Distal (posterior) occlusion is referred to sagittal occlusion anomalies and is characterized by a great variety of clinical forms and presentations.The type of occlusion, at which the upper jaw is protruding excessively, was described for the first time in 1886 by V.V. Dementyev, and in 1889 Sternfelf applied the term “prognathism”, which has been widely used in orthodontics ever since. The term “posterior occlusion” was introduced by Licher in 1926, and now it has a lot of synonyms in literature: the 2nd class, anomaly of the 2nd group, posterior occlusion, distal bite, etc.
Posterior occlusion is one of the most widespread anomalies and makes on average from 3.6 to 65 % of all the types of pathologic occlusions. The given data is rather variable, which is explained by the absence of a single technique of examination and criteria difference in the diagnostics of dentognathic anomalies.
Posterior occlusion cases frequency varies in age aspect as well, but, according to many scholars, it takes place in the period of transitional dentition occlusion most often — from 15 to 20 %. This is explained, on the one hand, by unstable relative physiological equilibrium of the dentognathic apparatus in the period of transitional dentition, and on the other hand, by the fact that some anomalies in the period of mastication apparatus final formation disappear as a result of self-recovery.
The clinical symptom of posterior occlusion is the prognathic correlation between the dental arches, which may arise as a result of different interrelations between dentognathic apparatus elements, and also location of the apparatus in the cranium.
Thus, Angle in his anatomico-morphological classification refers the prognathic correlation between the dental arches to 2nd class anomalies, when the lower 1st molars are located distally relative to the upper ones. Angle considers this correlation to be caused by the lower jaw as the only movable bone of the facial skeleton. The author singles out two varieties of the 2nd class: 1) protrusion with frontal upper teeth diaereses and 2) frontal part retrusion.
A.Y. Katz recommends taking into account the functional state of mastication muscles during dentognathic anomalies diagnostics. At prognathic jaws correlation the functional insufficiency of the muscles protruding the lower jaw {m. pterygoideus lateralis) takes place. He refers such dental arches correlations to 2nd group anomalies.
L.V. Ilyina-Markosian, diagnosing prognathic occlusion forms, offers taking into account lower jaw displacement at usual location. She refers prognathic dental arches correlation to sagittal occlusion anomalies, applying the term “posterior occlusion” and singling out its three varieties:
o without lower jaw displacement;
o with lower jaw displacement;
0 mixed form.
D.A. Kalvelis takes account of etiological agents when diagnosing dentognathic anomalies. The author refers prognathism to sagittal occlusion anomalies, emphasizing its hereditary nature.
On the basis of etiological signs A. Kantorowicz singles out posterior occlusion arising because of the distal position of the lower jaw or the 1st molars during their eruption.
According to V.Y. Kurliandskyi classification, dental arches correlation anomalies are to be evaluated by the signs of underdevelopment or excessive development of jaws and their combination with normal development. Therefore prognathic dental arches correlation may be caused by excessive development of the upper jaw or lower jaw underdevelopment.
A.I. Betelman refers posterior occlusion to sagittal anomalies and depending on the jaws development degree singles out four clinical forms:
1 — lower micrognathia;
2 — upper macrognathia;
3 — upper macrognathia and lower micrognathia;
4 — upper prognathism with narrowing in the lateral parts.
S.I. Kryshtab offered a pathogenetic classification of sagittal lower jaw deformations. It is based on the degree of the articular process, as the centre of lower jaw longitudinal growth, being included into the pathologic process, and divided this deformation into two nosologic groups: condylar and extracondylar. The author considered typical of condylar ones to be characterised by jaws bodies underdevelopment, and of supracondylar — alveolar process reduction.
In recent years teleroentgenography is widely used in the diagnostics, prognosis, and choosing the method of treating an orthodontic pathology. Teleroentgenography is used as an additional investigation method, which allows characterizing facial skeleton growth peculiarities, localization, patient’s individual profile.
A. El-Nofeli (1964), analyzing teleroentgenograms data, singles out two forms of posterior occlusion:
1) dental posterior occlusion with normal correlation of facial elements;
2) skeletal posterior occlusion with pathologic correlation of facial elements.
