Periodontal Considerations in the Evaluation and Treatment of Dentofacial Deformities
Degeneration of the periodontium is likely to accelerate in the presence of specific intrinsic biologic factors (i.e., the individual’s biotype or predisposition of the periodontium), including the following: (1) a baseline jaw discrepancy with malocclusion; (2) the crowding of the teeth (i.e., the dental roots) within limited alveolar bone; (3) a forced mouth-breathing pattern in combination with a limited ability to close the lips together (i.e., inadequate incisor coverage) caused by anterior skeletal vertical (height) excess; and (4) an inadequate amount of attached gingiva at the clinical crown interface of the teeth. When attempting to achieve a favorable alignment of the teeth in each arch as well as improved occlusion through orthodontic maneuvers, these factors should be considered. Additional compounding factors that may also negatively affect the periodontium include the following: (1) active infection or inflammation of the periodontium; (2) non-biologic restorations at the dental–gingival interface; (3) para-occlusal habits (e.g., bruxism, clenching); (4) the use of medications that effect the saliva (e.g., antipsychotics); (5) local toxins (e.g., nicotine); (6) poor oral hygiene; and (7) the effects of age.
Teeth are hard structures that are made up of an enamel-covered surface called the crown and a cementum-covered surface called the root. The root of the tooth is attached to the alveolar bone (i.e., the jaw bone) via the periodontal ligament (PDL). Teeth are primarily used for chewing, speech, and swallowing. The maxillary and mandibular arches both contain teeth. Humans have two sets of teeth during their lifetimes: the deciduous teeth, which are also known as the primary dentition, and the permanent teeth, which are known as the secondary dentition. Between the ages of 6 and 12 years, there is a mixed dentition during which both the primary and permanent teeth are present in the oral cavity at the same time.
Figure 6-1 Illustration of a sagittal view of a maxilla and mandible with the outer cortex of bone removed to demonstrate a fully erupted deciduous (primary) dentition and the location of the developing permanent tooth buds. Also indicated on the illustration are the usual ages of dental eruption for each tooth of both the deciduous and the permanent dentitions. From www.netterimages.com. © Elsevier Inc. All rights reserved.
There are 20 total deciduous teeth, which are composed of two incisors, one canine, and two molars in each of the four quadrants of the oral cavity. Under normal circumstances, no deciduous teeth are present at birth. Generally, by the third year of life, all 20 deciduous teeth have erupted.
There are 32 total permanent teeth, which are composed of two incisors, one canine, two premolars, and three molars in each of the four quadrants of the oral cavity. Usually the first permanent tooth to erupt into the oral cavity is the mandibular first molar. The first molar typically erupts at approximately 6 years of age. The molar erupts distal to the primary dentition and behind the second primary molar. The primary teeth eventually are replaced by the permanent teeth. If a permanent tooth is congenitally absent, then the primary tooth typically remains in the arch for an extended period of time.
Figure 6-2 Illustrations of the fully erupted permanent dentition in the maxilla and mandible. The palate and the lingual view illustration are used to define terminology for the surfaces of a tooth. From www.netterimages.com. © Elsevier Inc. All rights reserved.
Figure 6-3 Illustration of a cross-sectional view through a permanent molar and the associated alveolus. Pertinent anatomic terminology is labeled. From www.netterimages.com. © Elsevier Inc. All rights reserved.
• The dentin is the hard tissue that underlies both the enamel and the cementum and that constitutes the major portion of the tooth. Dentin is a modification of osseous tissue. It is composed of a number of dental tubules (small, wavy, and branching tubes) that are located in a dense matrix.
