Sagittal Plane Malocclusions: Progenic Syndromes and Mandibular Retrognathism Study Guide

Definition and Classification of Progenic Syndromes

Progenic syndromes represent a group of sagittal plane anomalies characterized by mesialized dental or skeletal relationships and frontal inverse occlusion. Within this group, clinicians distinguish between true prognathism, which involves an excessive development of the mandible in all three spatial planes, and false prognathism, also known as mandibular pseudoprognathism. According to Glăvan, approximately $33\text{--}43\%$ of these cases are skeletal forms. This condition can result from an insufficient development of the upper maxilla, a combination of maxillary deficiency and mandibular excess, or functional anomalies. Functional variants may present a clinical picture similar to mandibular excess but are actually a consequence of mandibular pro-sliding.

The terminology surrounding these anomalies varies across different academic schools. Researchers such as Cauhépé and Firu refer to it as anatomical or total prognathism, whereas Ballard classifies it as Skeletal Type III. Aquilar describes it as hereditary prognathism, while Häupel uses the term true progeny, and Planas refers to it as congenital progeny. In the works of Hoffer, it is called morsus inversus basalis. In Anglo-Saxon literature, the condition is commonly termed an underbite or negative overjet.

Classification systems differ by region and historical school of thought. The German School distinguishes between true progeny, characterized by sagittal mandibular overgrowth, and false progeny, which stems from insufficient maxillary development or functional habits that force the mandible into an anterior position. Western classifications, such as the American School, categorize these under Angle Class III. Sub-type III/1 involves inferior prognathism due to excessive mandibular growth, while III/2 involves a false mandibular prognathism. Boboc offers a classification based on the anatomical site involved: mandibular prognathism via macrognathia, mandibular pseudoprognathism via maxillary deficiency, intermaxillary relationship abnormalities (articular or cuspid-guided fording), or axial modifications of the anterior teeth, such as frontal inverse engagement.

Prevalence and Etiopathogenesis of Mandibular Prognathism

The frequency of progenic anomalies in the European population is estimated between $1.5\% \text{ and } 5.3\%$ according to Baccetti (2004). Boboc's research indicates a prevalence of $9.9\%$, which rises significantly to $14.7\%$ in populations with cognitive disabilities (oligophrenics). Generally, false progeny is more prevalent than true progeny. Within the spectrum of inverse occlusions, inverse engagement is the most common, followed by forced inverse occlusion, and finally false progeny resulting from maxillary developmental deficiency.

The etiology of mandibular prognathism via macrognathia is heavily influenced by heredity, as noted by Galippe, Pont, Kantorowicz, Korkhaus, and Schwartz. Korkhaus posits that it is the tendency toward mandibular evolution that is inherited rather than the fully formed anomaly. Historical examples include the Habsburg family line, such as Ernest the Iron (Duke of Austria, 1377–1424) and Charles II of Spain (The Bewitched, 1661–1700). Other causes include neuro-endocrine disorders like juvenile acromegaly, where an excess of somatotropic hormone modifies the condyle and glenoid cavity shape (Sudaka Lespin) or affects the condylar growth cartilage (Boboc). Hypothyroidism can also contribute via macroglossia. In some cases, a functional pseudoprognathism may transform over time into a skeletal anomaly.

Pseudoprognathism through maxillary deficiency is often hereditary (Schwartz, Hoffer) and related to the constitutional intra-maxillary position of tooth germs. It is also a feature of genetic syndromes such as Down syndrome and achondroplasia, which involve developmental disturbances at the cranial base. Binder syndrome (maxillo-nasal dysostosis) is another specific genetic cause. Local factors include the anodontia of upper incisors (Weinemann, Sicher, Fernex) and the detrimental action of the upper lip and buccinator muscles when not compensated by the tongue (Müller). Retractile scars from cheilognathopalatoschisis or other causes, as well as adenoid vegetations (Case, Nevrézé, Turner), also play a significant role.

Clinical Manifestations of Progenic Anomalies

Clinical signs of mandibular prognathism via macrognathia include a characteristic "galosh" shape of the horizontal mandibular branch, a concave facial profile, and a smoothed labiomental groove. The labial step is inverted, the lower third of the face is enlarged, and the mandibular angle is widened to approximately $140\text{--}145^\circ$. Conversely, in pseudoprognathism due to maxillary deficiency, the face appears flattened with sunken cheeks (from a frontal view). From a lateral view, the profile is concave, and the subnasale (Sn) point is posterior to the Dreyfuss plane. While there is an inverted labial step and superior retrocheilia, the lower facial height and mandibular angle remain largely unchanged.