A.M. Schwarz (1969) and F.Y. Khoroshilkina (1976) during studying lateral head
teleroentgenograms detected three basic forms of posterior occlusion: dentognathic, gnathic, and combined.
A.S. Shcherbakov (1967) differentiates dentognathic and skeletal forms of posterior occlusion.
According to the WHO systematics (
o jaw size anomalies (upper jaw macrognathia, lower jaw micrognathia);
o anomalies of jaws position relative to the skull base (upper jaw prognathism, lower jaw retrognathia);
o dental arches correlation anomalies (posterior occlusion).
Posterior occlusion may be caused by different etiological agents and be the consequence of many functional and morphological dentognathic apparatus damages. Heredity is of big importance in prognathism development. Studying twins, some scholars (Siemens, Praeger, Kantorowicz, Korkhaus, 1939) concluded that anomalies, including prognathism, may be inherited. Not only face type, but also jaw size and occlusion form may be alike. Prognathism is also caused by constitutional peculiarities of the organism, the state of the patient’s reactivity to environmental factors influence.
Intrauterine factors are also significant in posterior occlusion formation, first of all that is mechanical fetal injuries. In the womb the fetus is in the amniotic fluid protecting it from shakings and strokes. Fluid quantity changes in different periods of intrauterine development — from
At typical fetal position the upper and lower extremities are pressed to the face, and due to the high pressure of the amniotic fluid or mechanical pressure from outside there may appear a deformity or growth inhibition of the maxillofacial skeleton.
Schwarz considers that the ventral fetus position may lead to distal lower jaw position.
Special attention must be paid to the mother’s level of health during pregnancy. The influence of radioactive, pharmacological, and other external agents, hard working conditions, irrational unbalanced diet, metabolic disorder and endocrine glands dysfunction, injuries, early pregnancy toxemia may lead to dentognathic apparatus development deviations.
The parents’ age, especially the mother’s, at the time of child’s birth, presence of hereditary, chronic, and specific diseases also mean a lot.
Posterior occlusion may appear at difficult prolonged labor. Obstetric intervention at abnormal labor (forceps or vacuum delivery) sometimes causes an injury of the dental germs or TMJ, which not infrequently leads to prognathism.
Etiological agents, arising as a result of extrauterine agents influence, are the main ones causing posterior occlusion.
The character of child’s feeding considerably influences jaws growth and development. A child is known to be born with distal lower jaw location (physiological ret- rognathia).
The function of sucking is a big load on the infant’s mastication muscles. Due to the functional tension of muscles and intensive transfer of the lower jaw forward, by the end of the lactation period neutral position of jaws is noted. At artificial feeding lower jaw growth is inhibited and it takes the distal position, which leads to physiological retrognathia preservation. Artificial feeding from a bottle violates favorable functional irritation and the mastication apparatus is inhibited in its development
sucking movements do not require lower jaw displacement, mixture from the bottle pours into the infant’s mouth, and rubber nipples caot substitute natural feeding.
The character of food also matters in posterior occlusion development. Feeding children with soft, grinded food, which does not require intensive mastication, develops mastication “laziness” in children. This leads to underdevelopment of the mastication muscles, which not infrequently causes underdevelopment of the lower jaw alveolar process.
Nasal breathing violation may be one of the reasons for prognathism. At mouth breathing the tongue changes its position — it is adjacent not to the palatine surfaces of the upper teeth, but to the lower teeth. Without inner tongue support the upper dental arch narrows from the sides, becomes elongated and protrudes in the frontal part. Negative pressure forms in the nasal cavity at nasal duct obstruction. As a result of reinforced drawing in of the air and constant pressure of the air flow from the side of the oral cavity high palate forms and dental arches form changes. Posterior occlusion formation is promoted by infantile diseases, especially rachitis. Vitamin D deficiency violates calcium and phosphorus metabolism. Bones become “soft” and are easily deformed. At that, growth zones activity is considerably disturbed.
