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 disease sites may occur with use of orthodontic devices.¹³¹ Even without banded bracket appliances, an active and diligent oral hygiene program for the patient that includes frequent periodic checkups by an appropriate dentist is required throughout orthodontic treatment.

Dental Restorations: Gingival Interface

The relationship between bacterial plaque accumulation and gingival inflammation has been documented since at least the 1960s.¹³² A patient’s susceptibility to gingival inflammation is not based solely on the mere quantity of dental plaque but also on the virulence of the resident plaque microorganisms. The bacterial composition of dental plaque is dynamic, and the pathogenicity of each specific organism is subject to change over time. It is a dental dictum that creating a confluent restorative–gingival interface is an important factor that allows patients’ oral hygiene efforts to reduce the accumulation of plaque and microorganisms and to decrease—if not eliminate—the resulting gingivitis. For this reason, emphasis should be placed on the marginal integrity of dental restorations; the coronal contour of the restoration; the embrasure and contact; and the marginal location of the restoration. The proper marginal location of a restoration relative to the alveolar bone is thought to be one of the most important parameters for achieving and maintaining long-term gingival health.^{92,124–126,139} Similarly, all patients who are undergoing dental therapy should be philosophically taught and technically trained to perform effective plaque-removal practices.

• Inadequate attached gingiva surrounding the clinical crowns of the teeth

• Inadequate alveolar bone to house the roots of the full complement of teeth in each arch

• Inadequate nasal airflow with a forced mouth-breathing pattern, often in association with vertical (skeletal) excess and inadequate lip closure, with limited coverage of the incisors and the gingiva

• The effects of malocclusion associated with a jaw deformity

Effects of Inadequate Attached Gingiva

There are significant intrinsic biologic variations between humans with respect to the morphologic characteristics of the gingiva; this is known as the gingival biotype.52,73,138 The evaluation of the individual’s gingival biotype is important to orthodontic treatment planning, because thick and thin gingival biotypes are frequently associated with varied osseous patterns. These two tissue types are likely to respond very differently to similar orthodontic forces by demonstrating different patterns of osseous remodeling. With an understanding of the nature of the individual’s biologic risk factors (e.g., gingiva, alveolar bone, breathing pattern, degree of malocclusion), appropriate periodontal, orthodontic, and surgical preventative procedures and precautionary measures may be instituted to provide a more favorable tissue environment to minimize alveolar bone loss and gingival recession. Historically, Ochsenbein and Maynard discussed the importance of thick versus thin gingiva with regard to restorative treatment planning.¹⁵⁰ In addition, in a group of patients reviewed by Olsson and colleagues, a thick periodontal biotype (85% of population) was found to be more prevalent than a thin periodontal biotype (15% of population).¹⁵² Thick gingival tissue is dense in appearance, with a fairly large zone (length) of attachment. The gingival topography is relatively flat, which is suggestive of a full underlying bony architecture. Thin gingival tissue tends to be delicate and almost translucent in appearance. The tissue is friable, with a minimal zone of attachment; this is suggestive of minimal bone over the labial roots of the teeth. The diametrically opposite thin and thick gingival biotypes will respond differently when subjected to inflammation, mechanical trauma, orthodontic forces, or surgical insults. Results from at least some clinical studies indicate that, as long as a tooth is being orthodontically moved with light forces and within or into (and not out of) the alveolar process, then the risk of harmful side effects on the marginal (gingival) soft tissues is minimal.^212–215 In current clinical practice, pretreatment gingival augmentation (i.e., free gingival grafts, lateral pedicled flaps, and autogenous and allogenic connective tissue grafts) to improve the presenting thin keratinized gingiva—in combination with light orthodontic force—generally achieves objectives and limits recession and alveolar bone loss.

Effects of Inadequate Alveolar Bone (Alveolar Bone/Dental Root Ratio)

There will be inherent biologic variations among individuals with regard to the extent of alveolar housing as compared with the cumulative dental root volume of the compliment of teeth within each arch; this is known as the alveolar bone/dental root ratio.184,199 When the roots are crowded into limited available alveolar housing, the periodontal tissues are less able to withstand the routine inflammatory processes and the mechanical demands that they experience. In turn, the periodontium may recede (i.e., experience bone loss and gingival recession). To prevent this, either the space within the arch must be increased (e.g., rapid palatal expansion, surgically assisted rapid palatal expansion, segmental osteotomies) or extractions must be carried out as part of orthodontic treatment to limit the risk of periodontal deterioration.^{50,58,101,103,114,119,147,168,217} Orthodontic relief of dental crowding in the upper jaw by simply expanding the crown arch form in the presence of an inadequate alveolar arch form may align the dental crowns, but it will predictably result in cortical plate thinning, with the potential for dehiscence, fenestrations, loss of alveolar ridge height, and gingival recession (Fig. 6-8). Under these circumstances, successful dental uncrowding without extractions requires the initial expansion of the maxillary (skeletal) arch (e.g., rapid palatal expansion, surgically assisted rapid palatal expansion, segmental osteotomy).¹⁰⁸ By following these principles, the achievement of improved arch form with the preservation of periodontal health should be possible.¹⁴⁷

Effects of Nasal Obstruction and Mouth Breathing With Resulting Vertical Maxillary Excess, Lip Incompetence, and Inadequate Incisor/Gingiva Coverage

There is considerable variation among humans with respect to biologic respiratory patterns (i.e., mouth breathing versus nasal breathing). In the presence of significant nasal obstruction, a forced mouth-breathing pattern will occur and have the potential to cause detrimental effects on the periodontium.7,102,113,206 The existence of these two very different airway biotypes (i.e., nasal breathing and mouth breathing) and the secondary effects that may result should be recognized. Mouth breathing is an important etiologic factor for chronic gingivitis and chronic marginal periodontitis as well as for the formation of dental plaque and calculus. The presence of marginal gingivitis in individuals with mouth breathing was described in the literature by Coleyer in 1920. Warwick and Hastings (1933) also claimed that the surfaces of teeth and gingiva that were constantly exposed to air (i.e., in individuals who breathe habitually through the mouth) did not have the benefit of normal irrigation with saliva; these surfaces also did not benefit from the normal friction effects that result from the vestibular mucosa moving against the teeth and gingiva that would normally occur during lip closure.