In functional frontal inverse occlusions (articular or cuspid-guided), facial signs are similar to macrognathia but significantly less pronounced. The profile may be straight or only slightly concave, the chin occupies an anterior position, and the labial step is slightly inverted, although the sub-nasal region is not sunken. The mandibular angle and lower facial height are generally normal or only slightly increased. In those with axial modifications of the incisors, the primary facial sign is the inverted labial step, while the chin position and lower facial height remain normal. Inverse engagement (angrenaj invers) typically results in only minor interlabial relationship changes that become visible mainly during smiling or speaking.

Oral manifestations differ by dental age. In macrognathia, the permanent dentition shows an overall excess of mandibular development in both sagittal and transverse planes. In the deciduous dentition, inverse occlusion relationships are often established as soon as the teeth erupt, which is frequently a sign of hereditary nature; large diastemas are typically seen in the lower arch. At the start of mixed dentition, there is a dissociation in eruption rhythms, with lower permanent teeth erupting earlier and often with spaces between them. In cases of maxillary deficiency, the deciduous dentition lacks physiological diastemas, and the arch length is shortened (as measured by the Bogue index). In permanent dentition, the upper arch remains short and narrow, often with retro-inclined upper incisors showing vestibular wear facets due to friction.

Differential Diagnosis and Functional Assessment

The diagnostic process includes functional tests such as the mandibular retropulsion test. In this test, the examiner applies pressure to the chin while the mandible is in a resting position. A total positive result occurs if the mandible can be moved back to a psalidodont (normal) relationship, indicating articular-guided inverse occlusion. A partial positive result occurs if a head-to-head relationship is reached, suggesting cuspid-guided forced occlusion. A negative result occurs if retropulsion is impossible, suggesting other skeletal forms of progeny. Functional disturbances also impact phonation, mastication (reducing efficiency and creating a "chopping" stereotype), and the temporomandibular joint (TMJ), which may exhibit clicking, crepitations, and inverted anterior guidance.

Periodontal changes often appear early in inverse engagement, such as the "elimination groove" and dental mobility. In macrognathia, periodontal issues appear later and are more severe, including horizontal bone atrophy and gingival recession on the lower incisors. However, these changes may spontaneously regress after successful orthodontic correction (articular leap). Lingual modifications are also specific: acromegaly presents macroglossia, hypothyroidism presents a hypotonic tongue, and maxilary deficiency often results in a lower tongue position in the mandibular arch and anterior thrust during swallowing.

Cephalometric and Radiographic Analysis

Radiographic exams like the orthopantomogram (OPG) in macrognathia show large spaces between the germs of successional teeth in the support zones. Teleradiography (cephalometry) provides definitive metrics. For macrognathia, indicators include $Go\text{-}Gn > N\text{-}Se + 3\,mm$, a condylar angle greater than $137^\circ$, a mandibular angle between $140\text{--}145^\circ$, and an increased Schwartz base angle ($> 20^\circ$). The Tweed angle, also known as the prognostic angle, is normally $22\text{--}25^\circ$ but is modified in these cases. The mandibular profile angle $SN\text{-}M$ decreases below $60^\circ$.

For pseudo-prognathism due to maxillary deficiency, cephalometry reveals a decreased $SNA$ angle (normally $85^\circ$ according to Schwartz) and an $NSA\text{-}NSP$ distance less than $7/10$ of the $N\text{-}Se$ distance. The sagittal dimension of the maxillary base is significantly reduced compared to the mandibular base, deviating from the normal $2/3$ ratio. For axial modifications of the anterior teeth, there is a decrease in the angle between the upper incisor axis and the $OF$ plane, an increase in the angle between the upper incisor axis and $NSA\text{-}NSP$, and an increase in the angle formed by the lower incisor axis and the mandibular basal plane. The interincisal angle is typically less than $130^\circ$.

Treatment of Progenic Syndromes

Prophylactic treatment focuses on correcting sleeping postures, deconditioning bad habits (tics), and ensuring clear nasal passages for proper respiration. It also involves selective grinding of deciduous canines (at ages $5\text{--}7$ years), preventing premature contacts, and performing selective extractions of deciduous upper incisors that might deviate permanent teeth. In cases of cleft lip/palate, excising retractile scars and applying vestibular pads is necessary. Families with progenic syndromes may use a chin cup (bărbiȑă cu capelină) preventatively for several days a week.

Interceptive treatment often involves exercises with a lingual spatula during the early mixed dentition stage, specifically for isolated inverse engagement of $1\text{--}2$ erupting upper incisors where space and vertical overbite are sufficient. Curative treatment depends on age and skeletal severity. Objectives include inhibiting mandibular growth, stimulating three-dimensional maxillary development, achieving the "articular leap," and ensuring sufficient incisor overbite for natural retention. Growth inhibition is achieved using a chin cup with occipito-mental extraoral traction.

