8: Diseases of the Periodontium

Diseases of the Periodontium

Diseases of periodontium comprise of a group of heterogeneous disorders, and majority of them are caused by bacteria. Periodontal diseases have been known since antiquity. Skulls of some ancient cave dwellers show evidence of chronic periodontal disease, while an acute form now known as acute necrotizing ulcerative gingivitis, or ‘Vincent’s infection,’ was reported as early as 400 BC in soldiers in the Greek army of Xenophon. Man suffers to a greater extent from periodontal disturbances than lower animals.

Though there are many distinct types, chronic diseases of the periodontal tissues exist, chronic plaque associated gingivitis and periodontitis are most common. Inflammation confined only to the marginal gingiva is known as gingivitis. Once it extends to involve the connective tissue attachment and alveolar bone loss, it is called periodontitis. Chronic periodontitis causes more teeth loss than any other disease for adults does. Classification of the various periodontal diseases is difficult, because in nearly every case the condition begins as a minor localized disturbance, which unless adequately treated, may gradually progress until the alveolar bone is resorbed and the tooth is exfoliated. Also, a variety of local irritating factors and underlying systemic situations may alter the progress of the disease. The various resulting pathologic conditions are generally similar regardless of the etiologic factors involved. In other words, the reaction to injury that occurs in the gingiva and the supporting tissues of the teeth is usually a chronic inflammatory response. Histologic studies of the periodontium seldom indicate the type of irritant causing the disease or suggest a specific method of therapy.

The Healthy Periodontium

The periodontium (peri—around, odonto—tooth) or ‘the attachment apparatus’ includes the following tissues: (1) the gingiva, (2) the periodontal ligament, (3) the root cementum, (4) the alveolar bone. Its main function is to attach the tooth to jaw bone and to maintain the integrity of the masticatory system.


A healthy gingiva is a part of the masticatory mucosa covering the alveolar process and surrounds the cervical portion of the tooth by snugly fitting into each interproximal space between the teeth (Fig. 8-1A).

Gingiva is anatomically differentiated into two parts; the free gingiva and the attached gingiva. The color of the gingiva is coral pink and it has a stippled ‘orange peel’ surface. In children, the gingiva is not stippled and appears redder and more delicate. The attached gingiva and the central portion of the interdental papillae are stippled but not the marginal gingiva. Stippling is a form of adaptive specialization or reinforcement for the function. So, reduction or loss of stippling is a common sign of gingival disease. Microscopically gingival epithelium is stratified squamous and parakeratinized except in the gingival sulcus and interdental area where it is nonkeratinized.

In the coronal direction, the gingiva terminates in the free gingival margin with a scalloped outline. In the apical direction it is separated from the loose, darker red alveolar mucosa, by a border termed as mucogingival junction or mucogingival line.

The free gingiva extends apically from the gingival margin to the free gingival groove at the level of the cementoenamel junction (CEJ). The free gingival margin is rounded and is located approximately 1.5–2 mm coronal to the CEJ. It comprises buccal or labial and lingual or palatal aspects and the interdental gingiva. The interdental gingiva also called as interdental papillae has a shape in conformity with the outline of the proximal interdental contact surfaces, as a concavity or a small depression called ‘col’, (a term used by mountaineers to describe a depression between two peaks) which is covered by non-keratinized epithelium. The col lies between the buccal and lingual papillae and is covered with a vestigial structure consisting of the epithelial remnants of the enamel organs of the two adjacent teeth.

Fish believes that a clinically healthy col is gradually replaced by stratified squamous epithelium unless interrupted by inflammation. According to him, a clinically healthy col covered with enamel epithelium is found only in adolescents or very young adults. If the col becomes inflamed or irritated from aggressive scaling at an early age, it might develop an infrabony pocket, since the col is a vulnerable area of the periodontium.

The attached gingiva is firmly attached to the underlying alveolar bone to form a tough mucoperiosteum and to the cementum by the connective fibers and extends apically to the mucogingival junction.

The epithelium of the free gingiva is microscopically differentiated as oral epithelium, facing the oral cavity, sulcular epithelium, which faces the tooth, and the junctional epithelium between the gingiva and the tooth.

