum disease DENTAL TRIBUNE 20 Clinical United Kingdom Edition · December 1–7, 2008 common – that airway obstruction caused by adenoid hypertrophy and malocclusion are related. The degree of that relationship and what it affects is still under debate. This paper attempts only to highlight the positive existence of this relationship and its possible effects regarding dentofacial growth and development. DT page 19 from these articles generally fall into three categories: • That hypertrophied adenoids have a definitive effect resulting in skeletal malocclusion3 • That hypertrophied adenoids, coupled with other factors, may aid in the development of skeletal anomalies4 • That adenoid hypertrophy has no effect on airway obstruction and malocclusion. Fig. 3 The research in this area is expansive, but largely inconsistent. Thus, the cause-and-effect relationship of adenoid hypertrophy and malocclusion must be carefully examined on a Fig. 4 case-by-case basis.5 Regardless of the various researchers’ conclusions, one theory remains Basic facial growth and development Fig. 5 Developments in the understanding of human craniofacial growth have stemmed from histological and embryologic studies, radiographic cephalometry, correlation of growth and facial anomalies analysis of surgical interventions, animal research and other science fields.6 Despite these studies, we are still waiting for a definite consensus regarding the controlling mechanism of craniofacial tissue. Seasons Greetings to all our dental customers and partners Postnatal facial growth is influenced by genetic and environmental factors.2 Most facial growth and development occurs during the two childhood growth peaks. The first growth peak occurs during the change from primary to permanent dentition (between five and 10 years of age) and the second growth peak occurs between 10 and 15 years of age.2 The study of the early years of life shows that by the age of four, 60 per cent of the craniofacial skeleton has reached its adult size. By the age of 12, 90 per cent of facial growth has already occurred.7 By age seven, the majority of the growth and development of the maxilla is complete and by age nine, the majority of the growth and development of the mandible is complete. Proper facial growth is affected either positively or negatively, early in life, by the sequential occurrences of four major factors: This year Henry Schein Minerva would all Suppliers to make donations to Brid rather than send gifts. Bridge2Aid is a registered charity operating den community development programme in North W It provides primary dental care and education w and training local people as health care professio As part of their year long commitment to Bridge2 chosen charity, Henry Schein Minerva will featur events throughout 2009 seeking to enhance even charity’s profile amongst the dental community. Please give generously at www.justgiving.com/henryschei Partnership in Practice nc ar es st .ju www Contribute to th e Henry Schein M inerva Bridge2Aid fun d raising target! Visit gi i vin he c g.co s m/henr y Practice Software Make your contribution Business Solutions visit: www.justgiving.com/henryscheincares www.bridge2aid.org.uk Consultancy Services Surgery Design & Installation Best Value Dental Consumables Henry Schein Minerva Dental Centurion Close Gillingham Kent ME8 0SB 08700 10 20 43 London Cardiff Glasgow Belfast • The cranial base must develop properly • The naso-maxillary complex must grow down and forward from the cranial base • The maxilla must develop in a linear and lateral fashion • A patent airway must develop properly. The relationship between the naso-maxillary complex and the cranial base is significant for aesthetic reasons and proper facial bone, muscle and soft tissue support. To allow proper downward and forward rotation of the mandible, the maxilla must be adequately developed, in width, for acceptance of the mandible. Any limitation on mandibular rotation may affect the relationship of the condyle to the glennoid fossae (in the temporal bone) resulting in multiple TMJ problems. An improper airway will affect the global individual growth.8 The simultaneous growth of these factors is not nearly as significant as how these factors interrelate during facial growth and development. For example, the basic design of the face is established by a series of interrelated factorial developments. The naso-maxillary Clinical Orascoptic HiRes Rudy Revolution The Revolution is Through-the-Flip! Fig. 8 complex is associated with the anterior cranial fossae. The posterior boundary of the maxilla determines the posterior limits of the midface. This structural plane is significant to facial and cranium development. The basic structural format of facial growth and development is dependent on, and governed by, the interrelation of multiple functional matrices. These functional matrices include a phenomenon of bone