In a normal human physiologic state, nasal breathing is a primary source of air intake; it is essential for the supply of properly cleansed, moist, warm air to the lungs. The mouth is considered the secondary emergency source of air for breathing. Individuals who primarily breathe through the mouth also tend to have an excessively open lip posture (i.e., >4 mm), and they often have reduced lip coverage of the incisors and the gingiva. Epidemiologic studies suggest an increased susceptibility to gingival inflammation among mouth breathers. The exact mechanism of these effects is not entirely known, but it is thought that the gingiva of the anterior teeth in particular is prone to drying out as a result of a lack of saliva. This scenario will also lead to an absence of the natural protective action of the saliva and the lips.

Gulati and colleagues undertook a study to assess the effects of mouth breathing, lip seal, and upper lip coverage on the gingival health of children.⁹⁸ School-aged children between the ages of 10 and 14 years (n = 240) were selected for the study. After clinical examination, they were divided into two major groups: mouth breathers and normal breathers. These two groups were further subdivided into six subgroups on the basis of lip-seal ability and upper incisor lip coverage. The results of the study indicate a gingival index that is higher in mouth breathers with lip incompetence than in normal breathers. Increased lip separation and decreased upper lip coverage (i.e., excess exposure of the maxillary incisors) were also associated with higher plaque and gingival indices.

Alexander completed clinical research with the intent of understanding habitual mouth breathing and its effect on gingival health.7–9 The study included 200 patients with a mean age of 30 years who were attending a clinic for routine dental treatment. Each of the subjects underwent systematic examinations to evaluate the presence of gingival inflammation, supragingival and subgingival calculus, and bacterial plaque. Each detailed examination was carried out under standardized conditions. Individuals were questioned carefully regarding the manner in which they usually breathe (i.e., mouth breathing versus nasal breathing). Mean gingival inflammation scores, calculus surface indices, and bacterial indices (with erythrosine disclosing solution) were calculated for each of their individual teeth. The study results confirm that habitual mouth breathing is highly associated with an increase in gingival inflammation and the prevalence of supragingival and subgingival calculus (see Figs. 6-15 through 6-22).

Fukuda and colleagues completed a study to evaluate the influence of mouth breathing on the periodontal tissues.⁷⁶ Ten patients with chronic marginal periodontitis who were found to be habitual mouth breathers were included in the study, and they were evaluated for 30 days. During the experimental time frame, the study patients underwent taping of the lips to accomplish lip seal and to limit the mouth breathing option while sleeping. Oral examinations were completed and biopsy specimens of the gingiva were taken before and after nighttime lip tapings. The study indicates that, with satisfactory lip seal (i.e., lip taping), forced primary nasal breathing was achieved in these individuals while they were sleeping. This resulted in the following:

Effects of Malocclusion on Periodontal Health

Bollen completed a systematic review of the literature to answer the question, “Does a malocclusion affect periodontal health?”³⁵ An electronic search included all publications from 1960 through 2006. A total of 25 studies that evaluated the association between a malocclusion and periodontal health were of sufficient quality for inclusion in the review.* Only 5 of these 25 studies adjusted for factors such as age, socioeconomic status, and oral hygiene. The total number of subjects included in the 25 studies was 35,300, and they had a mean age of 22 years (range, 3 to 60 years). Pertinent results of the review included the following:

The conclusions drawn by Bollen suggest that there is often a correlation between the presence of malocclusion and periodontal disease. However, the extent of this correlation, which is found in large population studies, should not be interpreted as demonstrating a clear cause and effect for any given individual.4,5

Long Face Growth Pattern

In the individual with a long face growth pattern, orthodontic camouflage maneuvers may attempt to correct maxillary arch–width deficiency via the buccal tipping of the posterior teeth (see Figs. 6-15 through Fig 6-19). If more than a few millimeters are required, this may result in the remodeling of the alveolar process with dehiscence and fenestration of the buccal cortex, followed by gingival recession.^{27,205,207,209}

Orthodontic mechanics that are carried out in an attempt to manage the skeletal component of an anterior open bite often “extrude” the incisors. A biologic consequence may be the remodeling of the alveolar process with dehiscence and fenestration of the mandibular labial cortex, followed by gingival recession. Maxillary incisor root resorption may also occur.

Maxillary Deficiency With Relative Mandibular Excess Growth Pattern

With a maxillary deficient and relative mandibular excess growth pattern, orthodontic camouflage maneuvers often attempt to correct upper arch–width deficiency via the buccal tipping of the posterior teeth (see Figs. 6-14 and 6-20 through 6-23). If more than a few millimeters are required, this may result in the remodeling of the alveolar process with dehiscence and fenestration of the buccal cortex, followed by gingival recession.^{27,205,207,209}

Orthodontic mechanics that are carried out to manage the skeletal component of the negative overjet often result in the proclination of the maxillary incisors and retroclined mandibular anterior teeth. This approach may result in the remodeling of the alveolar process with dehiscence and fenestration of the mandibular labial cortex, followed by gingival recession. The remodeling of the alveolar process with a loss of maxillary labial cortex may also be seen.185,194,210

Primary Mandibular Deficiency Growth Pattern

In the individual who presents with a primary mandibular deficiency growth pattern, orthodontic camouflage maneuvers often attempt to uncrowd the mandibular arch by “flaring” the anterior dentition and to then decrease the overjet by proclining the incisors even further (see Figs. 6-24 through Fig. 6-28). This may result in the remodeling of the alveolar process with dehiscence and fenestrations of the labial cortex, followed by gingival recession.^{10–15,18,26,64,65,72,178,195,211}

Another common error occurs when mandibular advancement surgery is planned to correct the excess overjet. Often an inter–arch-width discrepancy will be unmasked (i.e., in approximately 30% of cases). It is not uncommon for clinicians to then avoid maxillary surgery through the process of orthodontic buccal tipping the maxillary posterior teeth to relieve the crossbites. If more than a few millimeters are required, this may result in remodeling of the alveolar process with dehiscence and fenestration of the buccal cortex followed by gingival recession¹⁸⁰ (see Figs. 6-24 through 6-28).

1. Addy, M, Dummer, PMH, Griffiths, G, et al. Prevalence of plaque gingivitis and caries in 11-12-year-old children in South Wales. Community Dent Oral Epidemiol. 1986; 14:115–118.

2. Addy, M. Plaque control as a scientific basis for the prevention of caries. J R Soc Med. 1986; 79(Suppl):6–9.

3. Addy, M, Griffiths, G, Dummer, PMH, et al. The distribution of plaque and gingivitis and the influence of toothbrushing hand in a group of 11-12-year-old school children. J Clin Periodontol. 1987; 14:564–572.