The most coronal portion of the attachment apparatus is called the ‘epithelial attachment’ or ‘epithelial cuff.’ This is a band of modified stratified squamous epithelium (normally about 0.2 mm. in vertical dimension) wrapped around the neck of the erupted tooth in the adult. This epithelium is continuous with the epithelium lining the gingival crevice (crevicular epithelium). The attached epithelium, like all other surface epithelium throughout the body, is continuously replaced by multiplication of the basal cells to compensate for the desquamation of the surface cells. This epithelium has relatively high turnover rate. Whether this band is organically attached to the tooth or not is controversial, but the nature of its attachment does not seem to be as important as the fact that the epithelium is present at the site where the tooth extrudes into the oral cavity and that when healthy it forms an effective seal, protecting the underlying connective tissues. The epithelium in this area, whether attached firmly or lightly, is an external cover for the oral cavity, which is resistant to the invasion of irritants and bacteria into the underlying connective tissues. It is a continuous, living, protective device around the neck of the tooth.

Lamina Propria

The connective tissue (lamina propria) components of the gingiva consist of collagen fibers (60%), fibroblasts (5%), vessels and nerves (35%). They are embedded in amorphous ground substances. Cells of the connective tissue include fibroblasts, mast cells, macrophages and the inflammatory cells.

The connective tissue fibers produced by the fibroblast are collagen fibers, reticulin fibers, oxytalan fibers and the elastic fibers. The collagen fibers of the gingiva are oriented in bundles and run in specific direction. Accordingly they are divided into the following groups:

1. Circular fibers, these fiber bundles are contained in the free gingiva and encircle the tooth in a cuff or ring-like fashion.

Gingival fluid (sulcular fluid)

Gingival fluid is present at the gingival sulcus in minute amounts. It is not considered as secretion. It is a fluid that exudates and increases during inflammation. Gingival crevicular fluid is a complex mixture of substances derived from serum, leukocytes, cells of the tissues of periodontium, and microbial flora inhabiting the marginal gingiva or the sulcus (pocket). It also contains significant amounts of antibodies, cytokines, enzymes, and tissue degradation products. The amount of gingival fluid is less in healthy sulcus. Gingival fluid helps to cleanse material from the sulcus, and the presence of plasma proteins may improve adhesion of the epithelium to the tooth, thereby maintaining the structure of junctional epithelium. By its antimicrobial property it defends the periodontium.

Defense mechanisms of gingiva

Nature of the gingival epithelium (i.e. the degree of keratinization, permeability, etc.), presence of leukocytes, salivary components, and gingival crevicular fluid guard the periodontal tissues against the various microbial threats.

Gingival crevicular fluid exhibits both cell mediated and humoral immune responses in healthy and diseased periodontal state by having cytokines. Interferon-α in gingival crevicular fluid inhibits the bone resorption activity of interleukin-1β in periodontal diseases.

Leukocytes, predominantly polymorphonuclear leukoctyes (PMN) are present in the healthy gingival sulci. Apart from PMN a smaller amount of B lymphocytes, T lymphocytes, and mononuclear phagocytes are also present. They have phagocytic and killing property and prevent the extension of plaque and bacterial toxins into the gingival sulcus.

Saliva contains antibodies, enzymes, other antibacterial substances, and leukocytes, which protect the oral tissues by its cleansing, buffering, and antibacterial property. It exerts influence on initiation, progression, and maturation of bacterial plaque.

2. Dentogingival fibers are embedded in the cementum and project in a fan-like configuration into the free gingival tissue.

3. Dentoperiosteal fibers are also embedded in the cementum as dentogingival fibers, but run apically and terminate at the periosteum of the alveolar crest.

4. Alveologingival fibers extend from the crest of the alveolar bone to the lamina propria of the gingiva.

5. Transseptal fibers, these fibers run straight across the interdental septum and are seen embedded in the cementum of the adjacent teeth.

Periodontal Ligament

The periodontal ligament is a soft, richly vascular, dense fibrous connective tissue and is attached to the cementum on one end and alveoloar bone on the other end and occupies the space between the root cementum and the alveolar bone proper. The embedded portion of the periodontal ligament fibers is known as Sharpey’s fibers and the diameters of these fibers are smaller in the cementum than in the alveolar bone proper.

