Normal gingiva (Fig. 5-1)—exhibiting no fluid exudate or inflammation caused by bacterial plaque—is pink and stippled. It varies in width from 1 to 9 mm and extends from the free margin of the gingiva to the alveolar mucosa. The gingiva and alveolar mucosa are separated by a demarcation called the mucogingival junction (MGJ), which marks the differentiation between stippled keratinized tissue and smooth, shiny mucosa; the latter contains more elastic fibers in its connective tissue. Apical to the MGJ, the alveolar mucosa then forms the vestibule and attaches to the muscles and fascia of the lips and cheeks.

Fig. 5-1 Normal gingiva.

The gingiva (Fig. 5-2) consists of three parts:

1. Free (marginal) gingiva, which extends from the most coronal aspect of the gingiva to the epithelial attachment with the tooth.

2. Attached gingiva, which extends from the level of the epithelial attachment to the junction between the gingiva and the alveolar mucosa (the MGJ).

3. Interdental papillae, which are triangular projections of gingivae filling the area between adjacent teeth and consisting of a buccal and a lingual component separated by a central concavity (the col).

Fig. 5-2 Normal gingival structure and anatomic landmarks. MG, Marginal gingiva; FGG, free gingival groove; AG, attached gingiva; MGJ, mucogingival junction; AM, alveolar mucosa.

(Redrawn from Schluger S, et al: Periodontal Disease: Basic Phenomena, Clinical Management, and Occlusal and Restorative Interrelationships, 2nd ed. Philadelphia, Lea & Febiger, 1990.)

A V-shaped depression on the labial or buccal surface of the gingiva at or somewhat apical to the level of the epithelial attachment to the tooth is called the free gingival groove. It is not always readily apparent clinically but can be seen histologically and may serve as a reference point for dividing the free gingiva from the labially or buccally attached gingiva.^2,³

The gingiva consists of dense collagen fibers, sometimes referred to as the gingivodental ligament, which can be divided into alveologingival, dentogingival, circular, dentoperiosteal, and transseptal groups. These fibers firmly bind the gingiva to the teeth and are continuous with the underlying alveolar periosteum. A more detailed description can be found in standard periodontal texts.⁴^–⁸

Periodontium

The periodontium is a connective tissue structure attached to the periosteum of both the mandible and the maxilla that anchors the teeth in the mandibular and maxillary alveolar processes. It provides attachment and support, nutrition, synthesis and resorption, and mechanoreception. The main element of the periodontium is the periodontal ligament (PDL), which consists of collagenous fibers embedded in bone and cementum, giving support to the tooth in function (Fig. 5-3). These fibers, also known as Sharpey’s fibers, follow a wavy course and terminate in either cementum or bone. There are five principal fiber groups in the PDL that traverse the space between the tooth root and alveolar bone, providing attachment and support⁴:

1. Transseptal fibers, which extend interproximally between adjacent teeth. (Their ends are embedded in cementum.)

2. Alveolar crest fibers, which begin just apical to the epithelial attachment and extend from cementum to the alveolar crest.

3. Horizontal fibers, which course at right angles from cementum to the alveolar bone.

4. Oblique fibers, which extend in an oblique direction apically, attaching cementum to the alveolar bone. (They are the most numerous fibers.)

5. Apical fibers, which radiate from cementum into the alveolar bone at the apex of the root.

Fig. 5-3 Normal tooth-gingival interface and coronal periodontium. CEJ, cementoenamel junction; PDL, periodontal ligament. B, bone; C, cementum.

There are also smaller, irregularly arranged collagen fibers interspersed between the principal fiber groups. In addition, the PDL contains elastic fibers ⁹ as well as oxytalan fibers.¹⁰

Cellular elements found in the PDL include fibroblasts (the main synthetic cells, which produce collagen and other proteoglycans), cementoblasts and cementoclasts, osteoblasts and osteoclasts (which maintain the viability of their respective tissues), and mast cells and epithelial rests (which play a role in pathologic conditions of the periodontium).¹

Dentogingival Junction

At the base of the gingival sulcus (crevice) is the epithelium-tooth interface, also known as the dentogingival junction (DGJ). This structural relationship between hard and soft tissues is unique in the body. At the ultrastructural level, it is made up of hemidesmosomes and a basal lamina, which anchor the epithelial cells to the enamel and cemental surfaces.^4,¹¹

The depth of the sulcus varies in healthy individuals, averaging 1.8 mm.¹² In general, the shallower it is, the more likely the gingiva is to be in a state of health. Sulcular depths up to 3 mm are considered maintainable. The continued maintenance of the gingiva in a state of health depends on tight, shallow sulci, which in turn depend on optimal plaque control and ensure the success of periodontal therapy, as well as affording a good prognosis for subsequent restorative treatment.