4. Addy, M, Griffiths, GS, Duramer, PMH, et al. The association between tooth irregularity and plaque accumulation, gingivitis, and caries in 11-12-year-old children. Eur J Orthod. 1988; 10:76–83.

5. Ainamo, J. Relationship between malalignment of the teeth and periodontal disease. Scand J Dent Res. 1972; 80:104–110.

6. Albander, JM. A 6-year study on the pattern of periodontal disease progression. J Clin Periodontol. 1990; 17:467–471.

7. Alexander, AG. Habitual mouth breathing and its effect on gingival health. Paradontologie. 1970; 24:49–55.

8. Alexander, AG, Tipnis, AK. The effect of irregularity of the teeth and the degree of overbite and overjet on gingival health. Br Dent J. 1970; 128:539–544.

9. Alexander, AG. The effect of lack of function of teeth on gingival health, plaque and calculus accumulation. J Periodontol. 1970; 41:438.

10. Allais, D, Melsen, B. Does labial movement of lower incisors influence the level of the gingival margin? A case-control study of adult orthodontic patients. Eur J Orthod. 2003; 25(4):343–352.

11. Alstad, S, Zachrisson, BU. Longitudinal study of periodontal condition associated with orthodontic treatment in adolescents. Am J Orthod. 1979; 76:277–286.

12. Andlin-Sobocki, A, Bodin, L. Dimensional alterations of the gingiva related to changes of facial/lingual tooth position in permanent anterior teeth of children: a 2-year longitudinal study. J Clin Periodontol. 1993; 20:219–224.

13. Andlin-Sobocki, A, Persson, M. The association between spontaneous reversal of gingival recession in mandibular incisors and dentofacial changes in children: a 3-year longitudinal study. Eur J Orthod. 1994; 16:229–239.

14. Årtun, J, Osterberg, SK, Kokich, VG. Long-term effect of thin interdental alveolar bone on periodontal health after orthodontic treatment. J Periodontol. 1986; 57:341–346.

15. Årtun, J, Krogstad, O. Periodontal status of mandibular incisors following excessive proclination. A study in adults with surgically treated mandibular prognathism. Am J Orthod Dentofacial Orthop. 1987; 91:225–232.

16. Årtun, J, Osterberg, SK. Periodontal status of teeth facing extraction sites long-term after orthodontic treatment. J Periodontol. 1987; 58(1):24–29.

17. Årtun, J, Urbye, KS. The effect of orthodontic treatment on periodontal bone support in patients with advanced loss of marginal periodontium. Am J Orthod Dentofacial Orthop. 1988; 93(2):143–148.

18. Årtun, J, Grobety, D. Periodontal status of mandibular incisors after pronounced orthodontic advancement during adolescence: a follow-up evaluation. Am J Orthod Dentofacial Orthop. 2001; 119:2–10.

19. Asikainen, S, Jousimies-Somer, H, Kanervo, A, Summanen, P. Certain bacterial species and morphotypes in localized juvenile periodontitis and in matched controls. J Periodontol. 1987; 58:224–230.

20. Atherton, JD, Kerr, NW. Effect of orthodontic tooth movement upon the gingiva. Br Dent J. 1968; 124:555–560.

21. Atherton, JD. Gingival response to orthodontic tooth movement. Am J Orthod. 1970; 58:179–186.

22. Axelsson, P, Lindhe, J, Nystrom, B. On the prevention of caries and periodontal disease: results of a 15-year longitudinal study in adults. J Clin Periodontol. 1991; 18(3):182–189.

23. Badzian-Kobos, K, Stepien-Szczepanska, J, Strzelecka, E. Oral hygiene, condition of periodontium, and malocclusion in children aged 7-15 years from a region of mining and power production. Czas Stomatol. 1987; 40:309–315.

24. Baer, PN, Cocarro, PJ. Gingival enlargement coincident with orthodontic therapy. J Periodontol. 1964; 34:436–439.

25. Baker, DL, Seymour, GJ. The possible pathogenesis of gingival recession: a histological study of induced recession in the rat. J Clin Periodontol. 1976; 3:208–219.

26. Beagrie, CS, Thompson, GW, Basu, MK. Tooth position and anterior bone loss in skulls. Br Dent J. 1970; 129:471–474.

27. Beagrie, GS, James, GA. The association of posterior tooth irregularity and periodontal disease. Br Dent J. 1962; 113:239–243.

28. Behlfelt, K, Ericsson, L, Jacobson, L, Linder-Aronson, S. The occurrence of plaque and gingivitis and its relationship to tooth alignment within the dental arches. J Clin Periodontol. 1981; 8:329–337.

29. Bergström, J, Eliasson, S, Preber, H. Cigarette smoking and periodontal bone loss. J Periodontol. 1991; 62:242–246.

30. Bergström, J, Preber, H. Tobacco use as a risk factor. J Periodontol. 1994; 65:545–550.

31. Bernimoulin, JP, Curiloviec, Z. Gingival recession and tooth mobility. J Clin Periodontol. 1977; 4(2):107–114.

32. Bibb, CA. Occlusal evaluation and therapy in the management of periodontal disease. In: Newman MG, Takei HH, Carranza FA, eds. Carranza’s clinical periodontology. ed 9. Philadelphia: W. B. Saunders Company; 2002:698–701.

33. Bilimoria, KF. Malocclusion: its role in the causation of periodontal disease. J All India Dent Assoc. 1963; 35:293–300.

34. Bolin, A, Eklund, G, Frithiof, L, Lavstedt, S. The effect of changed smoking habits on marginal alveolar bone loss: a longitudinal study. Swed Dent J. 1993; 17(5):211–216.

35. Bollen, AM, Cunha-Cruz, J, Bakko, DW, et al. The effects of orthodontic therapy on periodontal health: a systematic review of controlled evidence. J Am Dent Assoc. 2008; 139(4):413–422.

36. Bondemark, L. Interdental bone changes after orthodontic treatment: a 5-year longitudinal study. Am J Orthod Dentofacial Orthop. 1998; 114(1):25–31.

37. Boyd, RL. Are your patients healthier periodontically because of orthodontic treatment? Bull Pac Coast Soc Orthod. 1984; 56:54–57.

38. Boyd, RL, Leggott, PJ, Quinn, RS, et al. Periodontal implications of orthodontic treatment in adults with reduced or normal periodontal tissues versus those of adolescents. Am J Orthod Dentofacial Orthop. 1989; 96(3):191–198.