Specific appliances include the Br0ckl-Reichenbach plate, Schwartz's double plates (Doppelplatte), and the M0ller system for retropulsion. Removable appliances may include palatal plates with inverted vestibular arcs, trapezoidal split plates, or plates with S-shaped or mushroom-shaped springs. Fixed appliances often utilize Class III intermaxillary elastics. Functional fixed tools include Schlesinger-Phleps orthodontic rings with inclined planes or frontal gutters. For maxillary stimulation, split Y-plates with Bertoni screws or Delaire facial masks for maxillary propulsion are used. Functional regulators include Fr0nkel Type III, Balters Type III, and the Eschler, Wunderer, or Karwetzky II activators. Surgical options for adults include mandibular osteotomies (oblique ramus or vertical/staircase horizontal resections) and Le Fort I osteotomy for maxillary advancement.

Mandibular Retrognathism: Definition and Classification

Mandibular retrognathism is characterized by the retrusion of the mandible relative to the midface. The French school classifies this into total mandibular retrognathism (rarely a total micrognathia, more often changes in the ascending ramus) and partial retrognathism (inferior retroalveolia), where only the lower incisors are lingualized. Firu distinguishes between functional resting retrognathism and anatomical retrognathism.

Etiology and Pathogenesis of Retrognathism

Functional retrognathism is driven by habits such as finger sucking, resting the chin on a fist, or sleeping with the head in hyperextension. It can also be caused by distalized terminal occlusion due to abnormal cusp slopes. Anatomical retrognathism has genetic roots, such as Trisomy 15 or 17 (causing ramus development deficits) and Turner syndrome. Endocrine factors like pituitary dwarfism are also relevant. Local factors include the destruction of mandibular growth cartilages, TMJ ankylosis, and hypofunction of the propulsor muscles as described by Eschler. Firu notes that functional forms can evolve into anatomical forms if support zone teeth are lost prematurely.

Clinical Signs and Radiographic Diagnosis of Retrognathism

In functional retrognathism, the extraoral exam reveals a convex profile due to chin retrusion (Gnathion is posterior to Simon's orbito-frontal plane) and a reduced lower facial third. Endobucally, distalized occlusion and sagittal inoclusion are found, often accompanied by oral respiration and infantile swallowing. Anatomical retrognathism presents a more severe convex profile. In cases of TMJ ankylosis, the "bird profile" (profil de pasăre) emerges. A characteristic pre-angular notch may be present on the lower mandibular border. The mandibular angle is decreased, and the ears may appear low-set due to the short ascending ramus. The lower arch is typically short/narrow, and the lower incisors may contact the palatal vault.

Radiographic findings in functional retrognathism show an increased angle between the Y-axis and the Frankfurt horizontal ($SGn\text{-}F > 65^\circ$), but the branches are usually normally developed. In anatomical retrognathism, the ascending ramus is underdeveloped. Cephalometric markers include a reduced $SNB$ angle ($73\text{--}75^\circ$), an increased $ANB$ angle, and a mandibular profile angle ($SN\text{-}M$) greater than $60^\circ$. The Tweed angle exceeds $28^\circ$, the mandibular angle is less than $110^\circ$, and the condylar angle is less than $130^\circ$. Chateau notes that if the anterior margin of the ascending ramus is more oblique downward and backward compared to the pterygomaxillary plane, it signifies retrognathism.

Therapeutic Management of Retrognathism

Treatment for functional retrognathism begins with prophylaxis: natural breastfeeding and deconditioning habits like finger sucking or lip interposition. Curative objectives focus on mandibular propulsion and myotherapy for the propulsor muscles. Appliances used include the Hotz vestibular plate, palatal plates with anterior inclined planes, and double propulsion plates (M0ller, Schwartz). Functional appliances like the Andresen-H0upel monoblock are standard intervention tools.

For anatomical retrognathism, the goal is significant mandibular propulsion and, if necessary, inhibition of maxillary growth. Removable functional elements include the Chateau bi-block and palatal plates with functional lingual arcs. Other functional devices include the Balters Type I bionator, M0hlemann propulsor, Stockfisch kinetor, and Bimler Type A conformator. Fixed techniques such as Edgewise or Straight-Wire utilize Class II intermaxillary elastics. Surgical treatment is reserved for severe cases, involving mandibular ramus osteotomies, TMJ interventions to correct ankylosis, or plastic surgery (genioplasty) to improve facial aesthetics.