**3. Periodontal disease**

Periodontal disease is a condition that affects the periodontium, therefore the structures that surrounds the teeth, whose role is to protect and provide support to it (De Marco & Gioso, 1997). It is an infectious disease (Mitchell, 2005) that affects more than 80% of dogs (Riggio, 2011), and climbing to about 85% of dogs over four years old (Roman et al., 1995; De Marco & Gioso, 1997). This fact makes it the most prevalent disease in dogs (Harvey & Emily, 1993; Gioso & Carvalho, 2004; Mitchell, 2005). It has been described as a multifactorial infection with aetiological factors such as bacterial plaque, microflora, immune status, the amount of saliva, breed, age, routine of prophylactic cleaning and type of food. However, plaque is the primary aetiological agent, which consists predominantly of gram-positive, aerobic, nonmotile bacteria early in the infection, and anaerobic, gram-negative and motile bacteria in the later stages of infection (Harvey & Emily, 1993; Gioso, 2007).

The disease is caused by the accumulation of bacterial plaque on teeth and gingiva (Harvey & Emily, 1993; Gioso & Carvalho, 2004), by toxic metabolism products of these microorganisms and the host immune response against infection (Mitchell, 2005) that triggers the inflammatory process. Initially this process affects only the gingiva tissue, which characterises the gingivitis that later may worsen and develop into a process of periodontitis

Periodontal Disease in Dogs 125

positive rods (non-motile) gradually increase, surpassing the cocci, and the number of gramnegative bacteria also grows. This change continues to go on until the periodontium involvement phase (periodontitis), when the more pathogenic gram-negative microorganisms become the majority, so that the spirochetes represent almost half of the bacteria, while gram-positives are underrepresented (Niezengard et al., 1997; Riggio et al.,

Fig. 2. Formation phases of dental plaque: A) Adhesion of Gram-positive cocci and rods; B) cellular proliferation and exopolysaccharide production; C) adhesion of Gram-negative

Without interference in the plaque formation an inflammatory process can occur, which marks the beginning of a periodontal disease and that provides a favourable environment for change in the microbial composition of the plaque, that become a biofilm with more pathogenic characteristics, continuing with later stages of the disease (Sans & Newman,

The main bacteria involved in the formation of dental plaque are *Streptococcus* sp. (Gibbons, 1972; Tanzer et al. 1974; Duchin & Houte, 1978; Slee & O'Connor, 1983; Slee et al. 1983; Corner et al., 1988; Murray et al., 1992; Harvey & Emily, 1993; Lang et al., 1997; Loesche &

bacteria; D) maturation of plaque with increase of bacterial biodiversity.

1997; Loesche & Grossman, 2001; Gioso, 2007).

2011).

which involves changes in other periodontium tissues and can cause bone, periodontal ligament, and in some cases, cementum or even tooth loss (Harvey & Emily, 1993).

Bacterial plaque is a sticky, yellowish material that colonises the entire mouth (Gioso, 2007), the faces of the teeth in their enamel structure (Slee & O'Connor, 1983; Katsura et al., 2001) and gingival sulcus (Domingues et al., 1999). This plaque is a biofilm (Dupont, 1997; Roza, 2004) or an undefined microbial community associated with the tooth surface (Wilderer; Charaklis, 1989, Lang et al., 1997), and is considered the leading cause of pathological process (aetiologic agent) (Tanzer et al. 1977; McPhee & Cowley, 1981). The plaque has as its main constituents: salivary glycoproteins, minerals, oral bacteria, extracellular polysaccharides that adhere to the tooth surface, desquamated epithelial cells, leukocytes, macrophages and lipids (Harvey & Emily, 1993; Roza, 2004)

Initially there is a pellicle formation upon the tooth surfaces and other areas of the mouth, called attached pellicle, which is an organic film derived from the saliva that, at first, has no micro-organisms (Sans & Newman, 1997). In the acquired pellicle begins the formation of a biofilm through the adhesion of the first microorganisms that are mostly gram-positive aerobic bacteria (Figure 2) (Lang et al. 1997; Sans & Newman, 1997; Gioso, 2007), mainly of the *Streptococcus* genus, which produce an exopolysaccharide, a substance that acts like a "glue", facilitating the attachment of these bacteria to the surfaces in question (Wiggs & Lobprise, 1997; Gioso, 2007; Roza, 2004) especially in places where there are small irregularities, cracks or roughness (Sans & Newman, 1997).