The periodontium includes the investing and supporting tissues of the teeth. It consists of two parts: the attachment apparatus (the cementum, the alveolar bone, and the intervening PDL) and the dentogingival unit (the gingival connective tissue that inserts into the supracrestal cementum and the sulcular and junctional epithelium as well as the latter’s attachment to enamel) (Fig. 6-4). The cementum covers the root surfaces. It serves as the attachment for the fibers of the PDL to the tooth as does the (cortical) alveolar bone of the alveolar socket. The periodontium is affected by the individual’s unique maxillofacial skeletal anatomy, by functional (occlusal) forces, and by degenerative cellular changes that occur with age. The greatest modifier of the periodontium is inflammatory disease.
Figure 6-4 Intraoral view demonstrating the normal width of attached gingiva in the human permanent dentition. From Newman MG, Takei HH, Klokkevold PR, Carranza FA: Carranza’s clinical periodontology, ed 11, St. Louis, 2012, W.B. Saunders Company, Figure 2-3.
Figure 6-5 Diagram showing the anatomic landmarks of the gingiva. From Newman MG, Takei HH, Klokkevold PR, Carranza FA: Carranza’s clinical periodontology, ed 11, St. Louis, 2012, W.B. Saunders Company, Figure 2-2.
Figure 6-6 Histologic appearance of healthy gingiva. A photomicrograph of a demineralized tooth with the gingival tissues in situ (hematoxylin and eosin stain, low magnification). The amelocemental junction (A) and the enamel space (ES) are shown. Gingival health is characterized by the organization of the epithelium into distinct zones: the junctional epithelium (A to B), the sulcular epithelium (B to C), the free gingiva (C to D), and the attached gingiva (D to E). The gingival connective tissue is composed of densely packed, organized, and interlacing collagen bundles. There are a few scattered inflammatory cells, but there is no significant inflammatory cell infiltrate. From Newman MG, Takei HH, Klokkevold PR, Carranza FA: Carranza’s clinical periodontology, ed 11, St. Louis, 2012, W.B. Saunders Company, Figure 21-1.
1. Masticatory mucosa (keratinized tissue): This includes the gingiva, the hard palate, and the dorsal surface of the tongue. The gingiva is a fibrous investing tissue that immediately surrounds and is contiguous with its PDL and with the mucosal tissues of the mouth. Keratinized epithelium also covers the hard palate.
• Junctional epithelium: This involves a single layer or multiple layers of non-keratinized cells that adhere to the tooth surface at the base of the gingival crevice. This was formerly called the epithelial attachment.
The gingiva is the part of the oral mucous membrane that covers the occlusal aspect of the alveolar processes of the jaws and that surrounds the necks of the teeth. The junctional epithelium and the connective tissue attachment have a characteristic dimension of 2 to 4 mm; this zone of tissue is called the biologic width. In general, an individual can only maintain health when the sulcus depth is no more than 3 to 4 mm. Greater depth provides a safe haven for bacteria that cannot be easily removed through normal oral hygiene maneuvers. A lower-than-average alveolar crest level is acceptable as long as it is stable (i.e., not progressive) and the periodontium is free of active disease. On the palatal surface of the teeth, the attached gingiva blends with the equally firm and highly keratinized palatal (masticatory) mucosa. The interdental gingiva occupies the gingival embrasure (i.e., the interproximal space beneath the area of tooth contact). It consists of the facial papilla, the lingual papilla, and the valley-like depression that connects the two in the interproximal contact area, which is called the col. In the absence of proximal tooth contact, the gingiva is firmly bound over the interdental bone; it forms a smooth, round surface without a triangular interdental papilla. The connective tissue of the gingiva is densely collagenous, and it contains collagen fiber bundles called gingival fibers (Fig. 6-7). When these fiber bundles insert into the tooth’s cementum, they are called Sharpey’s fibers, and they result in the mechanical attachment of the sulcular and supracrestal (i.e., crestal to the alveolar process) gingiva. These fibers are able to withstand masticatory forces without deflection or detachment from the tooth surface. The connective tissue attachments extend from just apical to the junctional epithelium of the sulcular (crevicular) gingiva to the supracrestal cementum of the root.