displacement and growth at the TMJ with the maxillary forward and downward movement equaling mandibular growth upward and downward. The displacement and growth phenomenon is responsible for the spatial relationship necessary for functional joint movement resulting in the final result of facial growth.9 Additionally, muscle adaptions affect dentoskeletal development. The integration of the musculoskeletal system affects respiration, mastication, deglutition, and speech.2 This basic understanding of facial growth and development is relevant as adenoidal tissue enlargement coincides with major facial growth, for example, they occur simultaneously. Facial growth may be restricted by abnormal development of adenoidal tissue resulting in abnormal swallowing and breathing patterns (Fig. 5). Adenoidal growth and development Lymphoid tissue is normally present as part of the Waldeyer’s tonsillar ring in the form of a nasopharyngeal tonsil (Linder-Aronson 1970). The Waldeyer’s ring is the system of lymphoid tissue that surrounds the pharynx. This system of tissue includes adenoids and pharyngreal tonsils; lateral pharyngeal tonsils; lateral pharyngeal bands; palatine tonsils and lingual tonsils (Fig. 6). Tonsils and adenoids have disparate embryonic origins and cytology even though they are both part of Waldeyer’s ring.10 Bacteria may play a role in adenoid hyperplasia. Specifically, different pathogens, such as Haemophilus influenza and Staphylococcus aureus, have been associated with lymphoid tissue hyperplasia. The adenoid lymphoid structures are lined with ciliated respiratorytype epithelium which is normally distributed throughout the upper and posterior nasopharynx walls. During the presence of disease, the distribution of the dendritic cells (antigen presenting cells) is altered. The result is that there is Fig. 7 an increase in dendritic cells in the crypts, and extrafollicular areas, and a decrease in surface epithelium dendritic cells. Lymphoid tissue is normally not apparent in the early infant stage of life. Marked symptoms of adenoid development are most common in the childhood age range of two to 12. During adolescence, a decrease in adenoid size is noted as current with the growth of the nasopharynx. Rarely is adenoid tissue present in adults and when it is noted it is usually in an atrophic condition. The cause of the involution of the Waldeyer’s ring is still under investigation.12 The imbalance in the relationship between the enlargement of the nasopharynx/nasopharyngeal airway and the concomitant growth of adenoid tissue can result in reduced patent nasopharyngeal airway and increased nasopharyngeal obstruction.10 The growth of adenoidal tissue as demonstrated by a bell curve, peaks at or near age six6 and also begins involution at or near this age as well (Fig. 7). Facial growth is coupled with adenoidal growth. As the cranial base forms the roof of the nasopharynx, a close examination of the growth and development of the craniofacial complex becomes significant for evaluation of the size and configuration of the nasopharyngeal airway. Any abnormal development regarding this craniofacial complex may affect the nasopharyngeal airway. Abnormal adenoidal growth that occurs during childhood, may consume the nasopharnx and extend through the posterior choanae in the nose.13 This excessive adenoidal growth usually interferes with normal facial growth and can result in abnormal breathing patterns, congestion, snoring, mouth breathing, sleep apnea.4 Eustachian tube dysfunction/otitis media, rhinosinusitis, facial growth abnormalities, swallowing problems, reduced ability to smell and taste, and speech problems.12 Theoretically, many clinicians believe the blockage should be removed as soon as possible through a surgical procedure called adenoidectomy. However, according to a study conducted by Havas and Lowinger one-third of child study patients, with traditional adenoidectomies, were ineffective with intranasal extensions of the adenoids obstructing the posterior choanoe. For this segment of the study population the “powdered-shaver adenoidectomy” was effective in the complete removal of the obstructive Fig. 8 adenoid tissue ensuring postural patency.13 Upper airway obstruction and mouth breathing During normal nasal respiration, the nose filters, warms and humidifies the air in preparation for its entry into the body’s lungs and bronchi. This nasal airway also provides a degree of nasal resistance in order to assist the movements of the diaphragm and intercostals muscles by creating a negative intrathoracic pressure. This intrathoracic pressure promotes airflow into the alveoli.7,15 Correct normal resistance is 2cm–3.5cm H2O/L/Sec and results in high tracheobronchial airflow which enhances the oxygenation of the most peripheral pulmonary alveoli. In contrast, mouth breathing causes a lower velocity of incoming air and eliminates nasal