Stain from Smoking

As a result of the collection of tobacco tars and resins, a yellowish-brown to black deposit forms on the tooth surfaces of persons who smoke often (Fig. 8-5B). This stain varying from a light brown, powdery deposit in the person who smokes an occasional cigarette to a dense black tarry deposit in heavy smokers. The deposit is harmless to the teeth, although it should be removed because of its objectionable appearance and may act as a nidus for calculus or have a mild, irritating effect on the gingiva. If the dentin is exposed, as in older patients by attrition, the staining may be severe.

Brown Stain

This is a thin, brown, delicate pellicle-like structure that occurs on the teeth and is thought to be composed of salivary mucin. Its occurrence on those surfaces of teeth that are closely adjacent to the orifices of the salivary gland ducts tends to confirm its relation to saliva.

A delicate pigmented dental plaque, called the mesenteric line by some, was described by Pickerill to be a plaque of brown or black dots that coalesce to form a thin, dark line on the enamel at the cervical margin of the tooth. Pickerill, F Bibby and Shourie noted that the presence of this line is often associated with a relative freedom from dental caries.

Black Stain

A thin, black deposit that forms in some patients, both children and adults, on the teeth, is usually in a narrow line or band, just above the free gingiva. It is not associated with smoking. This black stain may be caused by chromogenic microorganisms, although none has been identified or cultured from adult stains. The black stain on primary teeth is associated with a low incidence of dental caries. Slots in 1974 demonstrated that the microflora of black stain was dominated by Actinomyces species and showed that they could produce black pigment in culture.

Green Stain

In some persons, mostly children, there is usually a heavy gray-green stain especially prominent on the gingival third of the maxillary anterior teeth. This stain appears to be soft or ‘furry’ and is difficult to remove, suggesting its association with the enamel cuticle. Sometimes a green stain covers a decalcified area of the enamel. No chromogenic microorganism, which could cause this green stain, has been identified, although it has been assumed that such an organism is the cause. It has also been suggested that coloration of remnants of Nasmyth’s membrane, possibly by blood pigments, may be responsible for the stain.

Orange Stain

Occasionally, a light, thin deposit of a material of brick red or orange color is seen on teeth. The cause of this stain is not known, but it is also believed to be due to pigment-producing microorganisms. This stain can be easily removed, is of no apparent significance and may or may not recur.

Distribution of Calculus

Calculus is classified or divided into two general types according to its location. Deposits above the gingiva on the exposed coronal surfaces of the teeth are spoken of as supragingival calculus, while those covered by the free gingiva are called subgingival calculus. The subgingival calculus is generally much harder, denser, less extensive, flatter, more brittle, and darker in color while the supragingival calculus is white or whitish yellow in color and hard with clay-like consistency. Supragingival calculus can be easily detached from the tooth. Many investigators believe that both types of calculus result from a deposit of inorganic substances into bacterial plaque from saliva and that their physical difference is dependent only upon their environment. Many deposits include both types of calculus; one shading into the other, so any actual division is indistinguishable. Others believe that saliva does not penetrate the gingival crevice and that the source of the inorganic salts in calculus is the blood or tissue fluid from the gingival tissues.

The greatest accumulations of calculus, both supragingival and subgingival, occur on those surfaces of the teeth that are closest to the orifices of the major salivary gland ducts. Thus the lingual surfaces of the mandibular anterior teeth opposite the submandibular and sublingual gland openings and the buccal surfaces of the maxillary molars opposite the parotid duct opening are the common sites of deposition of calculus (Fig. 8-9). It may be localized in its distribution or generalized over many tooth surfaces.

Incidence of Calculus Deposition

Careful clinical observations have indicated that calculus is deposited at irregular intervals throughout life. Patients will sometimes demonstrate a rapid deposition for a short time and then no deposition of calculus for days or weeks.

Although there have been few epidemiological studies on the incidence of calculus, several indices to evaluate the quantity of calculus have been developed. The Simplified Calculus Index of Greene and Vermillion and the Probe Method of Calculus Assessment of Volpe and his coworkers were developed to measure the quantity of calculus formed in long-term longitudinal studies, whereas the Calculus Surface Index of Ennever and his coworkers was developed for short-term clinical trials of calculus inhibitory agents. In fact, the WHO proposed in 1978 that since plaque and gingivitis were so closely correlated, it was unnecessary to assess plaque (and presumably calculus) in population studies and field trials.