The first layer is usually single-celled and appears irregularly distributed on the tooth surface. With the microbial growth, the layer starts to come out of these areas of irregularities onto the enamel surface and increases in volume. The isolated plaques start to coalesce, forming a single plate. Over time in the process of plaque formation, a new phase is present, where new microbial strains with less ability to adhere to tooth structure, adhere to the already formed plaque, featuring new microcolonies and increasing the biodiversity of the plaque (Figure 2) (Sans & Newman, 1997). This process is called the organisation of the bacterial plaque, in which the bacteria need approximately 24 to 48 hours to get organised enough to cause the disease (Gioso, 2007). At this stage, the fight against bacterial plaque, with the simple disruption of it, is able to stall and reverse the process (Slee et al., 1983).

According to the location, the plaque can be classified as supra or sub-gingival. The supragingival plaque corresponds mainly to microbial aggregates found on tooth surfaces (mostly in the gingival third of the crown), however may extend into the gingival sulcus, where they are in immediate contact with the marginal gingiva. The subgingival plaque corresponds to bacterial aggregates found entirely within the gingival sulcus or periodontal pockets (Harvey & Emily 1993).

The bacterial constituents present in dental plaque are modified according to the disease evolution. In healthy gingiva, the cocci represent nearly two-thirds of the bacteria, followed by non-motile small rods. The bacteria present are mostly gram-positive and there is no significant representation of more virulent bacterial types. A new work from Federal University of Viçosa, Brazil, identified bacteria that are present in initial supra-gingival plaque in ten young dogs and found the genera *Streptococcus*, *Staphylococcus* and *Enterococcus* as the main components (personal data). At the stage of gingivitis, the gram-

which involves changes in other periodontium tissues and can cause bone, periodontal

Bacterial plaque is a sticky, yellowish material that colonises the entire mouth (Gioso, 2007), the faces of the teeth in their enamel structure (Slee & O'Connor, 1983; Katsura et al., 2001) and gingival sulcus (Domingues et al., 1999). This plaque is a biofilm (Dupont, 1997; Roza, 2004) or an undefined microbial community associated with the tooth surface (Wilderer; Charaklis, 1989, Lang et al., 1997), and is considered the leading cause of pathological process (aetiologic agent) (Tanzer et al. 1977; McPhee & Cowley, 1981). The plaque has as its main constituents: salivary glycoproteins, minerals, oral bacteria, extracellular polysaccharides that adhere to the tooth surface, desquamated epithelial cells, leukocytes,

Initially there is a pellicle formation upon the tooth surfaces and other areas of the mouth, called attached pellicle, which is an organic film derived from the saliva that, at first, has no micro-organisms (Sans & Newman, 1997). In the acquired pellicle begins the formation of a biofilm through the adhesion of the first microorganisms that are mostly gram-positive aerobic bacteria (Figure 2) (Lang et al. 1997; Sans & Newman, 1997; Gioso, 2007), mainly of the *Streptococcus* genus, which produce an exopolysaccharide, a substance that acts like a "glue", facilitating the attachment of these bacteria to the surfaces in question (Wiggs & Lobprise, 1997; Gioso, 2007; Roza, 2004) especially in places where there are small

The first layer is usually single-celled and appears irregularly distributed on the tooth surface. With the microbial growth, the layer starts to come out of these areas of irregularities onto the enamel surface and increases in volume. The isolated plaques start to coalesce, forming a single plate. Over time in the process of plaque formation, a new phase is present, where new microbial strains with less ability to adhere to tooth structure, adhere to the already formed plaque, featuring new microcolonies and increasing the biodiversity of the plaque (Figure 2) (Sans & Newman, 1997). This process is called the organisation of the bacterial plaque, in which the bacteria need approximately 24 to 48 hours to get organised enough to cause the disease (Gioso, 2007). At this stage, the fight against bacterial plaque, with the simple disruption of it, is able to

According to the location, the plaque can be classified as supra or sub-gingival. The supragingival plaque corresponds mainly to microbial aggregates found on tooth surfaces (mostly in the gingival third of the crown), however may extend into the gingival sulcus, where they are in immediate contact with the marginal gingiva. The subgingival plaque corresponds to bacterial aggregates found entirely within the gingival sulcus or periodontal

The bacterial constituents present in dental plaque are modified according to the disease evolution. In healthy gingiva, the cocci represent nearly two-thirds of the bacteria, followed by non-motile small rods. The bacteria present are mostly gram-positive and there is no significant representation of more virulent bacterial types. A new work from Federal University of Viçosa, Brazil, identified bacteria that are present in initial supra-gingival plaque in ten young dogs and found the genera *Streptococcus*, *Staphylococcus* and *Enterococcus* as the main components (personal data). At the stage of gingivitis, the gram-

ligament, and in some cases, cementum or even tooth loss (Harvey & Emily, 1993).

