Understanding the Etiological Relationship Between Orthodontic Tooth Crowding and Mucogingival Pathologies, “Big Teeth in Small Jaws”

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Understanding the Etiological Relationship Between Orthodontic Tooth Crowding and Mucogingival Pathologies, “Big Teeth in Small Jaws”

Colin Richman DMD

Department of Periodontics, Practice Limited to Periodontics (Focussed on SFT, LANAP/LAPIP/Oral‐Systemic‐Condition), Diplomate, American Board of Periodontology, Augusta University, Augusta, Georgia, USA

Introduction

Profitt and Fields Jr (2000) postulated that malocclusion may be attributed to genetic and environmental factors. Beecher et al. considered malocclusion to be a condition of westernization (Beecher et al., 1983). In this chapter, we will examine the role of anthropology, genetics, and diet as primary etiological agents associated with dental tooth crowding, a consequence of “big teeth in small jaws,” due to factors listed above (Figure 11.1a, b).

Fundamental Etiological Factors Associated with Orthodontic Tooth Crowding

Numerous theories have been proposed relative to the etiology and pathogenesis of orthodontic tooth crowding. These include:

Anthropological Factors

Historically, after attaining humanoid status and evolving from hunters to gatherers, to farmers and industrialized food‐processing, from an epigenetic perspective our pre‐humanoid jaws started “shrinking” (Cramon‐Taubadel, 2011). Also, from an anthropological perspective, as our knowledge base increased and continues to increase, the frontal lobe of our brain, which governs our humanity, expanded, and continues to expand, resulting in an ongoing associated expansion of our forebrain and associated skull. The consequence of this phenomenon is that our skulls are expanding at the expense of our shrinking jaws. Concurrently, our jaws are simultaneously being displaced in an inferior direction. This phenomenon is known as klinorynchy (Pajević et al., 2019; Terris, 2005) (Figure 11.2a, b).

Genetic Factors

As humans became more “civilized,” we have transitioned from a genetically homogeneous to a genetically heterogeneous society. An example of this phenomenon might be demonstrated by the following example: Visualize an infant born to a large‐statured (football‐playing) father of perhaps Scandinavian origin with large jaws and associated teeth and a petite (ballerina) mother of Asian origin with small jaws, stature, and teeth. If this infant inherits the father’s large teeth and the mother’s petite small jaws, a major discrepancy could result from trying to accommodate the large teeth into the small jaws when considered from a three‐dimensional (3D) perspective. Cone beam computerized tomography (CBCT) analysis enables clinicians to evaluate these anatomical relationships in 3 dimensions from the clinical perspective. (Peck et al., 1998).

Two images of big teeth in small jaws. It is labeled as a and b.

Figure 11.1 (a) Ideal facial and lingual alveolar bone morphology, exceeding 1.5 mm thickness at both the facial and lingual aspects. (b) Substantial facial bony dehiscence, with adequate lingual alveolar bone “big teeth in small jaws.”

Two images of facial skeletons. It is labeled as a and b. It depicts the brain portion of a human.

Figure 11.2 Klinorhynchy: a downwardly oriented facial skeleton in relation to the cranial base, frequently resulting in skeletal–dental problems. Associated with anthropological epigenetic changes with increasing anterior frontal bone expansion and decreasing midfacial volumetric structure. (a) Homo heidelbergenesis, 300,000–600,000 years ago (Figure 11.11a). (b) Homo sapiens, 300,000 years ago up to and including the present (Figure 11.11b).

Advances in dentofacial phenotyping the comprehensive characterization of hard and soft tissue variations in the craniofacial complex together with the acquisition of large‐scale genomic data have started to unravel genetic and epigenetic mechanisms underlying facial variation (Moreno, Uribe and Miller, 2015; Neela et al., 2020).

Dietary Factors

A classical study by Corruccini and Lee evaluated malocclusion development in the next‐generation offspring of Chinese laborers when they were transported from China to the United Kingdom. In this review, as the genetic factors of the immigrant parents remained unchanged relative to their genetic status, it was noted that within one generation the deterioration in the offspring’s tooth alignment suggested environmental influences, such as diet to be a factor (Beecher et al., 1983). (Corruccini and Lee, 1984) studied squirrel monkeys, who were either raised on a naturally tough/rough or artificially softened diet. Significant craniofacial and occlusal development between hard and soft diet animals was found, including in the soft diet group’s maxillary arch narrowing, palatal arching, crowded and displaced teeth, and retarded cranial bone mineralization. They suggested that a similar situation occurs in humans and that dietary consistency may be an important factor in human craniofacial growth.