However, Marshall-Day reported that in a study of persons 13–60 years old, the 19–22-year age group showed an increase in calculus deposition over the younger age group and that there was a further sharp increase in the 31–34-year age group. The incidence of calculus reached a peak of 91% of persons studied in the 56–59-year age group. Of the entire group, 71% of men and 62% of women manifested calculus formation. 26% exhibited supragingival calculus only, with no significant difference between men and women. Persons with subgingival calculus alone were comparatively few, the incidence being 7% for men and 8% for women. The greater proportion of subjects studied exhibited both types of calculus after 30 years of age. Third National Health and Nutrition Examination Survey revealed that 91.8% of the subjects had detectable calculus and 55.1% had subgingival calculus based on their survey involving 9689 adults in the United States.

Composition of Calculus

Calculus is composed of approximately 75% calcium phosphate, 15–25% water and organic material and the rest calcium carbonate and magnesium phosphate with traces of potassium, sodium, iron, and other elements. When deposits of calculus are washed and analyzed, their basic structure and composition are about the same, regardless of their location. Chemical analyses of calculus varies widely, depending upon the age of the calculus studied, the amount of food debris, and bacterial elements present, and so forth. Calculus consists primarily of calcium phosphate arranged in a hydroxyapatite crystal lattice structure similar to that of bones, enamel, and dentin. The similarity of chemical analyses and physical characteristics of dentin, enamel, cementum, bone, and calculus indicates that removal of calculus from the enamel, cementum or dentin must be done with care, or the dental tissues, especially the cementum, might be damaged.

The organic stroma of the calculus in which the mineral salts are deposited consists of protein polysaccharide complexes, a tangled meshwork of microorganisms, especially gram-positive filamentous types, desquamated epithelial cells and other debris, and white blood cells. Gram-negative filaments and cocci are also present in varying numbers. Mucin has been identified in calculus, as expected from its universal presence in saliva. Mandel and Levy demonstrated a carbohydrate fraction, probably in combination with a protein, and lipid in calculus. Salivary proteins make 5.9–8.2% of the organic component. The composition of subgingival calculus slightly differs from the supragingival calculus. Though the hydroxyapatite content is similar in both types, the magnesium content is more and brushite and octacalcium phosphate is less in subgingival calculus with absence of salivary proteins.

Attachment of Calculus

The manner of attachment of calculus to the tooth surface is an interesting problem, since it is well known that calculus can be scaled from the teeth very easily in some people, but with great difficulty in others. This suggests that calculus has more than one mode of attachment. Acquired pellicle formation has already been discussed. It is important to reiterate McDougall’s findings that all plaques on enamel include an acquired cuticle or pellicle. Zander also investigated calculus attachment and observed four types of attachment of the organic calculus matrix to the tooth surface: (1) attachment to the secondary dental cuticle, (2) attachment to microscopic irregularities in the surface of the cementum corresponding to the previous location of Sharpey’s fibers, (3) attachment by penetration of microorganisms of the calculus matrix into the cementum, and (4) attachment into areas of cementum resorption. He also found that one piece of calculus seldom got attached by a single mode, but rather by a combination of modes. Calculus embedded deeply into the cementum may appear morphologically similar to cementum and has been referred to as calculocementum.

Bacterial Colonization and Plaque Maturation

Many theories have been formulated to explain calculus deposition, but none of them are completely acceptable. No one knows exactly why calculus forms in some persons and not in others, or in the same person at some times but not others.

Numerous studies indicate that the early plaque is composed of a preponderance of coccal microbial forms. As the plaque ages, fusobacteria and filamentous organisms increase in number and, by the second or third week of plaque formation, about half of the organisms in the plaque become filamentous. Gram-positive cocci and rods make up the remainder of the plaque population. The population dynamics of plaque development indicates a progressive decline in aerobic organisms with a concomitant increase in anaerobic organisms.

There is increasing evidence that the various diseases included under the term ‘chronic periodontal disease’ are in fact different diseases and are associated with distinct microbial organisms. Reports from the laboratories of Socransky and his colleagues, Slots and of Kornman and Loesche and others indicate that there is certain specificity to the combination of bacteria in this subgingival plaque in periodontal diseases like chronic gingivitis, acute necrotizing gingivitis, and juvenile periodontitis. The evidence for microbial specificity of individual periodontal diseases was well presented in a review by Loe in 1981.

There are several reports of microbial differences between clinical forms of periodontal disease. Studies by Tanner and his colleagues showed that the predominant cultivable organisms from periodontitis lesions varied among patients. Their studies were early attempts to distinguish ‘pathogens’ associated with different clinical features of destructive periodontal disease. Studies of the plaque in various forms of periodontal disease indicate that there are indeed differences not only in clinical and microbial features but also in host responses to microbial complexes. For example, it is possible that Peptococcus asaccharolyticus and Actinobacillus actinomycetemcomitans play significant etiologic roles in distinctly different destructive forms of periodontal disease.