macrophages and lipids (Harvey & Emily, 1993; Roza, 2004)

irregularities, cracks or roughness (Sans & Newman, 1997).

stall and reverse the process (Slee et al., 1983).

pockets (Harvey & Emily 1993).

positive rods (non-motile) gradually increase, surpassing the cocci, and the number of gramnegative bacteria also grows. This change continues to go on until the periodontium involvement phase (periodontitis), when the more pathogenic gram-negative microorganisms become the majority, so that the spirochetes represent almost half of the bacteria, while gram-positives are underrepresented (Niezengard et al., 1997; Riggio et al., 2011).

Fig. 2. Formation phases of dental plaque: A) Adhesion of Gram-positive cocci and rods; B) cellular proliferation and exopolysaccharide production; C) adhesion of Gram-negative bacteria; D) maturation of plaque with increase of bacterial biodiversity.

Without interference in the plaque formation an inflammatory process can occur, which marks the beginning of a periodontal disease and that provides a favourable environment for change in the microbial composition of the plaque, that become a biofilm with more pathogenic characteristics, continuing with later stages of the disease (Sans & Newman, 1997; Loesche & Grossman, 2001; Gioso, 2007).

The main bacteria involved in the formation of dental plaque are *Streptococcus* sp. (Gibbons, 1972; Tanzer et al. 1974; Duchin & Houte, 1978; Slee & O'Connor, 1983; Slee et al. 1983; Corner et al., 1988; Murray et al., 1992; Harvey & Emily, 1993; Lang et al., 1997; Loesche &

Periodontal Disease in Dogs 127

it is also possible to use mouthwash in conjunction with brushing to obtain increased efficiency of bacterial removal (Clarke, 2001). Periodontal disease can remain in this state or progress to the loss of insertion of the gingiva to the tooth, thus, the loss of the junctional epithelium adhesion and consequently the formation of periodontal pockets characterising

the beginning of the pathologic stage called initial periodontitis (Hennet, 2002).

Fig. 3. Periodontal disease progression: A) healthy periodontium; B) gingivitis; C) Initial periodontitis – begins with the loss of periodontal tissue; D) moderate and severe

appear cyanotic..

periodontitis - The loss of periodontal tissue is more severe (25 to 50% loss) and the gum can

Grossman, 2001; Katsura et al., 2001; Drummond et al., 2004; Swerts et al., 2005), *Actinomyces* sp. (Slee & O'Connor, 1983; Katsura et al., 2001), and *Lactobacillus* sp. (Drummond et al. 2004; Roza, 2004). These colonise initially the adhered film of the enamel and then start to multiply and aggregate. Thereafter, surface receptors on the cocci and gram-positive rods allow adherence of gram-negative bacteria and, over time, they present the greatest biodiversity and pathogenic potential (Lang et al., 1997). In dogs, the most important bacteria of this group are *Veillonella*, *Bacterioides*, *Prevotella* (Domingues et al., 1999), *Fusobacterium* (Murray et al., 1992; Braga et al., 2005) and *Porphyromonas* (Domingues et al., 1999; Katsura et al., 2001; Braga et al., 2005; Senhorinho et al., 2011).

The bacteria involved in the periodontal disease process may migrate to other regions of the body by bacteraemia and colonise there, causing various diseases such as endocarditis, nephritis (Harvey & Emily, 1993; Debowes, 1996; Gioso, 2007), hepatitis (Debowes, 1996; Gioso, 2007) and myocarditis (Harvey & Emily, 1993). Another disease that can be caused by the microorganisms involved in periodontal disease, is a pathological process known as periodontic-endodontic lesion. There is an infection and inflammation of the dental pulp caused by the migration of periodontal bacteria at the apex of the tooth and root canal penetration through the foramen, which are small holes through which the vascular supply, lymphatics and nerves of the tooth passes (Pieri, 2004).

In dogs, the progression of periodontal disease can be divided into stages based on the clinical appearance of the gingiva (classified according to an index ranging from zero degree representing healthy gingiva, to four, when there is severe involvement of it (Roza, 2004; Mitchell, 2005) and loss of adherence of the periodontium, which is measured by inserting a millimeter probe into the gingival sulcus. This measure represents how much the junctional epithelium has migrated toward the apex of the tooth. The result in millimeters is the distance between the bottom of the gingival sulcus or periodontal pocket to the cementoenamel junction. The rate of adhesion loss is expressed by the ratio between the loss and the total normal adhesion (Mitchell, 2005).