39. Boyd, RL. Periodontal screening examination guide. In: American Association of Orthodontists risk management program. St. Louis: American Association of Orthodontists; 1992:13.

40. Bragd, L, Dahlen, G, Wikstrom, M, Slots, J. The capability of Actinobacillus actinomycetemcomitans, Bacteroides gingivalis and Bacteroides intermedius to indicate progressive periodontitis; a retrospective study. J Clin Periodontol. 1987; 14(2):95–99.

41. Brägger, U, Lang, NP. Significance of bone in periodontal disease. Semin Orthod. 1996; 2(1):32–38.

42. Brezniak, N, Wasserstein, A. Root resorption after orthodontic treatment: Part 2. Literature review. Am J Orthod Dentofac Orthop. 1993; 103:138–146.

43. Brown, IS. The effect of orthodontic therapy on certain types of periodontal defects: I. Clinical findings. J Periodontol. 1973; 44:742–756.

44. Buckley, LA. The relationship between malocclusion and periodontal disease. J Periodontol. 1972; 43:415–417.

45. Buckley, LA. The relationship between irregular teeth, plaque, calculus and gingival disease. Br Dent J. 1980; 148:67–69.

46. Buckley, LA. The relationship between malocclusion, gingival inflammation, plaque and calculus. J Periodontol. 1981; 52:35–40.

47. Burch, JG, Bagci, B, Sabulski, D, Landrum, C. Periodontal changes in furcations resulting from orthodontic uprighting of mandibular molars. Quintessence Int. 1992; 23:509–513.

48. Burke, JL, Provencher, RF, McKean, TW. Small segmental and unitooth ostectomies to correct dentoalveolar deformities. J Oral Surg. 1977; 35:453.

49. Burkett, LW. Effects of orthodontic treatment on the soft periodontal tissues. Am J Orthod. 1963; 49:671.

50. Carroll, WJ, Haug, RH, Bissada, NF, et al. The effects of the Le Fort I osteotomy on the periodontium. J Oral Maxillofac Surg. 1992; 50:128–132.

51. Clarke, NG, Hirsch, RS. Personal risk factors for generalized periodontitis. J Clin Periodontol. 1995; 22(2):136–145.

52. Coatoam, GW, Behrents, RG, Bissada, NF. The width of keratinized gingiva during orthodontic treatment: its significance and impact on periodontal status. J Periodontol. 1981; 52:307–313.

53. Cohen, W. A study of occlusal interferences in orthodontically treated occlusions and untreated normal occlusions. Am J Orthod. 1965; 51:647–689.

54. Cooper, MB, Landay, MA, Seltzer, S. The effect of excessive occlusal forces on the pulp. II. Heavier and longer term forces. J Periodontol. 1971; 42:353–359.

55. Davies, TM, Shaw, WC, Addy, M, Dummer, PH. The relationship of anterior overjet to plaque and gingivitis in children. Am J Orthod Dentofacial Orthop. 1988; 93:303–309.

56. Davies, TM, Shaw, WC, Worthington, HV, et al. The effect of orthodontic treatment on plaque and gingivitis. Am J Orthod Dentofacial Orthop. 1991; 99(2):155–161.

57. Diamanti-Kipioti, A, Gusberti, FA, Lang, NP. Clinical and microbiological effects of fixed orthodontic appliances. J Clin Periodontol. 1987; 14:326–333.

58. Diedrich, PR. Guided tissue regeneration associated with orthodontic therapy. Semin Orthod. 1996; 2(1):39–45.

59. Dominiak, M, Kalecinska, E, Krzyszton, E, et al. Correlation between temporomandibular dysfunction, disturbances of occlusion, and gingival recession in a group of youth students. Bull Group Int Rech Sci Stomatol Odontol. 2006; 47:40–46.

60. Dorfman, HS. Mucogingival changes resulting from mandibular incisor tooth movement. Am J Orthod. 1978; 74:286–297.

61. Dorfman, HS, Turvey, TA. Alterations in osseous crestal height following interdental osteotomies. Oral Surg Oral Med Oral Pathol. 1979; 48:120–125.

62. Driel, WD, Leeuwen, EJ, Hoff, JW, et al. Time-dependent mechanical behavior of the periodontal ligament. Proc Inst Mech Eng H. 2000; 214:497–504.

63. Eliasson, LA, Hugoson, A, Kurol, J, Siwe, H. The effects of orthodontic treatment on periodontal tissues in patients with reduced periodontal support. Eur J Orthod. 1982; 4(1):1–9.

64. Emslie, RD. The incisal relationship and periodontal disease. Paradontologie. 1958; 12:15.

65. Engelking, G, Zachrisson, BU. Effects of incisor repositioning on monkey periodontium after expansion through the cortical plate. Am J Orthod. 1982; 82:23–32.

66. Engström, C, Granström, G, Thilander, B. Effect of orthodontic force on periodontal tissue metabolism. A histologic and biochemical study in normal and hypocalcemic young rats. Am J Orthod Dentofacial Orthop. 1988; 93:486–495.

67. Ericsson, I, Thilander, B, Lindhe, J, Okamoto, H. The effect of orthodontic tilting movements on the periodontal tissues of infected and non-infected dentitions in dogs. J Clin Periodontol. 1977; 4:278–293.

68. Ericsson, I, Thilander, B, Lindhe, J. Periodontal condition after orthodontic tooth movements in the dog. Angle Orthod. 1978; 48:210–218.

69. Ericsson, I, Thilander, B. Orthodontic forces and recurrence of periodontal disease. Am J Orthodont. 1978; 74:41.

70. Ericsson, I, Lindhe, J. Recession in sites with inadequate width of the keratinized gingiva: an experimental study in the dog. J Clin Periodontol. 1984; 11(2):95–103.

71. Feliu, JL. Long-term benefits of orthodontic treatment on oral hygiene. Am J Orthod. 1982; 82(6):473–477.

72. Ferro, A, Aronna, P. Isolated gingival recession “without cause” localized to the lower incisors in Class II, 1 dental malocclusion: further studies. Arch Stomatol (Napoli). 1988; 29:1049–1062.

73. Forsberg, A. A clinical study of the periodontal tissues of the upper incisors in two age groups. Acta Odontologjca Scand Suppl. 1951; 9(8):1–105.

74. Foushee, DG, Moriarty, JD, Simpson, DM. Effects of mandibular orthognathic treatment on mucogingival tissue. J Periodontol. 1985; 56:727–733.