resistance. Low pulmonary compliance results.7 According to blood gas studies, mouth breathers have 20 per cent higher partial pressure of carbon dioxide and 20 per cent lower partial pressures of oxygen in the blood, linked to their lower pulmonary compliance and reduced velocity.7,16. Contributing factors in the obstruction of upper airways include: anatomical airway constriction, developmental anomalies, macroglossia, enlarged tonsils and adenoids, nasal polyps and allergic rhinitis.5 However, for purposes of this paper the focus shall be on enlarged adenoids as the major contributing factor. There are numerous studies that link adenoid hypertrophy with nasopharyngeal airway obstruction to the development of skeletal and dental abnormalities.14 Airway obstruction, resulting from nasal cavity or pharynx blockage, leads to mouth breathing which results in postural modifications such as open lips, lowered tongue position, anterior and posteroinferior rotation of the mandible, and a change in head posture. These modifications take place in an effort to stabilize the airway. As previously discussed, facial structures are modified by postural alterations in soft tissue that produce changes in the equilibrium of pressure exerted on teeth and the facial bones (Fig. 8). Additionally, during mouth breathing, muscle alterations affect mastication, deglutition and phonation because other muscles are relied upon.2 DT page 22 Unique TTF design Versatile performance Sporty frame Orascoptic Rudy Revolution is the first hybrid loupe that combines through-the-lens and flip-up technology. 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Arrange a no-obligation consultation FreeCall 0500 321111 or visit our website www.evident.co.uk loupes & lights air abrasion ergonomic seating desirable consumables must-have technology T: 020 7722 0072 F: 020 7722 0976 E: [email protected] W: www.evident.co.uk FreeCall 0500 321111 Evident expandi ng hori zons DENTAL TRIBUNE 22 Clinical United Kingdom Edition · December 1–7, 2008 an added valuable diagnostic tool for the orthodontist in the evaluation of children with upper airway obstructions14 (Fig. 13). Treatment of nasal obstruction Fig. 9 DT page 21 Malocclusion – the issue still in debate Is there a cause and effect relationship between adenoids, nasal obstruction and malocclusion? Dentofacial changes associated with nasal airway blockage have been described by CV Tomes in 1872 as adenoid facies. Tomes coined this term based on his belief that enlarged adenoids were the principle cause of airway obstruction and resulted in noticeable dentofacial changes.7 Tomes reported that children, who were mouth breathers, often exhibited narrow V-shaped dental arches10 (Fig. 9). This narrow jaw is a result of mouth breathers keeping their lips apart and their tongue position low. The imbalance between the tongue pressure, and the muscles in the cheek, result in cheek muscles compressing the alveolar process in the premolar region. Simultaneously, the lower jaw postures back (Fig. 10). These simultaneous actions have been termed the compressor theory.11 Tomes’s views were supported in the 1930s by numerous leading orthodontists. These supporting clinicians reported airway obstruction as an important aetiologic agent in malocclusion. Rubin advocated that in order for these patients to fully be assessed they must be thoroughly evaluated by both a rhinologist and orthodontist.7 Malocclusion is the departure from the normal relation of the teeth in the same dental arch or to teeth in the opposing arch.3 Airway obstruction, coupled with loss of lingual and palatal pressure of the tongue, produces alterations in the maxilla. The positioning of the tongue also plays an important role in mandibular development. The tongue displaced downward can lead to a retrognathic mandible; and an interposed tongue can lead to anterior occlusal anomalies. Additionally, maxillary changes can be viewed in the transverse direction, producing a narrow face and palate often linked with cross bite; in the anteroposterior direction, producing maxillary retrusion; and in the vertical direction causing an increase in palatal inclination as related to the cranial base and excessive increases of the lower anterior face height. The most commonly found occlusal alterations are cross bite (posterior and/or anterior), open bite, increased over jet, and retroclination of the maxillary and mandibular incisors.2 Mahony Fig. 10 and Linder-Aronson’s findings were in agreement with the significant correlation between changed mode of breathing and diminished mandibular / palatal plane angle (ML/NL) found in adenodectomised children.22 Several authors have taken the position that alleged faces are not consistently found to be associated with adenoids, mouth breathing, nor a particular type of malocclusion; and that there is no cause and effect relationship between adenoids, nasal