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Etiology of Class II Malocclusions

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Etiology of Class II Malocclusions Etiology of Class II malocclusions Timothy Shaughnessy, DDS, MS, Workshop Leader Lawrence H. Shire, DDS, Workshop Recorder In reviewing the literature relative to the develop- sia, and mobius syndrome are a few of the more widely ment of Class II malocclusions, it can be learned that known. "not every Class II is a Class II." Wemust rememberthat Inter-arch problems such as Class II and Class III behind the soft tissue drape of the patient’s face is a malocclusions are genetic in nature, while intra-arch totally dynamic process that can be influenced by our problems also have an environmental component as heritage and altered by our environment. We realize well. when performing an occlusal evaluation of our young Looking at the importance of environmental vs. patients, findings like distal step molar relation or an inherited factors in the etiology of malocclusions, it was unusually large overjet may be presenting a false im- suggested that urbanization (and evolution) influence pression of what appears to be a true skeletal Class II malocclusions, making them more severe. The evolu- malocclusion. tionary factors involved are: a decrease in the size of the In addition to distal step molar relation, or an unusu- jaws, size and number of the teeth. We have no control ally large overjet, tooth size discrepancy with or without over these evolutionary factors (as well as the hereditary malrelated mandible and maxilla may also give the first factors), whereas the environmental factors can often be impression of a true skeletal Class II malocclusion. eliminated through preventive or interceptive treat- Skeletal Class II malocclusions can be found to have ment at the appropriate time. variants in one or more of the following regions: (1) Mandibular growth deficit following condylar frac- maxillo-mandibular relationship (mandibular tures or major trauma to the joint complex is highly retrognathism, midface protrusion or both); (2) the cra- likely. Proffit (1980) found between 5 and 10%of all nial base (increased length of the anterior cranial base severe mandibular deficiency or asymmetry problems will contribute to the midface protrusion, while length- were related to previous fracture of the mandibular ening of the posterior cranial base will tend to position condylar process. In this article, Proffit cites Walkerand the temporomandibular articulation more retrusively); also Gilhuus-Moeas noting that the younger the patient (3) vertical dysplasia (anterior upper face height often at the time of the injury, the greater the potential for greater than normal); (4) steep occlusal plane (a reflec- complete regeneration of the condyle, and healing with- tion of vertical skeletal dysplasia). out residual deficit. Proffit (1978) states that Lundfound Whatrole does genetics play in the etiology of Class essentially complete recovery in 75% of the children II malocclusions? According to the study by Lundstrom with early condylar fractures. The treatment goals for (1984), investigations published prior to that article patients with condylar fractures include the restoration have suggested that about 40% of commonanomalies in of joint function, occlusion, and facial symmetry. The tooth position and in the relationship between maxil- current theory on early treatment of condylar fracture in lary and mandibular dental arches are due to genetic the growingchild calls for firm fixation for only I week, differences between individuals. Corruccini and Potter with physical therapy and mouth opening exercises (1980), in studies of different dental and occlusal vari- beginning immediately after release of the rigid fixa- ables, found the heritability of dental overjet was re- tion. duced to zero. Several syndromes have Class II maloc- Condylar fractures often go unnoticed and result in clusions as a major finding. Of these syndromes, Class II malocclusions with asymmetry or severe Treacher Collins, hemifacial microsomia, achondropla- mandibular deficiency. Progressive deformity is associ- ated with mechanical limitations on growth and the resulting condition is referred to as "functional 336 SPECIALREPORT -- ETIOLOGY OFCLASS II MALOCCLUSIONS:Shaughnessy and Shire ankylosis." Ankylosis of the mandible can be thought of tal components. Changes in head, jaw, and tongue as fusion across the TMJ. This fusion restricts motion position could be seen in the experimental group. Some and inhibits growth. "In order to grow properly, the traits commonamong the sample were increased face mandible must be able to translate" (Proffit 1980). height, steeper mandibular plane angle, and larger Sometheories to explain the growth of the craniofa- gonial