DISEASES OF THE PERIODONTIUM

The general term periodontal disease is used to describe any condition of the periodontium other than normal. It covers such pathologic states as gingival hyperplasia, juvenile periodontitis (also known as periodontosis), and acute necrotizing ulcerative gingivitis—all distinct clinical entities that warrant specific treatment. Information concerning these disease states is available in any of the standard periodontal texts.⁴^–⁸ Periodontal disease must be recognized and treated before fixed prosthodontics so that the gingival tissue levels can be determined for proper margin placement, esthetics, and gingival displacement (with an AlCl₃-impregnated or plain cord; see Chapter 14). Only when the gingiva and periodontium are in an optimal state of health can these determinations be made with ease or predictability.

This discussion is limited to the etiology and progression of the inflammatory gingivitis-periodontitis lesion, which affects the majority of adults ¹³ and constitutes the bulk of pathologic disorders necessitating treatment before restorative dentistry.

Etiology

Most gingival and periodontal diseases result from microbial plaque, which causes inflammation and its subsequent pathologic processes. Other contributors to inflammation include calculus, acquired pellicle, materia alba, and food debris.^5,¹⁴

Terminology

Microbial plaque

Microbial plaque (Fig. 5-4) is a sticky substance composed of bacteria and their byproducts in an extracellular matrix; it also contains substances from the saliva, diet, and serum. It is basically a product of the growth of bacterial colonies and is the initiating factor in gingival and periodontal disease. If left undisturbed, it gradually covers an entire tooth surface and can be removed only by mechanical means.

Fig. 5-4 Gross plaque and calculus accumulation on the mandibular anterior teeth.

Pathogenesis

The pathogenesis or sequence of events in the development of a gingivitis-periodontitis lesion is very complex. It involves not only local phenomena in the gingiva, PDL, tooth surface, and alveolar bone but also a number of complex host response mechanisms modified by the bacterial infection and behavioral factors.²¹ Implicated in the pathogenic mechanism are phagocytic cells, the lymphoid system, antibodies and immune complexes, complement and clotting cascades, immune reactions, and the microcirculation. Detailed descriptions of host response in the gingivitis-periodontitis lesion are available in standard periodontal texts and reviews.⁵^–⁷

The chronic plaque-induced lesion has been investigated ^5,²² in great detail clinically, histopathologically, and ultrastructurally, and the model of disease activity has remained consistent over time. From these analyses, an indistinct division into initial, early, established, and advanced stages has been put forth. The salient features and approximate time frame for each stage are presented here.

Initial lesion

The initial lesion (Fig. 5-5) is localized in the region of the gingival sulcus and is evident after approximately 2 to 4 days of undisturbed plaque accumulation from a baseline of gingival health. The vessels of the gingiva become enlarged, and vasculitis occurs, allowing a fluid exudate of polymorphonuclear leukocytes to form in the sulcus. Collagen is lost perivascularly, and the resultant space is filled with proteins and inflammatory cells. The most coronal portion of the junctional epithelium becomes altered.

Fig. 5-5 Initial lesion of gingivitis-periodontitis. There is a predominance of polymorphonuclear leukocytes in the beginning stages of inflammation.

Early lesion

Although there is no distinct division between the stages of lesion formation, the early lesion (Fig. 5-6) generally appears within 4 to 7 days of plaque accumulation. This stage of development exhibits further loss of collagen from the marginal gingiva. In addition, an increase in gingival sulcular fluid flow occurs with increased inflammatory cells and the accumulation of lymphoid cells subjacent to the junctional epithelium. The basal cells of the junctional epithelium begin to proliferate, and significant alterations are seen in the connective tissue fibroblasts.

Fig. 5-6 Early lesion of gingivitis-periodontitis. The predominant inflammatory cells are lymphocytes subjacent to the junctional epithelium. The epithelium is beginning to proliferate into rete ridges.

(Redrawn from Schluger S, et al: Periodontal Disease: Basic Phenomena, Clinical Management, and Occlusal and Restorative Interrelationships, 2nd ed. Philadelphia, Lea & Febiger, 1990.)

Established lesion

Within 7 to 21 days, the lesion enters the established stage (Fig. 5-7). It is still located at the apical portion of the gingival sulcus, and the inflammation is centered in a relatively small area. There is continuing loss of connective tissue, with persistence of the features of the early lesion. This stage exhibits a predominance of plasma cells, the presence of immunoglobulins in the connective tissue, and a proliferation of the junctional epithelium (Fig. 5-8). Pocket formation, however, does not necessarily occur.