Periodontal ligament is made up of collagen fibers, oxytalan fibers, fibroblasts, amorphous ground substance, and interstitial tissue. Cells of the periodontal ligament include cementoblasts, osteoblasts, osteoclasts and epithelial remnants of Malassez (Figs. 8-2, 8-3). The shape of the periodontal ligament space is of an hourglass-like which is narrowest at the mid-root level. And width of the periodontal ligament ranges from 0.2 to 0.4mm.The mobility of the tooth is largely determined by the width, height and quality of the periodontal ligament.

The principal fibers of the periodontal ligament are collagenous bundles, with a wavy course in longitudinal sections. The principal fibers of the periodontal ligament are broadly grouped into:

The principal fibers of the periodontal ligament always develop conjunction with the eruption of the teeth.

The collagen fibers hold the tooth in position, suspend it in the alveolus, and transform occlusal pressures to tensile forces on the alveolar bone. Although these fibers are not elastic fibers, they are wavy in arrangement, and straighten under occlusal pressure. Sicher has stated that although fiber bundles extend from cementum to bone, the individual fibers do not. The fibers from the cementum and the bone are connected by an intermediate group of interlacing fibers in the middle of the periodontal ligament. The periodontal ligament also contains elastic fibres, associated with the blood vessels and the oxytalan fibers.

Oxytalan fibers are so named because they are acid-resistant, in contrast to collagen fibers and may be related to elastic fibers. An increase in the number of large oxytalan fibers in the transseptal region of periodontal ligaments supporting teeth, which serve as abutments for fixed bridges, suggests that they may be stress related. A concentration of these fibers is also observed to be inferior to the epithelial attachment, irrespective of its location on the tooth. Although oxytalan fibers may persist for a short time after the collagen fibers have been destroyed in periodontal disease, they ultimately disappear as well, and there is no evidence that they deter the progress of a periodontal lesion.

The functions of the periodontal ligament are the tooth anchorage, fibrous tissue development and maintenance, calcified tissue development and maintenance, nutritive and metabolite transport, and innervation.

The tooth is suspended in its position by the unique attachment (gomphosis) formed by strong connective fibers. Thus the functional arrangement is such that physiologic force from any direction will result in tension in the fiber groups and not compression on the bone or fiber groups.

The cells of the periodontal ligament are the fibroblast, osteoblast, cementoblasts, osteoclasts, nerve fibers, and the epithelial cells. The clusters of the epithelial cells are called as the epithelial cell rests of Malassez, a remnant of the Hertwig’s epithelial root sheath.

The epithelial rests are found in all people, but apparently their total number decreases with age. They vary in size from small resting types of larger proliferative masses of epithelial cells. Some are calcified and persist as cementicles. The majority of epithelial rests are located in the cervical area of the teeth at all ages except during the first and second decades, at which time the greatest number is found in the apical area. Reeve and Wentz have suggested that the greater persistence of epithelial rests in the cervical area may be correlated with and influenced by the constant inflammatory reaction present in the area of the gingival sulcus.

Root Cementum

Cementum is a mineralized tissue covering the root surfaces of the tooth. It does not contain blood or lymph vessels or nerves. The different forms of cementum are the cellular, acellular, and afibrillar cementum. The functions of the cementum are to attach the fibers of the periodontal ligament to the root and to repair of the damaged root surface. Cementum of erupted and unerupted teeth undergoes resorption and repair (Fig.8-4). Cementum resorption may be idiopathic or may be caused by local conditions such as occlusal trauma, orthodontic tooth movement, pressure from cysts and tumours, teeth without antagonists, embedded teeth, replanted and transplanted teeth, and tooth with periapical and periodontal diseases. Systemic conditions such as hypothyroidism, calcium deficiency, and Paget’s disease may predispose or induce cemental resorption. Bimstein E and coworkers have examined cemental surface under light microscope and found that teeth from children with leukocyte adhesion deficiency, Down’s syndrome, and aggressive periodontitis have narrower cementum areas and concluded that these cemental anomalies may facilitate the establishment and progress of periodontitis in children. In another study by Bimstein and coworkers on histologic characteristics of root surfaces of primary teeth from children with prepubertal periodontitis revealed bacteria inside dentin tubules or covering cementum, a cuticle, or resorbed dentin; normal, wider than normal, or hypoplastic cementum; resorption lacunae with various depths; aplastic root resorption; alternate resorption and repair; and active repair.

