General Information (Fig. 6-1)

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.

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.

Descriptions of the Surfaces of the Teeth (Fig. 6-2)

Basic Anatomy of a Tooth (Fig. 6-3)

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.

2. Lining mucosa (non-keratinized tissue): This epithelium makes up the majority of the mucosa of the mouth and is the primary lining of the oral mucosa.

3. Specialized mucosa: This is found specifically in the regions of the taste buds on the dorsum of the tongue.

The Periodontal Ligament

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

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.

The Alveolar Bone

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.

Gingivitis and Periodontitis

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.

Trauma from Occlusion

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 histopathologic lesion of occlusal trauma is called the lesion of the attachment apparatus, and it is characterized by the following:

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.

Effects of Orthodontic Appliances and Tooth Movement Forces

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/>