Fig. 5-7 Established lesion of gingivitis-periodontitis. The junctional epithelium is converted into pocket epithelium. Pocket formation may begin. The predominant inflammatory cells are plasma cells.

(Redrawn from Schluger S, et al: Periodontal Disease: Basic Phenomena, Clinical Management, and Occlusal and Restorative Interrelationships, 2nd ed. Philadelphia, Lea & Febiger, 1990.)

Fig. 5-8 Gingivitis. The interproximal gingiva is bulbous and inflamed. Note the erythematous and edematous tissue extending onto the labial portions of the lateral incisors.

Advanced lesion

It is difficult to pinpoint the time at which the established lesion of gingivitis results in a loss of connective tissue attachment to the tooth structure and becomes an advanced lesion or overt periodontitis (Fig. 5-9). Upon conversion to the advanced stage, the features of an established lesion persist. The connective tissue continues to lose collagen content, and fibroblasts are further altered. Periodontal pockets are formed, with increased probing depths, and the lesion extends into alveolar bone. The bone marrow converts to fibrous connective tissue, with a significant loss of connective tissue attachment to the root of the tooth. This is accompanied by the manifestations of immunopathologic tissue reactions and inflammatory responses in the gingiva.

Fig. 5-9 Advanced lesion of gingivitis-periodontitis. Pocket formation has begun, with a loss of connective tissue attachment apical to the cementoenamel junction. Bone is converted into fibrous connective tissue and is subsequently lost. The predominant inflammatory cells are plasma cells, and there are scattered lymphocytes present.

Periodontitis

When a loss of connective tissue attachment occurs, the lesion transforms from gingivitis into periodontitis (Fig. 5-10), a disease that may be characterized by alternating periods of quiescence and exacerbation. The extent to which the lesion progresses before it is treated will determine the amount of bone and connective tissue attachment loss that occurs. It subsequently affects the prognosis of the tooth with regard to restorative demands.

Fig. 5-10 Periodontitis. Plaque and calculus accumulation has resulted in a loss of connective tissue attachment apical to the cementoenamel junction.

EXAMINATION, DIAGNOSIS, AND TREATMENT PLANNING

Before treatment is rendered, all facts and findings related to the patient’s disease state should be recorded.^23,²⁴ These data can then be used to formulate a precise working blueprint for the proposed treatment. The diagnosis and treatment planning stages should be completed before therapy is initiated. In general practice, the data collection, diagnosis, and treatment planning for a patient’s restorative needs are accomplished at approximately the same time. Although laboratory assessments of gingival microflora and gingival crevicular fluid,²⁴ as well as genetic tests for susceptibility to periodontal diseases, are available,²⁵ traditional clinical assessments are most often employed to arrive at a periodontal diagnosis. These include such factors as probing depths, bleeding upon probing, clinical attachment levels, radiographic evidence of bone loss, and the presence or absence of the patient’s signs and symptoms.^26,²⁷ Once the diagnosis has been determined, a treatment plan is presented to the patient.

The treatment plan should be concise, logical, and rational—a realistic approach to therapy. It should not be a rigid or inflexible sequence of events, because often it must be emended as new information or changing circumstances dictate. The timing and sequencing of treatment are important in correcting the patient’s dental problems as efficiently as possible.

The following is a viable working model for periodontal treatment:

Evaluation of Initial Therapy

Evaluation of Surgical Therapy

Guided Tissue Regeneration (Hard and Soft Tissue Procedures)

Initial Therapy

Initial therapy consists of all treatment carried out before evaluation for the surgical phases of periodontal therapy. A number of procedures in each patient’s treatment regimen may be accomplished before more definitive or invasive approaches are undertaken.

Control of microbial plaque

The most crucial aspect of periodontal therapy is the control of microbial flora in the sulcular area. If the patient does not maintain excellent oral hygiene and thereby the optimum condition of soft and hard tissues, the success of subsequent periodontal and restorative treatments will be jeopardized.