Alveolar Bone

Alveolar process is the part of the maxilla and the mandible containing the sockets, which protects and supports the tooth. The main function is to distribute and resorb forces generated by mastication. Radiographs show that the alveolar bone has a definite cribriform plate with uniform trabeculae and it extends to a definite point between the teeth (Fig. 8-1B)

Isolated areas in which the root is denuded of bone and the root surface is covered by periosteum and overlying gingiva are termed as fenestrations. In fenestrations the marginal bone is intact. When such denuded areas extend through the marginal bone the defect is termed as dehiscence.

The layer of bone into which the principal fibers of the periodontal ligament are inserted is termed as ‘Bundle bone’. Alveolar bone is constantly renewed as a response to functional demands. Thus the periodontium is a site of continuous readaptation due to its function. The rate of this replacement is unknown, but is probably variable and related, in part at least to the physical forces applied to the periodontal ligament.

Deposits on Teeth

The organic coverings of tooth enamel are divided into two types: (1) anatomic structures, and (2) acquired pellicle. The anatomic covering, formed during the developmental and eruptive stages, is known as Nasmyth’s membrane or enamel cuticle, and remnants of this membrane persist throughout the life of the tooth.


The acquired pellicle is a thin deposit, which may form shortly after eruption on the exposed surface of teeth. It is usually invisible and is probably of no pathologic significance. It is reformed within minutes of polishing. It is fully formed in 30 minutes and reaches its mature thickness of 0.1–0.8 microns within 24 hours. It is free of bacteria and completely covers the tooth surface.

The pellicle has been thoroughly investigated by Meckle, by Leach and Saxton, and by Sonju and Rolla, utilizing electron microscopy, electron histochemistry, optical histochemistry, and chemistry. They found that the brownish stained, smooth, structureless deposits, in contradistinction to plaque, did not stain with basic fuchsin. The brown pigment forms due to the presence of tannins in the pellicle. The pellicle frequently penetrates into the enamel, especially on the proximal surfaces of the teeth. The histochemistry and the electron histochemistry indicated that pellicles are of salivary origin. The histochemistry of the pellicle was found to be practically identical with that of dried salivary films on glass. In addition, similar structures were formed in vitro by incubating enamel in saliva. The acquired pellicles were composed of mucoproteins or glycoproteins similar to those found in saliva and contained some lipid material. Primary amino acid groups and 1:2 glycol groups were also demonstrated by both electron histochemistry and chemical analysis. Bacterial enzymatic degradation of salivary glycoproteins did not take place, either because the material was rapidly deposited before bacterial enzyme action could occur or because the stereo-chemical structure of the glycoproteins enabled them to resist enzymatic degradation. A persistent extraneous calcification was always observed in pellicle from the lingual surfaces of lower anterior teeth, but was of such small magnitude that it could not be resolved by light microscopy.

Dental Stains

Pigmented deposits on the tooth surface are called dental stains or extrinsic stains. The oral cavity is subjected to many types of exogenous and endogenous substances that stain teeth. And since the oral flora in many cases contains chromogenic microorganisms, stained deposits are common on the teeth. The stains that are incorporated into tooth structure are known as intrinsic stains and are seen in porphyria, erythroblastosis fetalis and tetracycline therapy (Fig. 8-5A).

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.


In some children and most adults, varying amounts of a hard, stone-like concretion form on the surfaces of teeth or prosthetic appliances (Figs. 8-6, 8-7, 8-8). These deposits are called ‘calculus’, ‘odontolithiasis’, or ‘tartar.’ Calculus is mineralised dental plaque.

Mandel considers calculus formation to be a triphasic process, consisting of cuticle or pellicle deposition, bacterial colonization and plaque maturation, and mineralization, although all three steps may not always be essential. Frank and Brendel have indicated that bacteria can be attached directly to enamel without a cuticular intermediary. Theilade and his coworkers have shown that calcareous deposits can occur in germ-free animals. Nevertheless, the usual process in man is probably a triphasic one.