Figure 6-7 Diagram of the gingival dental fibers that extend from the cementum (1) to the crest of the gingiva, (2) to the outer surface, and (3) external to the periosteum of the labial plate. Circular fibers (4) are shown in cross-section. From Newman MG, Takei HH, Klokkevold PR, Carranza FA: Carranza’s clinical periodontology, ed 11, St. Louis, 2012, W.B. Saunders Company, Figure 2-20.
The junctional epithelium is connected to the tooth surface via a hemidesmosomal adhesion. These two ectodermal tissues and their interface act to block the flow of toxic chemicals and organisms from the oral cavity into the body.
The gingival sulcus contains a fluid that is derived from the gingival connective tissue and that flows through the thin epithelium of the sulcular wall. The gingival fluid is cleansing, and it contains sticky plasma proteins to increase the adhesion of the epithelial attachment to the tooth. The fluid possesses antimicrobial properties, and it is active in its defense of the gingiva. It may also serve as a medium for bacterial growth, which contributes to the formation of dental plaque and calculus. The amount of gingival fluid (exudate) increases with inflammation. The composition of gingival fluid has many similarities to that of blood serum.
The attached gingiva is continuous with the marginal gingiva, and it consists of stratified squamous epithelium and an underlying connective tissue stroma. The superficial layer is keratinized, parakeratinized, or both. The connective tissue of the gingiva is known as the lamina propria. It is densely collagenous, with few elastic fibers, and it consists of two layers: a papillary layer next to the epithelium and a reticular layer next to the periosteum of the alveolar process.
Each interdental papilla consists of a central core of densely collagenous connective tissue covered by stratified squamous epithelium. The facial and lingual papillae are joined with the connective tissue of the col and the stratified squamous epithelium from the adjacent interdental papillae. The epithelium of the col is not keratinized and therefore more susceptible to inflammation. The shape of the interdental gingival papillae correlates with the shape of the teeth and the embrasures. The interdental papillae may be broad or narrow, depending on dental positioning and points of connection.
In a normal physiologic state, the gingiva is firm and resilient. With the exception of the movable free margins (i.e., the marginal gingiva), it is tightly bound to the underlying bone. This is the result of the collagenous nature of the lamina propria and its integration with the periosteum of the alveolar process. The visual stippling that is seen when viewing the gingival surface represents the pulling of the superficial gingival layer by the tight connective tissue attachments to the underlying alveolar process.
The PDL is the connective tissue structure that surrounds the root and that connects the root with the bone in the tooth socket. It is continuous with the connective tissue of the gingiva, and it communicates with the bone through vascular channels. The principal fibers of the PDL are collagenous organized bundles that insert into the cementum on one side and into the bone on the other side; they are called Sharpey’s fibers. Cellular elements of the PDL include fibroblasts, endothelial cells, cementoblasts, osteoblasts, osteoclasts, tissue macrophages, and stratified epithelial cells. The PDL has physical, formative, nutritional, and sensory functions. These include the physical functions of the transmission of occlusal forces to the bone, the attachment of the teeth to the bone, the maintenance of the gingival tissues in relationship to the teeth, the resistance to the impact of occlusal forces, and the protection of the vessels and nerves from injury by mechanical forces. Destruction of the PDL and the alveolar bone by disease or injury disrupts the balance between the periodontium and the occlusal forces. The PDL supplies nutrients to the cementum, the bone, and the gingiva through the blood vessels; it also provides lymphatic drainage to the same structures. The innervation of the PDL provides proprioception and tactile sensitivity. The PDL includes transseptal, alveolar–crestal, oblique, and apical oriented fibers.
Cementum is the calcified mesenchymal tissue that forms the outer covering of the tooth root. There are two types of cementum: acellular and cellular. Both consist of a calcified interfibrillar matrix and collagen fibrils. The cellular type contains cementocytes in individual spaces (lacunae) that allow for communication with each other through a system of canaliculi. There are two types of collagen fibers. The first type is Sharpey’s fibers, which are the principal fibers of the PDL and which are formed by fibroblasts. The second group of fibers is thought to be produced by the cementoblasts and to form an interfibrillar substance. The distribution of acellular and cellular cementum varies. The coronal half of the root is usually covered by the acellular type of cementum, whereas the cellular cementum is more common in the apical half of the root. The inorganic content of cementum includes hydroxyapatite, a carbohydrate–protein complex, and acid mucopolysaccharides.