angle. It should be noted that someof the animals cial complexinclude: (1) Sicher’s role of sutural growth; in the experimental group developed other than Class II (2) Scott’s role of the cartilage and the knowledgethat malocclusions. Class III malocclusions as well as Class I bone growth is secondary to cartilage growth; or (3) malocclusions were also seen. It is not the change in Moss’s functional matrix hypothesis that cartilage and breathing pattern that caused the malocclusions, but bone respond secondarily to soft tissue growth. Still rather it is the change in related functional demandson another theory is that of the influence of mouth breath- the craniofacial musculature and their obligatory re- ing vs. nasal breathing to which Harvold (1980) eluded. sponse. Proffit (1978) states that the postural positioning Experiments on transplantation and obvious reac- of the head, mandible, and tongue are all at the subcon- tions to manipulation of the sutures have, to some scious level. Dentoalveolar morphology can be shown degree, ruled out the sutural growth theory. Cartilage to be related to head posture. The more the head is held studies have shown both positive and negative influ- forward, the more likely that the upper dentoalveolar ences on growth whentransplantation of cartilage is the height will be increased. Also, there will be an increase variable factor of the studies. This depends upon in the steepness of the occlusal plane related to forward whether the cartilage is primary (from the primordial posturing of the head. skeleton) or secondary cartilage. Primary cartilage is McNamara(1981) reviewed Linder-Aronson’ s work growth center where.as secondary cartilage, like that of from 1975 where it was shown, on a small sample size, the condyle, is a growthsite. It has been shownthat there that removal of nasal obstruction (adenoidectomy) in is a positive correlation betweenthe soft tissue influence children, followed for 5 years postoperatively, had an and the growth of the craniofacial complex. For ex- average°. reduction in the mandibular plane angle of 4 ample, excessive intracranial pressure will cause hydro- This was twice the reduction found in the control group cephaly, with a markedincrease in the size of the calvar- (those without nasal airway obstruction and without ium, whereas diminished growth of the brain causes adenoidectomy). microcephaly. Whenan eye is removed from a child for . Are there other environmental factors that cause treatment of a tumor, the orbit does not continue to grow Class II malocclusions? Early loss of maxillary primary in the normal fashion. molars can influence the development of Class II maloc- Normally, teeth are balanced between the tongue clusions by allowing the maxillary molar, that maybe in and the lips. Resting pressure must be considered more an end-on relation with the mandibular molar, to slip important than the pressure created during chewing, forward thus establishing a dental Class II situation. It swallowing, or speaking, since the time we are at rest far would appear that local environmental factors influ- outweighs the time we are performing these other func- ence a dental Class II morethan they influence a skeletal tions. Whencomparing forces necessary to moveteeth, Class II. Understanding the etiology of the malocclu- heavy intermittent pressure has less effect than light sion, should play a role in developing a treatment plan. continuous forces. Howdo habits relate to Class II malocclusions? As The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the was previously stated, the light continuous forces are views of the Department of the Armyor the Department of Defense. much more detrimental to the oral complex than are heavy intermittent forces. Habits such as thumb suck- Dr. Shaughnessyis in the private practice of orthodontics in Marietta, ing, when performed for fewer than 6 hr per day, have Georgia, and Dr. Shire is deputy director, U.S. ArmyPediatric Den- not been shownto be responsible for anterior open bites tistry Residency Program, Ft. Lewis, Washington. Reprint requests should be sent to: Dr. Lawrence H. Shire, QTRS2338 S. 3rd St., Ft. or Class II malocclusions. Forward positioning of the Lewis, WA98433. tongue (seen during swallowing in patients with ante- rior open bite) is morelikely to be an effect than a cause. Corruccini RS, Potter RH: Genetic analysis of occlusal variation in What is the mechanism by which nasal impairment twins. AmI Orthod 78:140-54. 1980. could alter dentofacial form? Harvoldet al. (1981), using Harvold EP etal: Primate experiments on oral respiration. AmJ rhesus monkeys, forced them to become mouth breath- Orthod 79:359-72, 1981. ers by mechanical obstruction of their nasal airway. He Lundstrom A: Nature versus nurture in dentofacial
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