Bacterial plaque occurs on all surfaces of the teeth but is especially prevalent on the gingival third.²⁸ It is strongly adherent to the tooth structure, which means that it is not removed by the chewing of fibrous foods.²⁹ The prevention of plaque accumulation, by either mechanical or chemical means, is crucial in the prevention of hard and soft tissue pathosis. Although there are chemical means for removing plaque accumulation, only mechanical methods are considered in this text. Excellent reviews of the subject of chemical plaque removal are contained in standard periodontal texts.^5,⁷

Toothbrushing

Plaque removal is accomplished with a toothbrush and other orophysiotherapy aids. Many types of toothbrushes can be used and are classified according to their size, shape, length, bristle arrangement, and whether they are manually or electrically powered. The many types of brushes and alternate techniques are reviewed in standard periodontal textbooks.⁴^–⁷ The soft-bristle brush is particularly effective for cleaning in the gingival sulci and at buccal and lingual surfaces of interproximal areas^30,³¹ without causing gingival damage and tooth abrasion, which can result from a hard-bristle brush.³²

Technique

In toothbrushing, effective placement of the bristles is more important than the amount of energy expended. The Bass sulcular method of brushing is preferred for most fixed prosthodontics patients because it cleans the sulci, where the margins of restorations are often placed.

The bristles are placed in the sulci at an angle of approximately 45 degrees to the tooth surface, directed gingivally, and moved back and forth with short scrubbing motions under light pressure. The brush is applied in a similar manner throughout the mouth on all buccal and lingual or palatal surfaces of the teeth. In the anterior area, where interproximal spaces are small and where it may seem impossible to place the brush horizontally against the gingiva, the brush can be turned vertically for better access. After the sulcular areas have been cleansed, the occlusal surfaces are brushed, as is the dorsal surface of the tongue. Excellent descriptions and illustrations of toothbrush placement appear in standard periodontal texts.⁵^–⁷

Flossing

Interproximal plaque can be controlled with dental floss.^33,³⁴ Both waxed and unwaxed types clean proximal surfaces, but the unwaxed floss has several advantages³⁵:

1. It is smaller in diameter and thus more easily passed through interproximal contact areas.

2. It flattens out under tension, and thus each separate thread effectively covers a larger surface area.

3. It makes a squeaking noise when applied to a clean tooth surface, which can be used as a guide to effective performance.

Other Aids

Plaque may also be controlled effectively by orophysiotherapy aids such as dental tape, yarn, rubber and wooden tips, toothpicks, interdental stimulators, interproximal brushes, and electric toothbrushes.

When plaque is removed around a fixed dental prosthesis or a restoration involving splinted teeth, a floss threader may be needed. Alternatively, special lengths of floss with stiffened ends are available and have been shown to be quite effective.

Disclosing agents may be used to provide better visualization of areas where plaque control is difficult or deficient. Erythrosin dye in tablet or liquid form stains plaque, rendering it readily observable. Ultraviolet light has been used in combination with fluorescein dye to reveal plaque deposits, precluding the undesirable red stain that remains after erythrosin use.

All the previously mentioned items are useful in removing and controlling inflammation-inducing microbial plaque. However, the most important aspect of plaque control is patient motivation. Without motivation, all orophysiotherapy aids and the knowledge to apply them are useless.

Scaling and polishing

Removal of supragingival calculus (scaling) and polishing of the coronal portion of the tooth are the first definitive steps in débridement of the teeth. Scaling consists of the removal of deposits and accretions from the crowns of teeth and from tooth surfaces slightly subgingival. This is accomplished with the use of sharp scalers or curettes. The gingiva responds to this removal of supragingival and slightly subgingival calculus with a decrease in inflammation and bleeding. Thus, the patient is able to observe the first signs of therapeutic gain, especially when part or half of the mouth is instrumented at one appointment and the remainder is done after a short time has elapsed.

Correction of defective and/or overhanging restorations

Overhanging restorations, open interproximal contacts, and areas of food impaction contribute to local irritation of the gingiva and, of greater importance, impede proper plaque control. These deficiencies (Fig. 5-11) should be corrected during the initial therapy phase of treatment by either replacement or reshaping and/or removal of the overhang (Fig. 5-12). Close cooperation and communication between the periodontist and the restorative dentist are essential during this treatment phase.

Fig. 5-11 Overhanging splinted restoration connecting the mandibular right and left central incisors, with obliteration of the interproximal space by the castings. The patient’s inability to clean this area properly has resulted in iatrogenic loss of attachment.

Fig. 5-12 Recontouring of the interproximal space of the castings seen in Figure 5-11 allows the patient to clean the area. Note the excellent gingival health between the central incisors as a result of good oral hygiene techniques.