The relationship of the interface between the cementum and the enamel at the crown–root interface varies. Cementum overlaps the enamel in about two thirds of cases. In the other third, there is an edge-to-edge arrangement in which a small percentage of the cementum and the enamel fail to meet.
When cementum resorption occurs, it is seen microscopically as concavities on the root surface. Multinucleated giant cells and large mononuclear macrophages are generally found adjacent to the cementum that is undergoing active resorption. The resorptive process may extend into the underlying dentin and even into the pulp. In a physiologic setting, embedded fibers of the PDL reestablish a functional relationship in the new cementum. Cementum repair requires the presence of viable connective tissue. If epithelium proliferates into an area of cementum, then resorption rather than repair will likely take place. Fusion of the cementum and the alveolar bone with obliteration of the PDL is termed ankylosis. When ankylosis does occur, it generally happens after chronic periapical inflammation, tooth replantation, or significant occlusal trauma. It may also represent a congenital failure of eruption.
The anatomic root is the portion of the tooth that is normally covered by cementum. The anatomic crown is the portion of the tooth that is covered by enamel. The clinical crown is the part of the tooth that includes the anatomic part of the crown and the part of the root that has been denuded of periodontium and that is visible in the oral cavity. The clinical root is that portion of the tooth that remains covered by periodontal tissues (i.e., the PDL, the cementum, and the gingiva). Exposure of the root via the apical migration of the gingiva margin is called gingival recession. Exposure of the root to the oral cavity via the apical migration of the junctional epithelium without apical migration of the gingival margin results in pocketing. In either case, periodontal degenerative changes result in the permanent exposure of connective tissue (i.e., the dentin and the cementum) to the external environment.
All parts of the alveolar process serve to support the teeth. Occlusal forces are transmitted through the PDL to the inner wall of the alveolus, which is then supported by the cancellous trabeculae. The cancellous trabeculae in turn are buttressed by the labial and lingual cortical plates. The alveolar process is the bone that supports the tooth socket, and it consists of the following:
The alveolar process consists of calcified matrix with osteocytes that are enclosed within spaces called lacunae. The canaliculi form an anastomosing system through the intercellular matrix of the bone, which brings oxygen and nutrients to the osteocytes and which removes metabolic waste products. In the cancellous trabeculae, the matrix is arranged in lamellae that are demarcated from each other by prominent cement linings. The compact alveolar bone (i.e., the bony lining of the alveolus) consists of closely arranged lamellae and Haversian systems. The principal fibers of the PDL that anchor the tooth in the socket are embedded into the alveolar bone and are referred to as Sharpey’s fibers. The socket wall consists of dense laminated bone. The cancellous portion of the alveolar bone consists of trabeculae, which enclose irregularly shaped marrow spaces that are lined with a layer of thin, flattened ostial cells.
The bony wall of the tooth socket appears radiographically as a thin radiopaque line; it is called the lamina dura. The alveolar bone is perforated by numerous channels that contain blood vessels, lymph vessels, and nerves, which link the PDL with the cancellous portion of the alveolar bone. The vascular supply of the bone is derived from blood vessels in the PDL and in the marrow spaces and from small branches of peripheral vessels that penetrate the cortical plates. The interdental septum consists of cancellous bone that is bordered by the socket walls of approximating teeth and the facial and lingual cortical plates.
The mesiodistal angulation of the crest of the interdental septum parallels a line drawn between the CEJs of the approximating teeth. The average distance between the crest of the alveolar bone and the CEJ in the mandibular anterior region in an individual who is periodontally healthy is approximately 1 mm. With disease progression, the distance between the bone ridge and the CEJ increases throughout the mouth.