Calculus is deposited as a soft, rather ‘greasy’ material, which gradually hardens by deposition of mineral salts in the organic interstices, until it becomes hard. It varies in color, from yellow to dark brown or black, depending upon the amount of stain present on or within the deposit.

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.

Halitosis: (Oral malodor, fetor oris, fetor ex ore)

Halitosis an unpleasant or foul odor exhaled while breathing or talking. It is one of the most common reasons for seeking dental aid. It is present in all mouth for some time (transient) and some mouth for all time (persistent). Transient halitosis occurs in fasting, eating certain foods such as garlic, onions, fish and the like, obesity, smoking, and alcohol consumption. Because the mouth is dry and inactive during the night, the odor is usually worse upon awakening (morning breath).

Causes of halitosis may be local or extraoral. Among local causes tongue and gingival sulcus are the major sources of oral malodor, which also include retention of food debris on and between the teeth, unclean prostheses and diseased states like chronic periodontitis, dental caries, abscesses, and dry socket.

Extraoral causes of halitosis include respiratory tract infections, hepatic disorders and excretion through breath of metabolites. The later includes the sweet odor of diabetes, alcoholic breath, and uremic breath of kidney diseases.

Proteins retained in the mouth are broken down by the anaerobic bacteria into amino acids which in turn is further broken down to produce volatile sulfur compounds namely hydrogen sulfide and methyl mercaptan, which are foul smelling.

The methods of detecting or diagnosing halitosis are organoleptic measurement, sulfide monitoring and gas chromatography.

In some patients no halitosis may be present in spite of their complaint of oral malodor. These non-genuine halitosis patients are either pseudo-halitosis patients or halitophobic. Causes include chemosensory dysfunction like taste or olfactory dysfunction or psychosomatic factor.

Classification of Periodontal Disease

Many classifications of periodontal disease have been proposed. The classification presented here (Table 8-1) is the most accepted and was presented and discussed at the International Workshop for the classification of the periodontal diseases organized by the American Academy of Periodontology in 1999.

Table 8-1:

Classification of periodontal disease

Gingival diseases

Plaque induced gingival disease

Nonplaque induced gingival lesions

Chronic periodontitis



Aggressive periodontitis



Periodontitis as a manifestation of systemic disease

Necrotizing periodontal disease

Necrotizing ulcerative gingivitis (NUG)

Necrotizing ulcerative periodontitis (NUP)

Abscesses of periodontium

Gingival abscess

Periodontal abscess

Pericoronal abscess

Periodontitis associated with endodontic lesions

Endodotic – periodontal lesion

Periodontal – endodontic lesion

Combined lesion

Developmental or acquired deformities and conditions

Localized tooth related factors that predispose to plaque induced gingival diseases or periodontitis

Mucogingival deformities and conditions around teeth

Mucogingival deformities and conditions on edentulous ridges

Occlusal trauma

Gingival Diseases

Gingival diseases are broadly classified into dental plaque induced and nonplaque induced. Plaque induced gingival diseases comprise of two categories namely those caused by local factors and those affected by local factors modified by the specific systemic factors of the host.

Plaque induced gingival disease is the most common form of gingival disease. This may occur on a periodontium with no attachment loss or on a periodontium with a previous attachment loss that is stable and not progressing. Plaque induced gingival disease is the result of the interaction of plaque bacteria and defense cells of the host.

This bacteria and host interaction is modified by local and systemic factors. The factors that have been most commonly cited are as follows:


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.

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.


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.

Table 8-2:

Incidence of pregnancy gingivitis

Looby (1946): 475 women (In percentage)
Slight gingivitis 40
Hypertrophic gingivitis 10
Pregnancy tumor 2
Ziskin and Nesse (1946): 416 women (In percentage)
Pregnancy gingivitis 37.9
Hypertrophic gingivitis 7.0
Raspberry-red gingiva 40.0
Combination 1.8
Maier and Orban (1949): 530 women (In percentage)
No pathosis 44.6
Mild inflammation 35.9
Moderate inflammation 17.5
Severe inflammation 1.5
Pregnancy tumor 0.5

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.


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.

Jan 12, 2015 | Posted by in Oral and Maxillofacial Pathology | Comments Off on 8: Diseases of the Periodontium
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