Plaque Mineralization

The soft dental plaque that is hardened by the precipitation of mineral salts usually starts between the 1st and 14th day of plaque formation. The investigations of Mandel and Levy, as well as Wasserman and his associates, on early developing calculus utilizing histochemical as well as histologic techniques have added to the knowledge of calculus formation. They studied calculus formation by placing contoured strips around lower anterior teeth in patients known to form calculus rapidly. It was noted that the calcifying areas were frequently laminated by alternating dark and light staining bands that produced a concentric ring-like appearance similar to that of pulp stones and urinary calculi. This lamination had been noted by Black in human calculus 70 years earlier.

The major mineral present in calculus is a carbonate apatite similar to that formed in bones and teeth. It is not known why some dental plaques mineralize and others do not. The bulk of the calculus mass consists of mineralized bacteria, and the earliest visible mineral deposition is usually associated with them. Certain microorganisms, such as Corynebacterium matruchotii and some strains of Streptococcus mutans, can be isolated from plaque, which forms an apatite intracellularly when cultured in a medium rich in calcium phosphate. In addition, dead microbial cells induce apatite formation when suspended in metastable calcium phosphate solutions. This finding suggested to Ennever and his coworkers that some component of the cell functions as a catalyst for apatite nucleation. They isolated such a catalyst from microbial cells and characterized it as a proteolipid, nonpolar protein-acidic phospholipid complex. Bacterial cells do not calcify if the proteolipid has been completely removed. The dental calculus matrix also contains proteolipid, which is essential for its remineralization in vitro after it has been decalcified. It is chemically similar to microbial proteolipid. Thus it appeared that proteolipid derived from plaque microbial membranes provided the catalyst for calculus formation. Isolated proteolipid and synthetically prepared analogs have been used to determine the mechanisms of calcification. An essential feature of the mechanism is the initial calcium binding by acidic phospholipids of the complex. The binding is followed by dehydration, which forms a microenvironment in which apatite nuclei are stabilized long enough for crystal growth.

Importance of Calculus

Calculus is always covered with the unmineralized plaque. This unmineralized plaque is the chief irritant and the underlying calculus acts as a significant contributing factor. Calculus is uniformly associated with periodontal diseases. Since it is adherent to the tooth surface, it moves with the tooth during its functions. Subsequently, injuries can occur to the adjacent or overlying gingival tissues that do not move in unison with the teeth. Also, when pressure is placed on the gingiva during mastication, the underlying calculus could irritate the gingival tissues. Thus calculus causes an inflammatory reaction in the gingiva with its overlying mat of microorganisms (Fig. 8-10). Occasionally, supragingival calculus collect in prodigious amounts with little more pathosis present than a superficial inflammation; possibly due to high tissue resistance. Removal of calculus results in rapid clinical improvement.

Prevention of formation of calculus is dependent primarily upon removal by the patient of the fresh, uncalcified deposits with toothbrush and dental floss.

Microorganisms

One must recognize the omnipresence of the many varieties of oral microorganisms that grow as biofilm or plaque, for the most part, on the nonself-cleansing areas of the teeth, particularly below the cervical convexity of the crown and in the cervical areas. Smears of the material taken from the normal gingival sulcus, the gingival sulcus in a case of marginal periodontitis or from the gingival pocket in advanced periodontal disease reveal myriad microorganisms of many different types. Prominent among these will be cocci, various types of bacilli, fusiform organisms, spirochetes, and in advanced periodontitis, amoebas and trichomonads. The normal oral flora is so vast; however, and is made up of so many varieties of microorganisms that it has never been possible to prove conclusively that any one type of microorganism is of greater importance than others as far as periodontal diseases are concerned. The plaque associated with gingivitis and early periodontitis is complex and heterogeneous. However, Slots and coworkers in 1978 demonstrated that in the early stages of gingivitis the Actinomyces group of organisms is the dominant genus in the supragingival plaque.