obstruction/mouth breathing and malocclusion. Proponents of this position believe that the V-shaped palate was inherited and not acquired through mouth breathing. Hartsooh (1946), on a review of literature related to mouth breathing, concluded that mouth breathing is not a primary etiological factor in malocclusion. Additionally, Whitaker (1911) found that in a study of 800 children, who underwent adenoidectomy or tonsillectomy only 30 per cent had dental anomalies that needed orthodontic intervention. There is some suggestion that adenoids and hypertrophic tonsils are a consequence of a thyroid hormone deficiency. This hormone deficiency acts as a catalyst for activating the organism’s de- Fig. 11 fense mechanisms, which include hypertrophy of lymphoid tissue.11 Another orthodontic clinician, Vig, took the position that without documented total nasal obstruction, any surgery or other treatment to improve nasal respiration is empirical and difficult to justify from an orthodontic point of view.7,17 Nasal respiratory evaluation The relationship of airway obstruction and dentofacial structures/malocclusion is still the subject of investigation and controversy amongst orthodontists. The correlation between functional problems and morphologic characteristics is yet to be solidified. Regardless of varied opinion in this area practitioners should observe each patient carefully. Suggested protocol As the patient enters the room, facial and head posture should be noted to see if the lips are closed during respiration. Signs of allergic rhinitis should be noted, as well as histories of frequent colds or sinusitis. Assessment of family history for allergies is important. Sleep history should be evaluated: sleep apnoea, loud snoring, openmouth posture while asleep. Patient is asked to seal their lips – difficulty breathing through nose should be noted. One nostril can be occluded and the response noted – same procedure on the other side. (Fig. 11) Fig. 12 The evaluation of nasal airway patency is complicated, especially when the possibility exists that airways may clinically appear inadequate but be quite functional physiologically. Lip separating or an open-mouth habit is not an infallible indicator of mouth breathing. Often complete nasal respiration is coupled with dental conditions that cause open-mouth posture.10 Adenoid evaluation Nasopharyngeal space and the size of adenoids have been evaluated using different methods of assessment: Fig. 13 Fig. 14 1. Determination of the roentgenographic adenoid/nasopharyngeal ratio (a lateral cephalometric xray) 2. Flexible optic endoscopes (Fig. 12) 3. Acoustic rhinometry 4. Direct measurements during surgery. Direct measurements are considered to be the most accurate because space can be assessed in three directions.12 A lateral cephalometic radiograph is Adenoidectomy with or without tonsillectomy is indicated if hypertrophied adenoids (and tonsils) are the cause of upper airway obstruction.7 Powered-Shaver Adenoidectomy – Adenoidectomy coupled with Endoscopic Visualization will assist in achieving adequate removal of adenoids particularly high in the nasopharnx. Use of the powered-shaver technique allows for better clearance of obstructive adenoids. The end result is more reliable restoration of nasal patency.13 Septal surgery (rarely indicated in the child) but may be considered in the presence of a marked nasal septal deflection with impaction. Conservative septal surgery in growing patients will not have an adverse effect in dentofacial growth.7,18,19,20 – Maxillary expansion (RME or SAME) – an orthodontic procedure that widens the nasal vault7,18 (Fig. 14). – Cryosurgery or electrosurgery – this is a viable option for patients with vasomotor rhinitis.7 – Bipolar Radiofrequency Ablation (allergic rhinitis) – performed under local anesthetic – Inferior turbinectomy – Using powered instrumentation – Use of nasal sprays. Fig. 15a Fig. 15b Fig. 15c Fig. 15d Conclusion The effect of adenoids on facial expression, malocclusion and mode of breathing has been a topic of debate and investigation by practitioners in the field for the last one hundred years. A review of the literature exposes several theories. A healthcare provider, with a practice philosophy based on prevention of malocclusion development, cannot ignore the early years of the patient’s growth cycle. By age twelve, 90 per cent of facial growth has already occurred. This is the age when many practitioners begin orthodontic treatment.7 This is the age when 80–90 per cent of craniofacial growth is complete, so most formation and/or deformation has occurred.21 To wait until 90 per cent of the abnormality has occurred, before beginning treatment, is not consistent with a preventive philosophy. Interceptive measures must be initiated sooner. Early intervention requires an acceptance of a multidisciplinary approach to total patient health. An integrated