In the process of disease formation, the healthy periodontium is considered stage 0 (Figure 3) (Harvey & Emily, 1993) when the gingiva presents a uniform colour, the bacterial plaque is imperceptible and there are little pathogenic characteristics, and there is no halitosis (De Marco & Gioso, 1997). With the increase in bacterial plaque and its change regarding the amount and specificity of the present microorganisms, such as its pathogenicity, begins to emerge an inflammation that marks the beginning of periodontal disease itself, which can be divided into stages of gingivitis (stage 1), initial periodontitis (stage 2), moderate periodontitis (stage 3) and severe periodontitis (stage 4) (Harvey & Emily, 1993).

The first stage of periodontal disease begins with the emergence of bacteria which, through its metabolites, cause inflammation of the gingival tissue, called gingivitis (Figure 3 and Figure 4). This is the first defence of the tooth, without much pathogenicity and without damaging the structures of the support periodontium. Such inflammation is similar to that seen in other connective tissues. Vasodilation, leukocyte marginalisation, cell migration, production of prostaglandins and destructive enzymes also occurs (Gioso, 2007), making the gingiva red, swollen and painful, and may cause halitosis (De Marco & Gioso, 1997). At this stage the possibility of regression of the disease remains through the proper management of the oral health of the animal with measures such as brushing, promoting removal of the aetiological agent (bacterial plaque) (Gorrel & Rawlings, 1996; Gioso, 2007). At this moment

Grossman, 2001; Katsura et al., 2001; Drummond et al., 2004; Swerts et al., 2005), *Actinomyces* sp. (Slee & O'Connor, 1983; Katsura et al., 2001), and *Lactobacillus* sp. (Drummond et al. 2004; Roza, 2004). These colonise initially the adhered film of the enamel and then start to multiply and aggregate. Thereafter, surface receptors on the cocci and gram-positive rods allow adherence of gram-negative bacteria and, over time, they present the greatest biodiversity and pathogenic potential (Lang et al., 1997). In dogs, the most important bacteria of this group are *Veillonella*, *Bacterioides*, *Prevotella* (Domingues et al., 1999), *Fusobacterium* (Murray et al., 1992; Braga et al., 2005) and *Porphyromonas* (Domingues et al.,

The bacteria involved in the periodontal disease process may migrate to other regions of the body by bacteraemia and colonise there, causing various diseases such as endocarditis, nephritis (Harvey & Emily, 1993; Debowes, 1996; Gioso, 2007), hepatitis (Debowes, 1996; Gioso, 2007) and myocarditis (Harvey & Emily, 1993). Another disease that can be caused by the microorganisms involved in periodontal disease, is a pathological process known as periodontic-endodontic lesion. There is an infection and inflammation of the dental pulp caused by the migration of periodontal bacteria at the apex of the tooth and root canal penetration through the foramen, which are small holes through which the vascular supply,

In dogs, the progression of periodontal disease can be divided into stages based on the clinical appearance of the gingiva (classified according to an index ranging from zero degree representing healthy gingiva, to four, when there is severe involvement of it (Roza, 2004; Mitchell, 2005) and loss of adherence of the periodontium, which is measured by inserting a millimeter probe into the gingival sulcus. This measure represents how much the junctional epithelium has migrated toward the apex of the tooth. The result in millimeters is the distance between the bottom of the gingival sulcus or periodontal pocket to the cementoenamel junction. The rate of adhesion loss is expressed by the ratio between the loss

In the process of disease formation, the healthy periodontium is considered stage 0 (Figure 3) (Harvey & Emily, 1993) when the gingiva presents a uniform colour, the bacterial plaque is imperceptible and there are little pathogenic characteristics, and there is no halitosis (De Marco & Gioso, 1997). With the increase in bacterial plaque and its change regarding the amount and specificity of the present microorganisms, such as its pathogenicity, begins to emerge an inflammation that marks the beginning of periodontal disease itself, which can be divided into stages of gingivitis (stage 1), initial periodontitis (stage 2), moderate

The first stage of periodontal disease begins with the emergence of bacteria which, through its metabolites, cause inflammation of the gingival tissue, called gingivitis (Figure 3 and Figure 4). This is the first defence of the tooth, without much pathogenicity and without damaging the structures of the support periodontium. Such inflammation is similar to that seen in other connective tissues. Vasodilation, leukocyte marginalisation, cell migration, production of prostaglandins and destructive enzymes also occurs (Gioso, 2007), making the gingiva red, swollen and painful, and may cause halitosis (De Marco & Gioso, 1997). At this stage the possibility of regression of the disease remains through the proper management of the oral health of the animal with measures such as brushing, promoting removal of the aetiological agent (bacterial plaque) (Gorrel & Rawlings, 1996; Gioso, 2007). At this moment

periodontitis (stage 3) and severe periodontitis (stage 4) (Harvey & Emily, 1993).