The alveolar bone contour normally conforms to the prominence of the roots of the teeth, with regions of mild depression in between. The height and thickness of the facial and lingual bony plates are affected by the alignment of the teeth and the angulation of the roots in the bone. For example, in the patient with mandibular deficiency and excessive incisor procumbency, the labial bone may be thin, and apical migration may be seen along the tooth surface. When the mandibular incisor teeth are lingually positioned (i.e., skeletal Class III), the facial bony plate is generally thicker than normal. Another example is seen when the maxillary molar roots are at acute angles to the palatal bone. The effects of the root location and angulation result in recession of the marginal bone.
An isolated area in which a tooth root is denuded of labial cortical bone, the root surface is covered only by periosteum and overlying gingiva, and the marginal bone remains intact is termed fenestration. An area of the tooth root in which there is denuded bone and where the root surface is covered only by periosteum where the root denudation extends to the margin is called dehiscence. Dehiscences are more common on the labial surface of the lower anterior teeth and on the molars and premolars of the maxilla. Congenital or developmental jaw hypoplasia with dental crowding and trauma from occlusal treatments or orthodontics are common etiologic factors for fenestrations and dehiscences.
Alveolar bone is a structure that is constantly in a state of flux. It is maintained by a delicate balance between bone formation and bone resorption, and it is controlled by local and systemic influences. Bone is resorbed in areas of pressure and deposited in areas of tension. With age and normal occlusal forces, there is a tendency for the mesial migration of the teeth. As a result, the associated alveolar bone is remodeled via resorption and deposition.
The purpose of the alveolar process is to support the teeth both while they are at rest and while they are functioning. Its structure is dependent on the stimulation that it receives from masticatory function, because it undergoes constant remodeling in response to occlusal forces. When force is applied to a tooth, that force is displaced against the resilient PDL, thereby creating areas of tension and compression. The facial and lingual walls of the tooth socket bend in the direction of the force. When the force is released, the tooth, the PDL, and the bone spring back toward their original positions. In response to these forces, osteoblasts and newly formed osteoid will line the socket in areas of tension, whereas osteoclasts position themselves and resorption occurs in areas of pressure. The bone trabeculae are aligned in the path of the tension and compressive stresses to provide maximum resistance to the occlusal force with the minimum of bone substance. Forces that exceed the adaptive capacity of the bone produce injury. When occlusal forces are increased, the cancellous trabeculae also increase in number and thickness to provide necessary support.
The prevalence of periodontal disease with tissue destruction and the loss of teeth and tooth structure tends to increase with age.106,155,160,171 Another consequence of age is reduced tissue elasticity through the degeneration of the elastic fibers. Hormonal changes also occur, and these change the local tissue environment. Traditional thinking is that the degenerative gingival changes associated with aging may include recession, diminished keratinization, reduced stippling, decreased connective tissue cellularity, increased intercellular substances, and reduced oxygen consumption. In the PDL, degenerative aging effects are thought to include a decrease in elastic fibers and a decrease in vascularity and mitotic activity. If these effects occur, the ability of the alveolar bone to withstand occlusal forces is diminished. Frequent changes in tooth structure with age are seen, including occlusal wear with a loss of enamel substance that reduces cusp height and inclination. The degree of attrition is influenced by the masticatory musculature, the consistency of the food eaten, and occlusal factors and habits such as clenching and bruxism. A degree of continued tooth eruption usually occurs as teeth wear. As a result, the clinical crown may become longer, which creates further leverage on the bone with masticatory forces. An opposing factor is the fact that the clinical crowns are simultaneously reduced through attrition, often with an equilibrium or balance being present between the teeth and their bony support. The wear of the teeth along the proximal surfaces may also occur, which results in mesial migration. On average, proximal wear reduces the anteroposterior length of the dental arch by approximately 5 mm by the age of 40 years and by twice that by life’s end. When chronic periodontal disease is added to physiologic degenerative aging, the destructive response of the periodontium is exacerbated. There may be continued gingival recession, attrition, and the reduction of alveolar bone height as a result of a combination of these factors.31