Children’s pernicious habits take significant place in prognathism etiopathogene- sis. These habits include sucking fingers, tongue, lips, rubber nipple and other objects. All these habits exist in the period of occlusion formation and, acting for a long period of time, provoke bone deformation. For instance, thumb sucking causes upper frontal teeth protrusion, excessive development of the interincisor bone because of mechanical pressure and trophism change on certain parts of the jaw bone. At that, the anterior part of the lower jaw is underdeveloped and flattened.
Head position during sleep is very important. If the head is thrown back, the lower jaw acquires the distal position as this increases the recoil of the muscles dislocating the lower jaw backwards. The tongue position and functional state also influence dental arches and occlusion formation. Posterior occlusion most often arises because of the slow growth and development of the lower jaw after an injury, chronic inflammation, congenital absence or death of dental germs, premature extraction of milk teeth, permanent teeth retention on the lower jaw, supplemental teeth on the upper jaw.
Posterior occlusion has characteristic facial and intraoral signs. The most significant facial sign of prognathic occlusion is upper jaw protrusion and lower jaw distal position.
As for other facial signs, e.g. the height of the lower part of face, it may change. Thus, if posterior occlusion combines with deep overbite, it has a tendency to reduction, and at combination with open bite — to increase. Nasolabial and mental folds expressiveness also depends on that.
At posterior occlusion combined with deep overbite the nasolabial folds and especially the mental one are more expressive. The lower lip looks valgus; the upper teeth are located on the red border of the lower lip, leaving imprints on it. The mandible angle is reduced.
If posterior occlusion is combined with open bite, facial expression is forced, the nasolabial folds are smoothed. Besides, the “thimble” symptom appears at swallowing saliva. The mandible angle is more than 123°.
At upper frontal teeth protrusion the orbicular muscle of mouth is underdeveloped, the upper lip is shortened, the oral cavity is opened. These signs expressiveness depends on upper teeth protrusion degree.
Intraoral signs of posterior occlusion are characterized by prognathic dental arches correlation in the frontal and lateral parts. Violations in the frontal part declare themselves by forward upper dental arch displacement. Sometimes this displacement is conditioned by upper teeth protrusion, in other cases it takes place at the expense of the bone base. At that the upper frontal teeth may be located fanlike with spaces, without spaces, densely, and with opisthognathic inclination. The crown part of the frontal teeth seems enlarged, its cutting edge may have defects because of mechanical injuries.
If the upper frontal teeth protrude, there appears the so-called sagittal fissure between them and the lower frontal teeth. It may be different by length and size, sometimes being
To detect the severity degree of this anomaly one should take into consideration the ” degree of mesiodistal displacement in the lateral parts. At posterior occlusion the lateral teeth are in distal correlation, at that the mesiobuccal tubercle of the upper 6,h tooth does not get into the fissure of the similar lower tooth, but is located in front. Mesiodistal displacement degree may be by 1/2 of the tubercle, 1 tubercle and more.
Besides, transversal lateral teeth correlation is very important. Posterior occlusion is often combined with jaw narrowing. The narrowed upper jaw may have different shapes (V-like, U-like). According to Kalvelis, upper jaw narrowing changes the form of both upper and lower dental arches, becoming trapeziform, which worsens the anomaly.
Functional violations are also important. Breathing function is violated in patients with posterior occlusion. As a result of chronic diseases of the upper air passages, and also adenoid tissue excrescence, nasal breathing is disturbed. According to statistics, in 50 % children with prognathism vital lung volume is reduced by more than 20 %. Insufficient oxygen supply and redox processes violation in the organism lead to the inhibition of somatic and psychic development of the child.
The orbicular muscle in patients with posterior occlusion is underdeveloped, the oral cavity is constantly opened. Because of mouth breathing and open lips mouth cavity impermeability is violated, tongue position changes, which leads to double chin formation. Besides, the function of swallowing is disturbed in 83.6 % of patients. When the oral cavity is closed, the face has a forced expression, and at swallowing — the “thimble” symptom, i.e. dotted recesses on the chin skin, which indicates expression muscles hypertonus.
Patients with posterior occlusion very often have speech impairment. According to Z.P. Vasylevska, at prognathism tongue articulation zones form and location change on the palate at vowels pronunciation.
Mastication impairment arises at prognathism because of the decrease of the functioning mastication teeth surfaces area. The time of chewing food becomes longer, mastication efficacy and quality reduce.