75. Fox, ME, Stephens, WF, Wolford, LM, Deeb, ME. Effects of interdental osteotomies on the periodontal and osseous supporting tissues. Int J Adult Orthodon Orthognath Surg. 1991; 6:39–46.

76. Fukuda, T, Yokomichi, K, Kato, H, Ishikawa, J. Studies on the influence of mouth breathing to the periodontal tissue. The effect of oral screen and lip-seal tape on the gingiva in mouth breathers. Nihon Shishubyo Gakkai Kaishi. 1975; 2:280.

77. Gardner, JH. A survey of malocclusions and some aetiological factors on 1,000 Sheffield school children. Dent Practit. 1956; 6:187–201.

78. Garib, DG, Henriques, JFC, Janson, G, et al. Rapid maxillary expansion—tooth-tissue-borne vs tooth-borne expanders: a CT evaluation of dentoskeletal effects. Angle Orthod. 2005; 75:548–557.

79. Geiger, AM. Occlusal studies in 188 consecutively treated cases of periodontal disease. Am J Orthod. 1962; 48:330–360.

80. Geiger, AM. Occlusion in periodontal disease. J Periodontol. 1965; 36:387–392.

81. Geiger, AM, Wasserman, BH, Thompson, RH, et al. Relationship of occlusion and periodontal disease: Part I. A system for evaluating periodontal status. J Periodontol. 1971; 42:371–378.

82. Geiger, AM, Wasserman, BH, Thompson, RH, Turgeon, LR. Relationship of occlusion and periodontal disease: Part V. Relation of classification of occlusion to periodontal status and gingival inflammation. J Periodontol. 1972; 43:554–560.

83. Geiger, AM, Wasserman, BH, Turgeon, LR. Relationship of occlusion and periodontal disease: Part VI. Relation of anterior overjet and overbite to periodontal destruction and gingival inflammation. J Periodontol. 1973; 44:150–157.

84. Geiger, AM, Wasserman, BH, Turgeon, LR. Relationship of occlusion and periodontal disease: Part VIII. Relationship of crowding and spacing to periodontal destruction and gingival inflammation. J Periodontol. 1974; 45:43–49.

85. Geiger, AM, Wasserman, BH. Relationship of occlusion and periodontal disease: Part IX. Incisor inclination and periodontal status. Angle Orthod. 1976; 46:99–110.

86. Geiger, AM, Wasserman, BH. Relationship of occlusion and periodontal disease: Part X. Relation of cross-bite to periodontal status. J Periodontol. 1977; 47:785–789.

87. Genco, RJ. Current view of risk factors for periodontal diseases. J Periodontol. 1996; 67(Suppl 10):1041–1049.

88. Goldberg, D, Turley, P. Orthodontic space closure of edentulous maxillary first molar area in adults. Int J Adult Orthodon Orthognath Surg. 1989; 4:255–266.

89. Goldie, RS, King, GJ. Root resorption and tooth movement in orthodontically treated, calcium-deficient, and lactating rats. Am J Orthod. 1984; 85:424–430.

90. Goldman, HM. The development of physiologic gingival contours by gingivoplasty. Oral Surg Oral Med Oral Pathol. 1950; 3:879–888.

91. Goldman, HM, Cohen, DW. Periodontal therapy, ed 4. St. Louis: The C. V. Mosby Company; 1968.

92. Gould, MSE, Picton, DC. The relationship between irregularities of the teeth and periodontal disease: a pilot study. Br Dent J. 1966; 121:20.

93. Graves, DT, Fine, D, Teng, YT, et al. The use of rodent models to investigate host-bacteria interactions related to periodontal diseases. J Clin Periodontol. 2008; 35:89–105.

94. Greenbaum, KR, Zachrisson, BU. The effect of palatal expansion therapy on the periodontal supporting tissues. Am J Orthod. 1982; 81:12–21.

95. Grewe, JM, Chadha, JM, Hagan, D, Zermeno, JA. Oral hygiene and occlusal disharmony in Mexican-American children. J Periodontal Res. 1969; 4:189–192.

96. Griffiths, GS, Addy, M. Effects of malalignment of teeth in the anterior segments on plaque accumulation. J Clin Periodontol. 1981; 8:481–490.

97. Grossi, SG, Genco, RJ, Machtei, EE, et al. Assessment of risk for periodontal disease: risk indicators for alveolar bone loss. J Periodontol. 1995; 66(1):23–29.

98. Gulati, MS, Grewal, N, Kaur, A. A comparative study of effects of mouth breathing and normal breathing on gingival health in children. J Indian Soc Pedod Prev Dent. 1998; 16(3):72–83.

99. Haber, J. Cigarette smoking: a major risk factor for periodontitis. Compendium. 1994; 15(8):1004–1008.

100. Hamp, SE, Lundstrijm, F, Nyman, S. Periodontal conditions in adolescents subjected to multiband orthodontic treatment with controlled oral hygiene. Eur J Orthod. 1982; 4:77.

101. Handelman, CS. Nonsurgical rapid maxillary alveolar expansion in adults: a clinical evaluation. Angle Orthod. 1997; 67:291–305.

102. Hanson, ML, Andrianopoulos, MV. Tongue thrust, occlusion, and dental health in middle-aged subjects: a pilot study. Int J Orofacial Myology. 1987; 13:3–9.

103. Harry, MR, Sims, MR. Root resorption in bicuspid intrusion: a scanning electron microscope study. Angle Orthod. 1982; 52:235.

104. Heimlich, AC. Selective grinding as an aid to orthodontic therapy. Angle Orthod. 1951; 21:76–88.

105. Helm, S, Petersen, PE. Causal relation between malocclusion and periodontal health. Acta Odontol Scand. 1989; 47:223–228.

106. Henrikson, PA. Periodontal disease and calcium deficiency: an experimental study in the dog. Acta Odontol Scand. 1968; 26(Suppl 50):1–132.

107. Hollender, L, Rönnerman, A, Thilander, B. Root resorption, marginal bone support and clinical crown length in orthodontically treated patients. Eur J Orthod. 1980; 2:197–205.

108. Hom, BM, Turley, PK. The effects of space closure of the mandibular first molar area in adults. Am J Orthod Dentofacial Orthop. 1984; 85:457–469.

109. Horup, N, Melsen, B, Terp, S. Relationship between malocclusion and maintenance of teeth. Community Dent Oral Epidemiol. 1987; 15:74–78.