Inflammation of the gingiva, which is also known as gingivitis, is the most common form of gingival disease (Figs. 6-8 through 6-12).1,19,177,183,216 This occurs as a result of local irritants, such as the toxins released by the microorganisms related to dental plaque and calculus. Foreign bodies (e.g., orthodontic appliances, irregular dental restorations) may also serve as local irritants as well as plaque traps. The inflammation caused by local irritants can result in ulcerative, necrotic, and proliferative changes in the gingival tissues.29,30,34,99,165,170,221 When there is deepening of the gingival sulcus, there can be injury to the supporting periodontal tissues; this may become an irreversible process. With continued inflammation, hyperplastic changes of the gingiva occur, and the crest of the gingival margin extends toward the crown. Inflammation causes a proliferation of and a change in the quality of the sulcus and the junctional epithelium such that their normal protective nature becomes dysfunctional. The sulcus becomes a pocket; ulceration through the epithelial barrier with exposure of the underlying connective tissue to the oral cavity is a frequent occurrence. The organisms and their toxins are then able to access the exposed connective tissue, which undergoes further pathologic changes.93,133,135,154,193 As the process continues, the epithelial junction may separate from the root, and the pocket will migrate downward. The epithelium of the lateral wall of the pocket proliferates with inflammatory tissue, which results in varying degrees of degeneration and necrosis. Intrabony periodontal pockets are said to be present when the base is apical to the level of the alveolar bone. The extension of inflammation from the margin of the gingiva into the supporting periodontal tissues marks the transition from gingivitis to periodontitis.6,40,41,107,117,175,200 The essential problem of periodontal disease is the destruction of alveolar bone with a loss of crestal height and PDL destruction. If periodontal disease is left untreated, it will lead to the loosening and loss of the teeth.
Figure 6-8 Photograph of the maxillary anterior dentoalveolar region. Dehiscence of the labial cortical plate of the canine and fenestration of the labial cortical plate of the first premolar are demonstrated. From Newman MG, Takei HH, Klokkevold PR, Carranza FA: Carranza’s clinical periodontology, ed 11, St. Louis, 2012, W.B. Saunders Company, Figure 2-60.
Figure 6-9 Illustration of pocket formation that indicates expansion in two directions (arrows) from the normal gingival sulcus (left) to the periodontal pocket (right). From Newman MG, Takei HH, Klokkevold PR, Carranza FA: Carranza’s clinical periodontology, ed 11, St. Louis, 2012, W.B. Saunders Company, Figure 13-1.
Figure 6-10 Different types of periodontal pockets. With a gingival pocket (A), there is no destruction of the supporting periodontal tissues. With a suprabony pocket (B), the base of the pocket is coronal to the level of the underlying bone, and bone loss is horizontal. With an intrabony pocket (C), the base of the pocket is apical to the level of the adjacent bone, and bone loss is vertical. From Newman MG, Takei HH, Klokkevold PR, Carranza FA: Carranza’s clinical periodontology, ed 11, St. Louis, 2012, W.B. Saunders Company, Figure 13-2.
Figure 6-11 Classification of pockets according to involved tooth surfaces. A, Simple pocket. B, Compound pocket. C, Complex pocket. From Newman MG, Takei HH, Klokkevold PR, Carranza FA: Carranza’s clinical periodontology, ed 11, St. Louis, 2012, W.B. Saunders Company, Figure 13-3.
Figure 6-12 Probing of a deep periodontal pocket. The entire length of the periodontal probe has been inserted into the base of a pocket in the palatal surface of the first premolar. From Newman MG, Takei HH, Klokkevold PR, Carranza FA: Carranza’s clinical periodontology, ed 11, St. Louis, 2012, W.B. Saunders Company, Figure 13-4.