At posterior occlusion carriage is often violated, bones ossification terms change.
Posterior occlusion should be viewed as a disease of the whole organism with local manifestations in the oral cavity, therefore it requires complex approach to differential diagnostics and treatment method choice.
In orthodontic practice, conducting differential diagnostics of posterior occlusion types, clinical tests, offered by Eschler—Bittner, are widely used. The tests consist in the following: the patient’s face form in profile is remembered at usual occlusion, then the patient is offered to protrude the lower jaw till the neutral correlation of lateral incisors:
o if face form improves at that, posterior occlusion is conditioned by lower jaw underdevelopment;
o if face form becomes worse, there are no indications to growth stimulation of the lower jaw, and the reason for occlusion anomaly lies in sizes violation or upper jaw and dental arch position;
o if face expression improves at first and then becomes worse, posterior occlusion is caused by the violation of both jaws growth and development. Here it should be found out to what degree lower jaw growth is to be stimulated.
Posterior occlusion treatment is a complicated task, which depends not only on the clinical form and degree of its expressiveness, but also on the patient’s age. The main efforts during posterior occlusion treatment are to be directed at: o avoiding the inhibiting influence of dysfunctional lips, cheeks, and tongue muscles on jaws growth and formation;
o normalization of dentognathic apparatus functions — breathing, swallowing, speech, mastication;
o correction of teeth position, dental arches form, occlusion; o stimulation of the growth of the dental arches apical bases in the parts of their growth inhibition;
o hampering upper jaw growth and stimulating lower jaw growth. Posterior occlusion treatment in the temporary period consists in prophylactic measures and comes to creating conditions promoting the normal development of the child’s dentognathic apparatus. At that, the oral cavity and nasal part of the pharynx are subject to sanation. In this period great attention must be paid to myogymnastics by the technique of V.S. Kurylenko and Z.F. Vasylevska, aimed at strengthening the orbicular muscle of mouth and the muscles protruding the lower jaw. In some time skeletal muscles training may be included into complex treatment — using the well- known myogymnastics, worked out by Rodgers, and also Dass’ apparatus.
As the child adapts to treatment procedures, both prophylactic and treatment devices may be used.
Prophylactic devices:
o to prevent lower lip sucking and biting — a device on the lower jaw with bandages on the vestibular arch;
o to prevent finger or tongue sucking — a plate on the upper jaw with a wire or plastic protective shield.
To treat children with posterior occlusion, complicated with deep overbite, such treatment devices are used: Muelle- man’s propulsor or a plate on the upper jaw with an elongated inclined plane. The inclined plane is to be shaped from the palatine side from the frontal teeth necks at 45° angle for the advanced sliding of the lower incisors to the upper ones. It is expedient to use this device with a sling cap to keep the lower jaw in such position.
At prognathic occlusion, complicated with open bite, the normalization of the breathing and swallowing functions is emphasized. A vestibular mantel (Korbitz’plate) and Kraus’ apparatus are used.
Frankel’s devices of the 1st and 2nd type are used till the end of temporary period, till permanent teeth eruption. The 1st type — in patients with posterior occlusion combined with dental arches narrowing and frontal teeth protrusion. The 2nd type (Fig. 167) — in patients with posterior occlusion complicated with deep overbite.
Transitional dentition period is the most favorable for treatment, because it is the period of the most important development stages and dentognathic apparatus establishment. The transitional dentition process is accompanied by increased jaw growth; biological potency to growth is realised to the biggest extent. All this should be taken into account when choosing a treatment method and an orthodontic appliance of efficient design.
In the period of transitional dentition together with myogymnastics and fight against pernicious habits different designs of orthodontic appliances are widely used: Schwarz’ plates with an inclined or biting platform (Fig. 168), Frankel’s apparatus of the Is‘ and 2nd type, Kraus’ apparatus, Muelleman’s propulsor (Fig. 169).
At the underdeveloped lower jaw, accompanied by compression in the lateral parts, there are applied removable devices for lower jaw dilation, which allow influencing teeth and dental arches, alveolar process and jaw selectively (Fig. 170).