110. Ingervall, B, Jacobsson, U, Nyman, S. A clinical study of the relationship between crowding of teeth, plaque and gingival condition. J Clin Periodontol. 1977; 4:214–222.

111. Iyer, VS. Reaction of gingiva to orthodontic force: a clinical study. J Periodontol. 1962; 33:26–28.

112. Jacobson, L, Linder-Aronson, S. Crowding and gingivitis: a comparison between mouthbreathers and nosebreathers. Scand J Dent Res. 1972; 80:500–504.

113. Jacobson, L. Mouth breathing and gingivitis I. Gingival condition in children with epipharyngeal adenoids. J Periodontal Res. 1973; 3:269–277.

114. Jager, A, Polley, J, Mausberg, R. Effects of orthodontic expansion of the mandibular arch on the periodontal condition of the posterior teeth. Dtsch Zahnarztl Z. 1990; 45(2):113–115.

115. Janson, G, Bombonatti, R, Brandao, AG, et al. Comparative radiographic evaluation of the alveolar bone crest after orthodontic treatment. Am J Orthod Dentofacial Orthop. 2003; 124(2):157–164.

116. Janson, M. Gingival and periodontal relationships after orthodontic therapy: a study of class-II patients. Dtsch Zahnarztl Z. 1984; 39(3):254–256.

117. Jenkins, SM, Dummer, PM, Addy, M. Radiographic evaluation of early periodontal bone loss in adolescents: an overview. J Clin Periodontol. 1992; 19(6):363–366.

118. Kalamparov, K, Gantsev, GA, Ershov, VN. Relationship between dentomaxillary deformities and periodontal diseases in children. Stomatologiia (Mosk). 1972; 51:47–50.

119. Karring, T, Numan, S, Thilander, B, Magnusson, I. Bone regeneration in orthodontically produced alveolar bone dehiscences. J Periodont Res. 1982; 17:309–315.

120. Katz, RV. An epidemiologic study of the relationship between various states of occlusion and the pathological conditions of dental caries and periodontal disease. J Dent Res. 1978; 57:433–439.

121. Kessler, M. Interrelationships between orthodontic and periodontics. Am J Orthod. 1976; 70:154–177.

122. KIoehn, JS, Pfeiffer, JS. The effect of orthodontic treatment on the periodontium. Angle Orthodont. 1974; 44:127.

123. Klassman, B, Zacher, HW. Treatment of a periodontal defect resulting from improper tooth alignment and local factors. J Periodontol. 1969; 40:401.

124. Kois, JC. The restorative-periodontal interface: biological parameters. Periodontol. 1996; 2000(11):29–38.

125. Kokich, VG. Esthetics: the orthodontic-periodontic restorative connection. Semin Orthod. 1996; 2(1):21–30.

126. Kraus, BS, Jordan, RE, Abrams, L. Dental anatomy and occlusion. Baltimore: Williams & Wilkins Company; 1969.

127. Kwon, H-J, Pihlstrom, B, Waite, DE. Effects on the periodontium of vertical bone cutting for segmental osteotomy. J Oral Maxillofac Surg. 1985; 43:952–955.

128. Langford, SR, Sims, MR. Root surface resorption, repair, and periodontal attachment following rapid maxillary expansion in man. Am J Orthod. 1982; 81:108–115.

129. Lau, D, Grimths, GS, Shaw, WC. Reproducibility of an index for recording the alignment of individual teeth. Br J Orthod. 1984; 11:80–84.

130. Lee, H, Silness, J. Periodontal disease in pregnancy: I. Prevalence and severity. Acta Odontol Stand. 1963; 21:533–551.

131. Listgarten, MA, Hellden, K. Relative distribution of bacteria at clinically health and periodontally diseased sites in humans. J Clin Periodontol. 1978; 5:115–132.

132. Loe, H, Theilade, D, Jensen, SB. Experimental gingivitis in man. J Periodontol. 1965; 36:177–187.

133. Loesche, WJ. The role of spirochetes in periodontal disease. Adv Dent Res. 1988; 2:275–283.

134. Lundeen, HC, Gibbs, CH. The function of teeth. Gainesville, Fla: L and G Publishers; 2005.

135. Magnusson, I, Marks, RG, Clark, WB, et al. Clinical, microbiological and immunological characteristics of subjects with “refractory” periodontal disease. J Clin Periodontol. 1991; 18:291–299.

136. Marshall-Day, CD. The epidemiology of periodontal disease. J Periodontol. 1951; 22:13.

137. Massler, M, Sen Savara, BS. Relation of gingivitis to dental caries and malocclusion in children 14-17 years of age. J Periodontol. 1951; 22:87–96.

138. Maynard, JG, Ochsenbein, LD. Mucogingival problems, prevalence and therapy in children. J Periodontol. 1975; 46:543–552.

139. McCombie, F, Stothard, D. Relationships between gingivitis and other dental conditions. J Can Dent Assoc. 1964; 30:506–513.

140. Melsen, B, Agerbaek, N, Eriksen, J, Terps, S. New attachment through periodontal treatment and orthodontic intrusion. Am J Orthod Dentofacial Orthop. 1988; 94(2):104–116.

141. Melsen, B, Agerbaek, N, Makenstam, G. Intrusion of incisors in adult patients with marginal bone loss. Am J Orthod Dentofacial Orthop. 1989; 96:232–241.

142. Melsen, B. Biological reaction of alveolar bone to orthodontic tooth movement. Angle Orthod. 1999; 69:151–158.

143. Miller, J, Hobson, P. The relationship between malocclusion, oral cleanliness, gingival conditions and dental caries in school children. Br Dent J. 1961; 111:43–52.

144. Motegi, E, Nomura, M, Miyazaki, H, et al. Gingival recession in long-term post-orthodontic patients. J Dent Res. 2002; 81:A372.

145. Musialowicz, KJ. Relation between malocclusion and periodontal diseases in school children from urban and rural areas covered and not covered by planned stomatological care. Ann Acad Med Stetin. 1983; 29:371–385.

146. Newman, WG. Possible etiologic factors in external root resorption. Am J Orthod. 1975; 67:522.

147. Northway, WM, Meade, JB, Jr. Surgically assisted rapid maxillary expansion: a comparison of technique, response, and stability. Angle Orthod. 1997; 67:309–320.

148. Nyman, S, Karring, T, Bergenholtz, G. Bone regeneration in alveolar bone dehiscences produced by jiggling forces. J Periodontal Res. 1982; 17:316–322.