Occlusal forces affect the condition and structure of the periodontium.53,54,59,104,129,134,160,181,191,204 To remain structurally and metabolically sound, the PDLs and the alveolar bone require the mechanical stimulation of occlusal forces. When occlusal forces exceed the adaptive capacity of the tissue, injury occurs. The injury that occurs to the periodontium is called trauma from occlusion, and it can be classified as either primary or secondary occlusal trauma. Primary occlusal trauma occurs when greater-than-normal occlusal forces are placed on teeth with a normal periodontal attachment apparatus (i.e., those that are periodontally stable). Secondary occlusal trauma occurs when normal occlusal forces are placed on teeth with compromised periodontal attachment (i.e., those with periodontal disease).
The periodontium attempts to accommodate the functional demands that are placed on it by the masticatory system. The adaptive capacity of the periodontium varies from person to person. The periodontium is influenced by the severity, direction, frequency, and duration of the force that is put on it and the patient’s specific anatomy. The principal fibers of the PDL are arranged so that they can best accommodate occlusal forces in the long axis of the tooth. Forces that are not aligned well with the tooth’s load-bearing capacity place increased compression on specific locations of the PDL. This may result in resorption of bone, depending on the extent and duration of the occlusal force. If the trauma is excessive, a destructive change in the periodontium will occur. If the injurious force is relieved rapidly enough, repair rather than destruction will occur. When trauma is combined with active infection, rapid irreversible destruction of the periodontium is more likely. The degree to which these factors interact and cause destruction remains controversial. There is a need for ongoing clinical research to clarify these issues.
Traditional thinking is that trauma from occlusion is caused by alterations in the occlusal forces, the reduced capacity of the periodontium to withstand what would otherwise be considered normal, or both. Malocclusion is a risk factor for occlusal trauma, but damage may also occur in the presence of a “normal” occlusion. Trauma from occlusion refers to the tissue injury rather than the specific occlusion. Increased masticatory forces are not traumatic if the periodontium can accommodate them. Trauma from occlusion and inflammation from an infectious or foreign-body process are different pathologic processes that can occur either in isolation or together. Inflammation typically starts in the gingiva and then spreads into the supporting periodontal tissues. Trauma from occlusion causes pathologic change of the attachment apparatus. When this occurs in the presence of inflammatory processes, these two pathogenic factors may act synergistically to cause greater damage to the periodontium than the sum of each factor’s singular effect. These combined components are called co-destructive factors.
The lesion of the attachment apparatus can occur and progress rapidly. It is believed that, when the lesion interacts with plaque-induced inflammatory responses, then the loss of the periodontium is likely to be accelerated.
Tooth movement during orthodontic therapy is the result of controlled forces placed on the teeth and then transmitted to the PDL. Strong or heavy forces (i.e., forces that far exceed capillary blood pressure) result in the crushing of the PDL on the compression side of the tooth, with local ischemia and degeneration (i.e., hyalinization). Moderate forces that exceed capillary blood pressure result in the compression of the PDL with a delay in bone resorption and the movement of the tooth.89 Light continuous forces that are less than the capillary blood pressure result in only limited ischemia to the PDL, with gradual bone resorption on the compression side.174 The patient’s age is not a contraindication to orthodontic treatment per se. Interestingly, in the adult, the hyalinized (necrotic) zones are formed more readily on the pressure side of the orthodontically moving tooth; this will temporarily slow tooth movement.62 The hyalinized zone is soon eliminated with the reorganization of the tissues, first through the resorption of the marrow spaces (thus undermining resorption) and then through the repair of the PDL and finally of the alveolar bone.172 The anticipated regeneration of the PDL on the compression side and the formation of new bone on the tension side will likely be hampered by the presence of active inflammation in the periodontal tissues (i.e., periodontitis).169 This pathologic response is dependent on how long the PDL remains compromised. This is the reason why inflammation should be controlled through effective periodontal treatment before orthodontic tooth movement.*
Until the mid 1980s, heavy intermittent orthodontic forces were routinely used, and this required patient visits every 3 to 4 weeks.176 This allowed the hyalinized fibers to recover before another heavy orthodontic force was applied. Contemporary orthodontics involves the use of light, continuous force. This moves the teeth with less discomfort and more rapidly, and it also allows visits to be spaced at longer intervals.