Root planing

Root planing (Fig. 5-13) is the process of débriding the root surface with a curette. It is a more deliberate and more delicately executed procedure than scaling and necessitates the administration of a local anesthetic for most patients. At present, it constitutes the primary mode of initial therapy in periodontics, and there is evidence that tooth loss is substantially reduced over time when root surfaces are débrided on a continuing basis.³⁶ Other work has also demonstrated that disease progression continues without root planing, even with effective oral hygiene.³⁷

Fig. 5-13 Root planing. A, Curette placed in the sulcus to address calculus. B, The curette, initially placed apical to the calculus, moves coronally to dislodge the calculus. C, Accretions removed and the root planed to a smooth finish. CA, calculus; CU, Curette; R, root surface; S, sulcus.

(Redrawn from Carranza FA Jr: Glickman’s Clinical Periodontology, 7th ed. Philadelphia, WB Saunders, 1990.)

The curette is a spoon-shaped instrument well suited to cleaning and smoothing root surfaces. It is applied apically on the root with regard to the accretion and is moved coronally to lift deposits off the root surface and to plane it to a glasslike smoothness. As the patient’s plaque-control techniques improve, the changes observed when root planing is completed may necessitate changing or modifying the treatment plan, and further therapy may not be indicated.

Root planing and the incidental curettage of soft tissue that accompanies it may be an end point of active periodontal therapy. In many cases, the combination of root planing and improved oral hygiene on the part of the patient leads to manageable probing depths, and no further treatment is necessary. For this reason, the initial therapy requires careful evaluation.

Strategic tooth removal

An important part of treatment sequencing is the elimination of teeth that are hopelessly involved periodontally or are nonrestorable. Although no hard-and-fast rules exist regarding the timing of such extractions, removing teeth early in therapy is often more advantageous, when the patient has recently been informed of the prognosis and is prepared for treatment.

Extractions can be accomplished during initial therapy when the quadrant being instrumented is anesthetized. The operator can make an excellent determination of questionable teeth at this time by “sounding” the periodontium and can inform the patient of the verdict immediately. The patient is thus prepared psychologically (and also pharmacologically) for the removal. Teeth can also be removed during periodontal surgery, when the same conditions exist.

Early extraction of teeth and/or roots allows the socket areas to heal and can provide better access for plaque control of adjacent tooth surfaces. A transitional or provisional partial removable dental prosthesis or fixed dental prosthesis can also be fabricated; this stabilizes the arch and potentially maintains or improves occlusion, function, and esthetics.^5,⁷

Stabilization of mobile teeth

Tooth mobility occurs when a tooth is subjected to excessive forces, especially when bony support is lacking. It is not necessarily a sign of disease, because it may be a normal response to abnormal forces, and it does not always need corrective treatment. However, it is sometimes a source of discomfort to the patient, and in these cases it should be treated by reduction of the abnormal forces after occlusal evaluation. Depending on the patient’s need, the teeth may also be treated by splinting with provisional restorations (see Chapter 15) or an acid-etch resin technique (see Chapter 26) in conjunction with occlusal adjustment (see Chapter 6). Such restorations should be carefully designed so they do not impede plaque control or future periodontal treatment. Close communication between the periodontist and the restorative dentist is crucial in this phase of treatment.

Minor tooth movement

Orthodontics can be of major benefit to periodontal therapy. Malposed teeth may be realigned to make them more receptive to periodontal treatment and to improve the efficacy of plaque-control measures. As described in Chapter 6, restorative procedures can also be aided by minor tooth movement. Thus, for the best treatment of a patient with complex dental problems, good communication among consulting dentists is essential.

Evaluation of Initial Therapy

The periodontium recovering from active disease should be regularly reexamined and reevaluated to determine the efficacy of treatment. Soft tissue responses to the initial therapy are observed along with the patient’s motivation and ability to maintain a relatively inflammation-free state. Probing depths should be recorded again, and the location of the MGJ noted in relation to the teeth. Changes must be assessed in regard to the necessity of further periodontal treatment.

Reevaluation gives the practitioner a firmer grasp on the progress of treatment, and if necessary, it allows revision of the initial treatment plan. At this time, the gingiva is healthier, probing depths may have decreased because of better plaque control and root planing, and the working knowledge of the patient’s abilities and desires should have improved. The combination of these factors facilitates decisions regarding further treatment of the periodontium and allows a more informed prognosis.

Gingivectomy is the removal of diseased or hypertrophied gingiva. Introduced by G. V. Black,^38,³⁹ it was the first periodontal surgical approach to gain widespread acceptance. Gingivectomy is essentially the resection of keratinized gingiva only, and it may be applied to the treatment of suprabony pockets⁴⁰ and to fibrous or enlarged gingiva, particularly when they result from diphenylhydantoin (Dilantin) therapy⁴¹ (see Fig. 1-4). However, it is unsuitable for the treatment of infrabony defects.