149. O’Leary, TJ, Badell, MC, Bloomer, RS. Occlusal characteristics and tooth mobility in periodontally healthy young males classified orthodontically. J Periodontol. 1975; 46:553–558.

150. Ochsenbein, C, Maynard, JG. The problem of attached gingiva in children. ASDC J Dent Child. 1974; 41:263–272.

151. Ogaard, B. Marginal bone support and tooth lengths in 19-year-olds following orthodontic treatment. Eur J Orthod. 1988; 10(3):180–186.

152. Olsson, M, Lindhe, J. Periodontal characteristics in individuals with varying forms of the upper central incisors. J Clin Periodontol. 1991; 118:78–82.

153. Omnell, ML, Tong, DC, Thomas, T. Periodontal complications following orthognathic surgery and genioplasty in 19-year-old: a case report. Int J Adult Orthodon Orthognath Surg. 1994; 9:133.

154. Paolantonio, M, Festa, F, di Placido, G, et al. Site-specific subgingival colonization by Actinobacillus actinomycetemcomitans in orthodontic patients. Am J Orthod Dentofacial Orthop. 1999; 115(4):423–428.

155. Papapanou, PN, Wennström, JL, Gröndahl, K. Periodontal status in relation to age and tooth type: a cross-sectional radiographic study. J Clin Periodontol. 1988; 15:463–478.

156. Parker, GR. Transseptal fibers and relapse following bodily retraction of teeth: a histologic study. Am J Orthod. 1972; 61:331–334.

157. Pearson, LE. Gingival heights of lower central incisors orthodontically treated and untreated. Angle Orthod. 1968; 38:337–339.

158. Pedrazzoli, V, Kilian, M, Karring, T, et al. Effect of surgical and nonsurgical periodontal treatment on periodontal status and subgingival microbiota. J Clin Periodontol. 1991; 18:598–604.

159. Pfeifer, JS. The reaction of alveolar bone to flap procedures in man. Periodontics. 1965; 3:135–140.

160. Pihlstrom, BL, Ramfjord, SP. Periodontal effect of nonfunction in monkeys. J Periodontol. 1971; 42:748.

161. Polson, AM. Long-term effect of orthodontic treatment on the periodontium. In: McNamara JA, Ribbens KA, eds. Orthodontic treatment and the periodontium. Monograph 15, Craniofacial Growth Series. Ann Arbor, Mich: Center for Human Growth and Development, The University of Michigan; 1984:89–100.

162. Pontoriero, R, Celenza, F, Ricci, G, Carvenale, G. Rapid extrusion with fiber resection: a combined orthodontic-periodontic treatment modality. Int J Periodontics Restorative Dent. 1987; 7:31–43.

163. Poulton, DR, Aaronson, SA. The relationship between occlusion and periodontal status. Am J Orthod. 1961; 47:690–699.

164. Preber, H, Bergström, J. The effect of non-surgical treatment on periodontal pockets in smokers and non-smokers. J Clin Periodontol. 1985; 13:319–323.

165. Preber, H, Bergström, J. The effect of cigarette smoking on periodontal healing following surgical therapy. J Clin Periodontol. 1990; 17:324–328.

166. Pritchard, JF. Gingivectomy, gingivoplasty, and osseous surgery. J Periodontol. 1961; 32:257–262.

167. Pritchard, JF. The effect of bicuspid extraction orthodontics on the periodontium. Findings in 100 consecutive cases. J Periodontol. 1975; 44:534–542.

168. Proffit, WR, Phillips, C, Fields, HW, Turvey, TA. The effect of orthognathic surgery on occlusal force. J Oral Maxillofac Surg. 1989; 47:457–463.

169. Reitan, K. Continuous bodily tooth movement and its histological significance. Acta Odontol Stand. 1947; 6:115.

170. Reitan, K. Tissue rearrangement during retention of orthodontically rotated teeth. Angle Orthod. 1959; 29:105–113.

171. Ren, Y, Maltha, JC, Von den Hoff, JW, Kuijpers-Jagtman, AM. Age effect on orthodontic tooth movement in rats. J Dent Res. 2003; 82:38–42.

172. Ren, Y, Maltha, JC, Kuijpers-Jagtman, AM. The rat as a model for orthodontic tooth movement: A critical review and a proposed solution. Eur J Orthod. 2004; 26:483–490.

173. Ribeiral, MBC, Bolognese, AM, Feres, EJ. Periodontal evaluation after orthodontic treatment. J Dent Res. 1999; 78(5):979.

174. Roberts, WE, Goodwin, WC, Jr., Heiner, SR. Cellular response to orthodontic force. Dent Clin North Am. 1981; 25:3–17.

175. Robertson, PB, Schultz, LD, Levy, BM. Occurrence and distribution of interdental gingival clefts following orthodontic movement into bicuspid extraction sites. J Periodontol. 1977; 48:232–235.

176. Roth, RH. Five-year clinical evaluation of the Andrews straight wire appliance. J Clin Orthod. 1976; 10:836–850.

177. Ruben, RP, Frankl, SN, Wallace, S. The histopathology of periodontal disease in children. J Periodontol. 1971; 42:473.

178. Ruf, S, Hansen, K, Pancherz, H. Does orthodontic proclination of lower incisors in children and adolescents cause gingival recession? Am J Orthod Dentofacial Orthop. 1998; 114:100–106.

179. Rugg-Gunn, AJ, MacGregor, IDM, Edgar, WM, Ferguson, MW. Toothbrushing behaviour in relation to plaque and gingivitis in adolescent school children. J Periodontal Res. 1979; 14:231–238.

180. Ryon, K. Effects of force, magnitude and direction of tooth movement on different alveolar bone types. Angle Orthod. 1964; 34:244.

181. Sadowsky, C, BeGole, EA. Long-term status of temporomandibular joint function and functional occlusion after orthodontic treatment. Am J Orthod. 1980; 78:201–212.

182. Sadowsky, C, BeGole, EA. Long-term effects of orthodontic treatment on periodontal health. Am J Orthod. 1981; 80(2):156–172.

183. Safkan-Seppala, B, Ainamo, J. Periodontal conditions in insulin-dependent diabetes mellitus. J Clin Periodontol. 1992; 19(1):24–29.

184. Salonen, LW, Frithiof, L, Wouters, FR, Hellden, LB. Marginal alveolar bone height in an adult Swedish population: a radiographic cross-sectional epidemiologic study. J Clin Periodontol. 1991; 18(4):223–232.