Corruccini, Potter and Dahlberg, writing in the American Journal of Biological Anthropology, compared the occlusal variables and arch measurements on Pima American Indians. The study consisted of two groups, one of older individuals raised on traditional diets and the other of younger individuals raised on refined commercial foods typical of modern urbanized communities. The permanent dental occlusion was significantly more variable in the younger group. Other variables noted in the younger group included narrower palates correlating with a general trend among industrialized populations, including among experimental animals fed soft diets (Corruccini et al., 1983). A treatise in Nature Magazine reviewing the impact of dietary factors on malocclusion includes a comprehensive review of the contemporary literature on this topic. The reader is referred to this publication for supplemental information (Kahn and Ehrlich, 2019).

Comparative Anatomical Observations Relative to Other Mammalian Species Nurtured and Living in Their Natural Habitats

This author has acquired from various natural history museums around the world, clinical data of mammalian species born, nurtured, and living in their natural environment in the wild (unpublished data). Over 1,000 different crania and matching mandibles have been evaluated using calibrated clinical photography. These mammals range from field mice to African elephants and numerous other mammalian species of varying stature. (Museums include Europe, Arctic Circle, North America (multiple), and South Africa). When reviewing these data, it is noted that less than 0.5% of specimens examined demonstrate dehiscences, fenestrations, dental tooth crowding, and/or impactions. It is rare to identify more than one abnormal factor listed above in any examined specimen. Figure 11.3a–c are representative of the ideal and non‐compensated dentitions of herbivore examples (gorilla), carnivore (panther), and omnivore (brown bear).

Vasculature of the Gingival Tissues

From a genetic perspective both the maxilla and mandible are derived from five precursor bones, which eventually fuse to form the maxilla and the mandible. Relative to the theme of this narrative, consideration will only be given to the alveolar bone component of both bones.

Three images of mammalian occlusion. It is labeled as a, b, and c. It depicts the occlusion on the Gorilla, the occlusion on the Panther, and occlusion on the Brown Bear.

Figure 11.3 Representative images demonstrate ideal mammalian occlusion, various species with no evidence of malocclusion or impactions plus abundant supporting alveolar bone. (a) Ideal tooth relationship and occlusion on Gorilla (herbivore). (b) Ideal tooth relationship and occlusion on Panther (carnivore). (c) Ideal tooth relationship and occlusion on Brown Bear (omnivore).

Alveolar bone consists of a dense outer bone cortical plate, both on the buccal and lingual aspects, covered with periosteum, in turn, protected by attached and unattached gingival tissues.

An inner bony component lining the tooth sockets is substantially perforated, where the perforations, known as Volkmann’s canals, facilitate the passage of end branches of the vascular system to provide appropriate blood supplies to the overlying spongy bone and gingival tissues.

Spongy bone lies between these two layers (Figure 11.4).

The component of alveolar bone housing the teeth is known as the alveolar process. The junction of the alveolar bone with the basal bone on the facial aspect of each jaw is the “A” point in the maxilla. The “B” point represents the same position in the mandible (Figure 11.5). The vascularity of the basal bone for both jaws is more robust than the vascularity of the facial and lingual alveolar bone, especially in the case of orthodontic tooth crowding. In these situations, facial alveolar blood supply may be compromised or deficient, especially when associated with dehiscences and fenestrations. This results in a relatively thin avascular layer of bone, known as bundle bone. This situation is more frequently noted on the facial aspect of crowded teeth (Figure 11.1b).

An image of periodontium anatomy. It depicts the supply of blood through tissues.

Figure 11.4 Anatomy of periodontium.

An image of cephalometry. It is labeled as A point and B point.

Figure 11.5 Cephalometry with points A and B.

Typically, the blood supply to gingival tissues is derived from three major sources:

Vessels radiating from branches of the interdental vascular channels located in the interdental bony segments. These vessels enter the facial and lingual alveolar plates and then exit through foramina to nourish the overlying gingival tissues.

Vessels derived from the major neurovascular bundles, for example, the facial artery, lingual artery, and greater palatine artery, eventually terminate anastomosing in the supra‐alveolar gingival tissues.

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Oct 27, 2024 | Posted by in Orthodontics | Comments Off on Understanding the Etiological Relationship Between Orthodontic Tooth Crowding and Mucogingival Pathologies, “Big Teeth in Small Jaws”

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