In a patient with a periodontally compromised dentition and with a baseline loss of alveolar bone, the center of resistance of the involved teeth moves apically.141,157 The net effect is that the involved teeth are more prone to tipping rather than to bodily movement when orthodontic forces are applied. To achieve improvement in the periodontium, orthodontic treatment requires a combination of light controlled forces as well as the movement of teeth more completely into the alveolar housing. In the presence of active disease, orthodontic therapy should be postponed until effective periodontal treatment is accomplished. This approach to orthodontic tooth movement has been shown to improve any preexisting compromised periodontium.
Interestingly, the orthodontic movement of endodontically treated teeth is not a risk factor to the periodontium, because the response of the PDL is not affected by the pulp. Some studies do indicate that endodontically treated teeth are slightly more prone to root resorption during orthodontic treatment as compared with teeth with normal vitality.
Teeth that are already tipped outside of the cortical plate (e.g., proclined mandibular incisors in the individual with Class II malocclusion) and that are orthodontically uprighted into sound alveolar housing are likely to improve in overall periodontal health, even when the gingiva levels remain borderline. Animal studies indicate that, without the presence of plaque, orthodontic forces on the teeth do not in themselves induce gingivitis.67 In the presence of plaque, however, similar forces can cause angular bone defects and, with tipping or torquing movements, gingival attachment loss (i.e., recession) can occur.68–70 Clinical studies have demonstrated that, with adequate plaque control, even teeth with longstanding reduced periodontal support can undergo successful tooth movement without further compromise.63 In patients with no active periodontal disease and with good oral hygiene—and even in adults with reduced but healthy residual periodontium—physiologic orthodontic treatment causes no significant detrimental long-term effects on the periodontal attachment, including the bone levels. Physiologic tooth movement involves light forces and the movement of teeth into (not outside of) alveolar bone.37–39
In a cross-sectional study, radiographic crestal bone levels in adults (N = 104) who completed orthodontic treatment at least 10 years previously were shown to be no different than those of matched control subjects (N = 76).161 In a 2-year post orthodontic study, Trosello and colleagues compared adult women who had multi-banded orthodontic therapy (N = 30) with age-matched (non-orthodontically treated) controls (N = 30).203 It was found that the orthodontically treated patients had a higher prevalence of root resorption (17% versus 2%), although there was a lower prevalence of mucogingival defects (5% versus 12%). The root resorption differences were most common in the maxillary incisors, followed by the mandibular incisors. It appears that, in adults, when biologically sound orthodontic maneuvers are carried out, minimal detrimental effects on the health of the periodontium occur. In the short term, gingivitis and gingival hyperplasia may occur, but there is no attachment loss or irreversible effects. In the long term, when the teeth are moved into (not out of) the alveolar bone, mild root resorption (i.e., 1.0 to 1.5 mm) may be documented, but attachment loss (i.e., irreversible change) only occurs in areas of active periodontitis.
It is known that plaque is the primary etiologic factor of gingivitis. A patient’s inability to clean adequately around orthodontic devices (e.g., banded teeth, brackets, wires, springs, coils, elastics, plates) will promote plaque accumulation, which can lead to gingival inflammation. Before the extensive use of bonded brackets, overgrowth of anaerobes in the patient’s sulcus was typical.57 Fortunately, the common practice of placing numerous subgingival orthodontic bands in each quadrant has gone by the wayside. Nevertheless, a shift in the subgingival microflora to a more pathogenic population that is similar to what is seen in periodontal/>