Plaque and plaque-derived endotoxins may act as irritants or antigens in both nonspecific acute inflammatory responses and immune mechanisms of defense. One of the prime functions of the immune response is to activate the inflammatory system. Both the nonspecific acute inflammatory reaction and the immune response are homeostatic mechanisms, each of which usually succeeds in restoring and maintaining homeostasis. The growing weight of evidence suggests that the breakdown in host resistance dental plaque is a result of tissue injury brought about by the immune reaction. When both nonspecific and immunologically mediated inflammatory lesions of the gingiva occur, the lesion is no longer a self-limiting and protective reaction becomes progressively tissue destructive. There are many destructive enzymes released by polymorphonuclear leukocytes (PMNs) and numerous tissue destructive lymphokines and lymphotoxins elaborated by B- or T lymphocytes. Thus, collagenase liberated by both PMNs and lymphocytes, other lysosomal enzyme secretions, lysosomal acid hydrolases (of macrophages), lymphotoxin-mediated cytotoxins, and osteoclast-activating factor (OAF) are all tissue destructive substances released as part of the inflammatory reaction to injury. The subject of host-parasite interactions in gingivitis and periodontitis was reviewed by MacPhee and Cowley in 1981.

Specific microorganisms sometimes cause an inflammatory reaction of the gingiva, although the clinical appearance may be entirely nonspecific. For example, a monilial or a tuberculous infection may affect the gingiva. The herpes simplex virus and the fusospirochetal organisms of necrotizing ulcerative gingivitis may also infect the gingiva. Furthermore, both streptococcal and staphylococcal gingivitis have been described as being due specifically to these organisms. Definite proof of a cause-and-effect relation here is difficult and questionable.

Calculus

Calculus, whether in a supragingival or a subgingival position, causes irritation of the contracting gingival tissue. This irritation is probably caused by the byproducts of the microorganisms, although the mechanical friction resulting from the hard, rough surface of the calculus may also play a role.

Food Impaction and General Oral Neglect

The impaction of food and the accumulation of debris on the teeth because of oral neglect result in gingivitis, through irritation of the gingiva by toxins of microorganisms growing in this medium. The degradation of food debris may also prove irritating to the gingival tissues.

Faulty or Irritating Restorations or Appliances

Faulty restorations may act as irritants to gingival tissues and thereby induce gingivitis. Overhanging margins of proximal restorations may directly irritate the gingiva and in addition allow the collection of food debris and organisms that further injure these tissues. Improperly contoured restorations may also produce gingival irritation by causing food packing or abnormal excursions of food against the gingiva during mastication. Prosthetic or orthodontic appliances impinging on the gingival tissues produce gingivitis as a result of the pressure and of the trapping of food and microorganisms.

Mouth Breathing

Drying of the oral mucous membrane due to mouth breathing, excessive environmental heat, or excessive smoking causes gingival irritation, with accompanying inflammation or sometimes hyperplasia.

Tooth Malposition

Teeth which have erupted or which have been moved out of physiologic occlusion, where they are repeatedly subjected to abnormal forces during mastication, are apparently very susceptible to the development of periodontal disease. For example, a lower incisor may be ‘bucked’ out of alignment in the second or third decade of life and suddenly, in its new position, receive much of the occlusal stress of one or two upper anterior teeth. Calculus may be deposited on the lingual surface of such a tooth; the bacteria present attack the tissue around this tooth. As a result the gingival tissues may become inflamed and may recede. Teeth in labial positions have less osseous coverage over their radicular surface and hence are more susceptible to trauma from toothbrushing and other local irritations. Abnormally high frenal attachments also contribute to gingival recession.

Chemical or Drug Application

Many drugs are potentially capable of inducing gingivitis, particularly an acute case of gingivitis, owing to a direct local or systemic irritating action. For example, phenol, silver nitrate, volatile oils, or aspirin, if applied to the gingiva, will provoke an inflammatory reaction. Others, such as dilantin sodium, produce gingival changes when administered systemically. These have been discussed specifically in the Chapter 12 on Physical and Chemical Injuries of the Oral Cavity.

An unusual type of gingivostomatitis termed ‘plasma cell gingivitis’ (q.v.) first appeared in the United States about 1968. Although a number of etiologic factors such as hypersensitivity, allergy, endocrine disease, specific infection, etc. were proposed, it remained for Kerr and his associates in 1971 to identify the most probable causative agent. They found that the disease represented an allergic reaction to some component of chewing gum. When the patients eliminated the use of chewing gum, the tissues returned to normal. The clinical features of the disease were so characteristic that it could be readily recognized as a specific entity, probably with a common etiology.

Nutritional Disturbances

Nutritional imbalance is frequently manifested in changes in the gingiva and deeper underlying periodontium. The effects of nutritional deficiencies on these structures as well as on the oral cavity as a whole have been considered in detail in Chapter 15 on Oral Aspects of Metabolic Disease. It is sufficient to point out that adequate intake, absorption and utilization of the various vitamins, minerals and other foodstuffs are essential to the maintenance of a normal periodontium.

Pregnancy

Many investigators have reported that the gingiva undergoes certain changes during pregnancy which have been termed ‘pregnancy gingivitis’ (Table 8-2). Among studies of relatively large numbers of pregnant patients, the following may be cited as representative.