Dankov’s appliance (Fig. 171) is used at lower jaw distal position. Orthodontic treatment at upper jaw overgrowth mainly consists in changing the axial inclination of the upper frontal teeth, dental arch form change, dental arch shortening, inhibiting upper jaw growth by means of extracting the lower premolars at canine teeth coming out.
ETIOLOGY, PATHOGENESIS, CLINICAL PRESENTATION, TREATMENT, AND PROPHYLAXIS OF MESIAL OCCLUSION
Mesial occlusion belongs to sagittal plane anomalies and is a rather widespread dentognathic pathology, observed in any period of occlusion formation.
The term “mesial occlusion” was introduced into orthodontic practice by Lisher in
The progenia part among all dentognathic anomalies and deformations comprises from 1.9 to 18 %.
Parents apply to hospitals with their children concerning mesial occlusion already at young age more often than at other types of deformations. This happens because parents pay attention to the lower teeth covering the upper ones even when the pathology is not full-blown yet, and any other anomaly, for instance, posterior occlusion or deep overbite, is still imperceptible (Fig. 175-177).
By Angle’s classification (1889) mesial occlusion belongs to the 3rd class and is detected by lower jaw mesial dislocation. As a result 1st molars correlation violation is marked. The mesiobuccal tubercles of teeth come upon the distal buccal tubercles of 6 6 teeth, and at more evident pathology the mesiobuccal tubercles of f>J6 teeth come into the space between 76 67 teeth. Thus, the 2nd premolar articulates with the intertubercular space of the 1st molar, and at more evident mesial lower jaw dislocation even the 1st premolar of the upper jaw articulates with it.
Lower jaw displacement may be both uni- and bilateral. At unilateral displacement median line correlation violation is observed. Unilateral displacement is mostly a consequence of the premature extraction of the 2nd temporary molar on the lower jaw on one side. Distally located teeth and teeth standing in front of the defect transfer to the side of the extracted tooth.
By Katz’ classification (1940) mesial occlusion belongs to the 3rd group of anomalies and arises because of excessive functioning of the muscles protruding the lower jaw, or insufficient function of retractors group.
Functional pathology of this deformation consists in the following: articulate movements prevail in the child — opening and closing of the mouth, and gliding movements are absent, impossible because of the protruded lower jaw. This condition leads to rearrangement in the joint. Besides, a certain group of teeth does not participate in mastication — incisors are excluded from mastication. Their function is taken by lateral teeth — premolars and molars, which consequently bear an increased load.
L.V. Ilyina-Markosian refers this pathology to sagittal occlusion anomalies, applying the term “anterior occlusion”, meaning lower jaw protrusion at usual location, and singles out its three varieties:
o without lower jaw displacement:
1) general anterior occlusion;
2) frontal anterior occlusion; o with lower jaw displacement; o combined form.
D.A. Kalvelis (1957), taking into account etiological factors and hereditary character, refers progenia to sagittal occlusion anomalies, dividing it into true and false.
V.Y. Kurliandskyi (1957) and A.I. Betelman (1956) based their classification on the degree of jaw development. Thus, according to V.Y. Kurliandskyi, progenia is referred to dental arches correlation anomalies and arises because of: o lower jaw overgrowth; o upper jaw underdevelopment.
According to A.I. Betelman’s classification mesial occlusion belongs to sagittal plane anomalies and has such clinical forms:
1) upper jaw micrognathia;
2) lower jaw macrognathia;
3) lower jaw macrognathia and upper jaw micrognathia.
A.M. Schwarz (1969) and F.Y. Khoroshilkina (1976) studying lateral teleroentgenograms of head detected dentoalveolar, gnathic, and combined forms of mesial occlusion.
A.S. Shcherbakov (1967) singles out dentoalveolar and skeletal forms. S.I. Doroshenko (1968) on the grounds of interpretation data of lateral head teleroentgenograms of patients with anterior dental arches correlation came to a conclusion that it may be caused by the degree of jaws development, their form, location in the skull, lower jaw location in the TMJ, various correlations of bones in the skull. On the basis of these facts the author singles out the following forms of mesial occlusion:
1) progenia as a consequence of lower jaw overgrowth:
a) its body and branch;
b) body;
c) branch;
d) frontal part of the jaw;
2) progenia caused by upper jaw underdevelopment:
a) its body;
b) frontal part of the jaw;
3) progenia caused by the anterior location of the lower jaw:
a) in the skull;
b) in the joint.