approach to patient evaluation, diagnosis and treatment is most effective. Primary care physicians, dentists, allergists, otorhinolaryngologists, and orthodontists must all work together for early prevention and management of young patients with increased nasal airway resistance. After diagnosis, a comprehensive risk benefit analysis re- Fig. 15e Fig. 15f garding early intervention must be considered. Although hereditary and environmental factors must be considered, the universal goal is the promotion of proper nasal respiration throughout a child’s early years of facial growth. Figure 15 (a–f) shows the before-and-after treatment results of a young girl who had her adenoids removed, and then underwent maxillary expansion before full-fixed braces. She was treated as a second opinion against the removal of four premolar teeth to relieve dental crowding. DT References 1. Mattar, SE, Anselmo-Lima, WT, Valera, FC and Matsumoto, MA, Skeletal and Occlusal Characteristics in Mouth-Breathing Pre- DENTAL TRIBUNE School Children, J Clin Pediatr Dent 2004 28(4):315-318. 2. Valera, FC, Travitzk, LV, Mattar, SE, Matsumoto, MA, Elias, AM, Anselmo-Lima, WT, Muscular, Functional and Orthodontic Changes in Pre-School Children with Enlarged Adenoids and Tonsils, Int J Pediatr Otorhinolaryngal 2003, Jul; 67(7):761-70. 3. Khurana, AS, Arora, MM, Gajinder S., Relationship Between Adenoids and Malocclusion, J Indian Dental Ass., April 1986; 58:143-145. 4. Pellan, P., Naso-Respiratory Impairment and Development of Dento-Skeletal, Int JO Fall; 16(3):9-11, 2005 Clinical 23 United Kingdom Edition · December 1–7, 2008 About the author About the author Dr Kevin Williams manages two general dentistry practices in Greenville and Spartanburg, South Carolina, with an emphasis on facial driven orthodontics and oral surgery. He received his dental degree from the Medical University of South Carolina in 1993. His interest in airway and malocclusion developed from his children’s airway issues. Dr Williams is a Fellow in the Academy of General Dentistry and a Certified Senior Instructor in the International Association of Orthodontics. Email [email protected]. Dr Derek Mahony is a graduate of the University of Sydney, Faculty of Dentistry, and an Alumnus of the University of London, masters programme in orthodontics. He is a Fellow of the International College of Dentists and is considered a pioneer, throughout the world, in raising dentist’s awareness of the need for early interceptive orthodontic treatment. Email [email protected]. 5. Soxman, JA, Upper Airway Obstruction in the Pediatric Dental Patient, Gen. Dentistry July-August; 313-315, 2004. 6. Ranly, DM, Craniofacial Growth, Dent Clin NA, July; 44(3):457-470, 2000. 7. Rubin, RM, Effects of Nasal Airway Obstruction on Facial Growth, Ear, Nose & Throat J, May;66:44-53, 1987. 8. Pistolas, PJ, Growth and Development in the Pediatric Patient, The Functional Orth. 12-22 Winter 2004/Spring 2005. 9. Enlow, DH, Hans, MG, Essentials of Facial Growth; 5, 79-98, 206, 1996 10. Diamond, O, Tonsils and Adenoids: Why the Delima? Am J. Orthod., Nov. 78(5) 495-503, 1980. 11. Linder-Aronson, S, Adenoids: Their Effect on the Mode of Breathing and Nasal Airflow and Their Relationship to Characteristics of the Facial Skeleton and the Dentition, Acta Oto-laryng Suppl, 265: 5-132, 1970. 12. Casselbrant, MC, What is Wrong in Chronic Adenoiditis/Tonsillitis Anatomical Considerations, Int J Pet. Oto 49(1):S133-S135, 1999. 1.5Hour CPDPoi s nts 13. Havas, T, Lowinger, D, Obstructive Adenoid Tissue an Indication for Powered-Shaver Adenoidectomy, Arch Otolaryngol Head Neck Surg: July 2002; 128:789791. 14. Oulis, CJ, Vadiaka, GP, Ekonomides, J, Dratsa, J, The Effect of Hypertrophic Adenoids and Tonsils on the Development of Posterior Crossbite and Oral Habits, J Clin Pediatr. Dent, Spring; 18(3) 197-201, 1994. 15. Adams, GL, Boies, CR, Papaiella, MM, Boies’ Fundamental Oto. Philadelphia WB Sanders 1978. 16. Ogura, JH, Physiologic Relationships of the Upper and Lower Airways, Ann Otgl Rhinol Laryngol, 79; 495-501, 1970. 17. Vig, PS, Sarver, DM, Hall, DJ, et al, Quantitative Evaluation of Nasal Airflow in Relation to Facial Morphology, Am J Orthod, 79:263-272; 1981. 18. Gary, LP, Brogan, WF, Septil Deformity Malocclusions and Rapid Maxillary Expansion, Orthodontist 4; 1-13, 1972. 19. Cottle, MH, Nasal Surgery in Children, Eyo, Ear, Nose and Throat Monthly; 30:32-38, 1951. 20. Jennes, JL, Corrective Nasal Surgery in Children: Long Term Results, Arch Otolaryngal; 79:145-151, 1964. 21. Mahony, D., Page, D. The Airway, Breathing and Orthodontics; Ortho Tribune,8-11. 22. Mahony, D., Linder-Aronson, S. Effects of adenoidectomy and changed mode of breathing on incisor and molar dentoalveolar heights and anterior face heights. AOJ; 20:93-98,2004. Dental Webinars Be Wherever You Want Let the Seminar Come to You... 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