185. Sarikaya, S, Haydar, B, Ciger, S, Ariyurek, M. Changes in alveolar bone thickness due to retraction of anterior teeth. Am J Orthod Dentofacial Orthop. 2002; 122:15–26.

186. Schneider, HG, Brendel, AK. Oral hygiene study of children under orthodontic treatment. Stomatol DDR. 1981; 31:258–264.

187. Schneider, HG, Mauersberger, I, Bruchmann, M. Relation between periodontal diseases and malocclusions. Stomatol DDR. 1981; 31:494–500.

188. Sergl, HG, Krause, H. Studies on the effects of malocclusions on the periodontium. Dtsch Zahnarztl Z. 1973; 28:149–154.

189. Shaw, WC, Addy, M, Ray, C. Dental and social effects of malocclusion and effectiveness of orthodontic treatment: a review. Community Dent Oral Epidemiol. 1980; 8:36–45.

190. Shefter, GJ, McFall, WT, Jr. Occlusal relationships and periodontal status in human adults. J Periodontol. 1984; 55:368–374.

191. Shinberg, OE, Saakian, S, Zapashnik, EK. The functional periodontal overload in bite anomalies in adults. Stomatologiia (Mosk). 1991; 42–44.

192. Sjolien, T, Zachrisson, BW. Periodontal bone support and tooth length in orthodontically treated persons. Am J Orthod. 1973; 64:28–37.

193. Slots, J. Microflora in the healthy gingival sulcus in man. Scand J Dent Res. 1977; 85:247–254.

194. Sperry, TP, Spiedel, TM, Isaacson, RJ, Worms, FW. The role of dental compensations in the orthodontic treatment of mandibular prognathism. Angle Orthod. 1977; 47:293–299.

195. Steiner, GG, Pearson, JK, Ainamo, J. Changes of the marginal periodontium as a result of labial tooth movement in monkeys. J Periodontol. 1981; 52:314–320.

196. Sten, IB. Tooth malpositions and periodontal pathosis: an evaluation of etiology and considerations in treatment. J Peridontol. 1958; 29:253.

197. Stuteville, OH. Injuries caused by orthodontic appliances and methods of preventing these injuries. J Am Dent Assoc. 1937; 24:1494–1507.

198. Tad, S, Zachrisson, BU. Longitudinal study of periodontal condition associated with orthodontic treatment in adolescents. Am J Orthod. 1979; 76:277–286.

199. Thilander, B, Nyman, S, Karring, T, Magnusson, I. Bone regeneration in alveolar bone dehiscences related to orthodontic tooth movements. Eur J Orthod. 1983; 5:105–114.

200. Thilander, B. Infrabony pockets and reduced alveolar bone height in relation to orthodontic therapy. Semin Orthod. 1996; 2(1):55–61.

201. Thompson, RH, Geiger, AM, Turgeon, LR. Relationship of occlusion and periodontal disease. Part III. Relation of periodontal status to general background characteristics. J Periodontol. 1972; 43:540–546.

202. Tirk, TM, Guzman, CA, Nalchajian, R. Periodontal tissue response to orthodontic treatment studied by panoramix. Angle Orthod. 1967; 37:94–103.

203. Trossello, VK, Gianelly, AA. Orthodontic treatment and periodontal status. J Periodontol. 1979; 50:665–671.

204. Vanarsdall, RL, Corn, H. Soft-tissue management of labially positioned unerupted teeth. Am J Orthod. 1977; 72(1):53–64.

205. Vanarsdall, RL, Jr. Periodontal/orthodontic interrelationships. In: Graber TM, Vanarsdall RL, eds. Orthodontics: current principle and techniques. ed 2. St. Louis: Mosby; 1994:712–749.

206. Wagaiyu, EG, Ashley, FP. Mouth breathing, lip seal and upper lip coverage and their relationship with gingival inflammation in 11-14 year-old schoolchildren. J Clin Periodontol. 1991; 18:698–702.

207. Wainwright, WM. Faciolingual tooth movement: influence on the root and cortical plate. Am J Orthod. 1973; 65:278.

208. Wasserman, BH, Geiger, AM, Turgeon, LR. Relationship of occlusion and periodontal disease: Part VII. Mobility. J Periodontol. 1973; 44:572–578.

209. Watson, WG. Expansion and fenestration or dehiscence. Am J Orthod. 1980; 77:330–332.

210. Wehrbein, H, Fuhrmann, RA, Diedrich, PR. Periodontal conditions after facial root tipping and palatal root torque of incisors. Am J Orthod Dentofacial Orthop. 1994; 106:455–462.

211. Wehrbein, H, Fuhrmann, RA, Diedrich, PR. Human histologic tissue response after long-term orthodontic tooth movement. Am J Orthod Dentofacial Orthop. 1995; 107(4):360–371.

212. Wennstrom, JL, Lindhe, J, Sinclair, F, Thilander, B. Some periodontal tissue reactions to orthodontic tooth movement in monkeys. J Clin Periodontol. 1987; 14(3):121–129.

213. Wennström, JL. The significance of the width and thickness of the gingiva in orthodontic treatment. Dtsch Zahnarztl Z. 1990; 45:136–141.

214. Wennström, JL, Lindskog-Stokand, B, Nyman, S, et al. Periodontal tissue response to orthodontic movement of teeth with infrabony pockets. Am J Orthod Dentofacial Orthop. 1993; 103:313–319.

215. Wennström, JL. Mucogingival considerations in orthodontic treatment. Semin Orthod. 1996; 2(1):46–54.

216. World Health Organization. Epidemiology, etiology and prevention of periodontal disease. Geneva: Report of WHO Scientific Group, Technical Report Series; 1978.

217. Yurkstas, A, Curby, W. Force analysis of prosthetic appliance during function. J Prosthet Dent. 1953; 3:82–87.

218. Zachrisson, BW, Alnaes, L. Periodontal condition in orthodontically treated and untreated children: 1. Loss of attachment, gingival pocket depth and clinical crown heights. Angle Orthod. 1973; 43:402–411.

219. Zachrisson, BW, Alnaes, L. Periodontal condition in orthodontically treated and untreated individuals. Angle Orthod. 1974; 44:48–55.

220. Zachrisson, S, Zachrisson, B. Gingival condition associated with orthodontic treatment. Angle Orthod. 1972; 42:26–34.

221. Zambon, JJ, Grossi, SG, Machtei, EE, et al. Cigarette smoking increases the risk for subgingival infection. J Periodontol. 1996; 67(Suppl 10):1050–1054.