In the WHO classification mesial occlusion is presented in the following chapters: jaw size anomalies:
— upper jaw micrognathia;
— lower jaw macrognathia;
anomalies of jaws location relative to the skull base:
a) lower jaw prognathism;
b) upper jaw retrognathia;
dental arches correlation anomalies: a) mesial occlusion.
Mastication apparatus development is tightly connected with the development of the whole organism. It begins from the fifth week of embryonal development (when the first teeth germs anlage takes place) and continues during many years after the child is born until complete formation of permanent occlusion in mature age (18—20 years). If after child’s birth the lower jaw alveolar process protrudes relative to the one of the upper jaw, this testifies to possible formation of mesial occlusion at temporary teeth eruption.
From the point of view of etiopathogenesis, all this period of time is expedient to be divided into three stages:
1) intrauterine, antenatal. During this time the fetus is under mother’s organism protection, and its development disturbance considerably depends on the mother’s state, and less — on environmental factors;
2) labor stage;
3) postnatal, when the child is under the influence of environmental factors, adapts to them at the expense of congenital and inherited properties.
In the intrauterine period the fetus is under “mother’s protectorate”, in a peculiar “microenvironment”, but it can create a number of different conditions, negatively influencing the development of the embryo as a whole, and in particular — facial part development. This influence may be conditioned by different factors:
o physical (fetus mechanical injury, radiation damage, thermal agents, vibration, etc.);
o chemical (intake of different pharmacological, and especially hormonal preparations, alcoholic beverages, smoking during pregnancy);
o biological (infectious diseases, genetic or hereditary diseases); o social (conditions and way of life and work of the pregnant woman, diet in this period).
These agents, influencing the organism, leave a certain trace, the so-called “phy- logenetic background”, which later declares itself in ontogenesis as congenital dentognathic anomalies.
Enumerated factors influence leads to specific and nonspecific diseases of the mother and father, which can be communicated from generation to generation by a dominant or a recessive character as a genetic disease of the whole organism or only of the dentognathic apparatus. Also progenia and upper jaw underdevelopment may be caused by the form, size and function of the tongue in the period of oral cavity embryonal development. The tongue, mainly pressing on the anterior part of the lower jaw, causes progenia, and its belated deepening onto the bottom of the oral cavity causes narrowing of the intermaxillary bone and upper jaw alveolar processes.
Besides, mesial occlusion may be caused by water-salt and vitamin metabolism disorders, early pregnancy toxemia. It has been established that pregnancy and labor pathologies frequency and progenia frequency are in direct proportion.
Labor stage: progenia is more often (33 %) observed in children, who were born at transverse lie, breech presentation or footling presentation, after prolonged labor with a long anhydrous period, augmentation of labor, or operative delivery.
Postnatal period: the most critical for a child are the first months, later on — two first years of life. In the first period the child is under the influence of the environment, and it is the time when permanent occlusion foundation is laid.
Mesial occlusion may be caused by congenital peculiarities of the facial skeleton bone structure, especially of the lower jaw, intermaxillary bone underdevelopment, calcium metabolism disorder because of rachitis or other diseases, partial or multiple adentia in the region of the upper jaw, multiple retention of the upper teeth or their premature loss, supplemental teeth on the lower jaw, late transitional dentition.
The shortened or irregularly attached tongue frenulum exerts constant pressure on the frontal part of the lower jaw, which leads to progenia. This is also promoted by macroglossia.
Palatopharyngeal tonsil hypertrophy leads to the reduction of the opening for air flow passage. Pressure is observed in the region of the epiglottis because of lingual tonsil enlargement, and the child, to ease breathing, instinctively protrudes the lower jaw, abducting the root of tongue together with the enlarged tonsil. Such mouth breathing causes mesial occlusion also because the habit of protruding the lower jaw appears.