The clinical appearance of the gingiva in the pregnant woman varies from an unchanged to a smooth, shiny, deeply reddened marginal gingiva with frequent focal enlargement, and intense hyperemia of the interdental papilla. Occasionally, a single tumor like mass will develop, the ‘pregnancy tumor,’ which is histologically identical with the pyogenic granuloma (q.v.). Pregnancy induces a hypersensitive response to a mild injury which otherwise would have been innocuous. This gingivitis, clinically nonspecific in appearance, may occur near the end of the first trimester and may regress or even completely disappear at the termination of the pregnancy.

Diabetes Mellitus

This has been repeatedly reported in association with severe periodontal disease, especially in younger people. It has not been proved that diabetes is a specific cause of severe periodontal disease, since many patients with diabetes have normal periodontal structures. However, in uncontrolled diabetes, many metabolic processes are affected, including those which make up resistance to infection or trauma. For example, a diabetic may suffer from persistent chronic ulcers of the skin of the legs, presumably because resistance is lowered and any minor irritation such as trauma or bacterial infection of the skin will result in injury greater than that in a normal person. Also, the effectiveness of the healing process is decreased, possibly as a result of a disturbance in cellular carbohydrate metabolism. Therefore, considering the periodontium located in the oral cavity with its many factors predisposing to disease, including calculus, bacteria, and trauma, it is not surprising that this structure appears to breakdown more readily in persons with uncontrolled diabetes than in normal people. Controlled experimental animal studies have been performed repeatedly in which the animals were made deficient in insulin production and yet no consistent special periodontal pathosis resulted. Perhaps the local factors were insufficient to overcome the inborn vitality of the periodontium in such cases.

It has been reported by Russell that nearly 40% of a group of 37 diabetics exhibited gingival angiopathy in the form of PAS-positive, diastase-resistant thickening of vessel walls, hyalinization of vessel walls and sometimes luminal obliteration. Similar changes were also found in the periodontal ligament vessels of patients with diabetes mellitus.

Other Endocrine Dysfunctions

Gingivitis is reported to occur with some frequency in puberty as the so-called puberty gingivitis. The gingiva appears hyperemic and edematous. The fact that many adolescents are chronic mouth-breathers as a result of lymphoid hyperplasia of the tonsils and adenoids has suggested that the endocrine basis is relatively unimportant, while the local irritant (drying of the mucosa because of the mouth breathing) being the actual cause of the condition. Gingivitis associated with menstruation has been reported by many. In addition, a nonspecific gingivitis with gingival bleeding, vicarious menstruation may occur sometimes. This phenomenon is rare.

Psychiatric disturbances appear to have a definite influence upon the severity of periodontal disease. Belting and Gupta reported that the severity of periodontal disease was significantly greater in psychiatric patients than in a controlled group of patients. Significant differences in severity were noted even when such variable factors as amounts of calculus, brushing frequency and bruxism were held constant in the two groups. The severity of periodontal disease increased significantly as the degree of anxiety increased. It was also noted that the severity of periodontal disease decreased significantly in both normal and psychiatric groups as the educational level of the patient increased.

Incidence

Numerous studies have been devoted to ascertaining the incidence or prevalence of gingival disease. It is generally accepted that periodontal disease is worldwide in distribution and that there is no age group (except in very young infants) in which it does not occur. Although all races are affected, there is some difference in incidence between different races and different countries.

Marshall-Day and his associates studied the incidence of periodontal disease in a group of 1,279 persons ranging in age from 13–65 years residing in the Boston, Massachusetts. Their investigations revealed that the incidence of gingivitis was extremely high even in the early age groups, ranging from 80% at age 13–15, to 95% at age 60. An interestingly significant reduction in incidence of gingival disease to 62% occurred in the late teens and early 20s. It was suggested that this reduction was associated with the end of puberty and/or social factors, where the adolescents placed a greater emphasis on oral hygiene and esthetics than they had previously. In 10 of the 13 different age groups, men were affected more frequently than women; the overall average being 88% for males and 80% for females.

Clinical Features

Acute gingivitis is painful uncommon lesion with sudden onset and shorter duration. Specific forms of acute gingivitis will be discussed separately, and the present considerations will be limited to the most common form of gingival disease, the chronic gingivitis.

In gingivitis the inflammation is limited only to the gingiva without underlying attachment loss. It may be localized or generalized. Beginning of periodontitis is marked by the spreading of inflammatory process from the gingiva to the underlying periodontal tissues. Although all forms of periodontitis are preceded with gingivitis, it is not ne/>