Irregular swallowing (infantile type), irregular tongue location in the oral cavity during speaking and in quiescence, uneven wearing down of temporary teeth tubercles at the beginning of transitional dentition occlusion, especially of the lower canine teeth, uneven transitional dentition on both jaws — all these are etiological agents of progenia.
Individual lower incisors torsion leads to dental arches closure disorder, causes lower jaw protrusion. Upper jaw underdevelopment in the frontal part because of chronic inflammatory processes, new formations, surgical interventions on the jaws, endocrine disturbances, hypophysis hyperfunctioning leads to anterior occlusion formation.
Pernicious habits are very important: sucking of the upper lip, tongue, fingers, and different objects, sleeping on a high pillow, putting a palm or a fist under the chin in sitting position.
There are differentiated physiological and pathological types of progenia.
Physiological progenia is characterised by multiple contacts between the dental arches both in the front and lateral parts. It is viewed as an anatomic variant, which does not require any orthodontic treatment.
At pathologic progenia contacts between teeth are violated. There occur morphological, functional, and esthetic changes of the dentognathic apparatus, which require orthodontist’s intervention.
Most authors differentiate two main progenia forms: true and false.
L..V. Ilyina-Markosian divides false progenia into two forms:
o anterior false progenia;
o forced occlusion.
Their etiology, pathogenesis, functional and morphological disturbances, and treatment differ. Some authors (L.V. Ilyina-Markosian, D.A. Kalvelis) view false
progenia as inverse overbite of individual upper frontal teeth at preserved correct correlation of both dental arches along the full length. A.I. Betelman, Y.M. Aleksan- drova, A.D. Mukhina refused from this term and classify false progenia as upper frontal teeth palatine position.
Forced occlusion is a kind of false progenia and develops as a result of the habit of protruding the lower jaw. This form of false progenia is also called articular.
Mesial occlusion has characteristic facial and intraoral features. The main facial feature is lower jaw protrusion. At external examination, in cases of lower jaw enlargement the disturbed harmony of face profile attracts attention: the chin and upper lip protrude considerably, at that the upper lip somewhat falls back relative to the lower one, the subnasal fold is deep, the lower lip red border is wide. At deep overbite the lower part of face is not infrequently shortened, as a result of which the lower lip is thickened. At increased lower jaw angles and open bite the lower part of face is elongated, the lips close tensely, the oral fissure not infrequently gapes. If mesial occlusion combines with forward lower jaw shift, facial signs of disturbances are fullblown.
Oral cavity examination shows that the lower jaw is located in front of the upper one, its dental arch is wider.
The closure of the 1st permanent molars and canine teeth by 3rd Angle’s type may be by 1/2 size of the lsf permanent molar tubercle, by one tubercle, by 1/2 of the lsl permanent molar crown and more.
Frontal teeth correlation may vary: in some cases the labial surface of the upper incisors touches the lower incisors lingual surfaces, in other cases there is an inverse sagittal gap between the frontal teeth by
Mesial occlusion is more often complicated with upper jaw narrowing, which causes lower lateral teeth prevailing over the upper ones. The upper jaw may be flattened in the frontal part. Uni- or bilateral crossed relation is observed in the lateral parts.
The upper frontal teeth as a result of microgenia are located with torsions, transfer vestibularly, there is often observed frontal teeth congestion orally. The lower incisors sometimes deviate vestibularly, as a result of which diastems and diaereses form between them, or they press the upper incisors, increasing their palatine inclination.
At a most evident anomaly the lower jaw as though absorbs the upper one. The contact in the region of lateral and frontal teeth is violated, only the gliding of the lower teeth lingual surface on the upper teeth buccal surfaces takes place.
Functional disorders are also very important at mesial occlusion. Face form is violated. At the absence of occlusive contact between incisors food biting becomes impossible. Because of the forward shift of the whole lower jaw dental arch and molars correlation violation the general mastication area decreases. Tubercular closure, which forms between the masticatory teeth, hampers food grinding.
Sometimes, because of lower jaw protrusion, functional disorders, conditioned by its articular heads location in the glenoid fossae, there appears pain in the joints, crunch, clickin
The speech of patients with mesial occlusion is violated, lisping appears.