1999; Katsura et al., 2001; Braga et al., 2005; Senhorinho et al., 2011).

lymphatics and nerves of the tooth passes (Pieri, 2004).

and the total normal adhesion (Mitchell, 2005).

it is also possible to use mouthwash in conjunction with brushing to obtain increased efficiency of bacterial removal (Clarke, 2001). Periodontal disease can remain in this state or progress to the loss of insertion of the gingiva to the tooth, thus, the loss of the junctional epithelium adhesion and consequently the formation of periodontal pockets characterising the beginning of the pathologic stage called initial periodontitis (Hennet, 2002).

Fig. 3. Periodontal disease progression: A) healthy periodontium; B) gingivitis; C) Initial periodontitis – begins with the loss of periodontal tissue; D) moderate and severe periodontitis - The loss of periodontal tissue is more severe (25 to 50% loss) and the gum can appear cyanotic..

Periodontal Disease in Dogs 129

Fig. 5. Into de red circle: root exposure in the upper left central incisor, indicating moderate

Marco & Gioso, 1997). In these stages the microbiota of dental plaque is completely different from the initial one, having only a small amount of non-motile gram-positive cocci and large percentages of motile gram-negative spirochetes, virtually absent in healthy individuals (Niezengard et al., 1997). This phase shows severe inflammation, eventually cyanotic (Figure 3), with bleeding in response to the minimum stimulus, greater accumulation of bacterial plaque, intense halitosis (De Marco & Gioso, 1997), mild (in moderate) or large (in severe) tooth mobility (Harvey & Emily, 1993 ), and in most cases, there is also receding gingiva and a large accumulation of dental calculus. The bacteria enter the bloodstream and cause damage to the heart, liver, kidneys, joints and other organs (De Marco & Gioso, 1997; Gioso, 2007). In moderate periodontitis, there is between a 25 and 50% loss of supporting periodontium (which can be masked by large gingival hyperplasia in some animals), creating the need for treatment and care for the maintenance of the teeth in the socket. In severe periodontitis there is a loss of more than 50% of the supporting periodontal tissue and furcation may be exposed in multirooted teeth and in many cases leading to exfoliation

Prevention s considered essential for the maintenance of the animals' teeth throughout their lives, making it impossible for the formation of the periodontal disease process (Lyon, 1991). Brushing, chewable products, promoters of friction and the use of antimicrobial substances

periodontitis in a poodle with five years.

of teeth (Harvey & Emily, 1993).

**4. Prevention of periodontal disease** 

Fig. 4. Dog with gingivitis: A) red line on the cervical region of the tooth indicating gingival inflammation in a two years old poodle

Initial periodontitis (Figure 3) is a sequel of the untreated gingivitis. It is the phase that begins with loss of the junctional epithelium insertion considered the first irreversible phase of the disease, and from this point it becomes only possible to stabilise it (De Marco & Gioso, 1997; Gioso, 2007; Roza, 2004). This phase is the extension of the inflammatory process toward the supporting periodontium (periodontal ligament, cementum and alveolar bone) and leads to progressive destruction of the reported tissues (Harvey & Emily, 1993; Hennet, 2002). The gingiva is still in its normal topography and may have slight gingival recession in some breeds, but when it is very sore it may bleed when touched. There is mild inflammation in the periodontal ligament and little evidence of bone loss (Harvey & Emily, 1993). Intensive halitosis is presented (De Marco & Gioso, 1997). There is also the formation of dental calculus, commonly called tartar, which is nothing more than the mineralisation of dental plaque by salts of the saliva that makes it easier for the adherence of new microorganisms with more pathogenic features, subsequently increasing the severity of injuries caused to the periodontal tissues. The amount of calculus should not be used for the classification of the disease, since it is not the aetiologic agent, but the bacterial plaque. Large amounts of calculus are not indicative of the stage of the disease, and the diagnosis must be established in the gingival poll to assess the loss of adhesion of the epithelium (Gioso, 2007; Roza, 2004).

Moderate (Figure 5) and severe (Figure 6) periodontitis are the most advanced stages of periodontal disease and differ only in the degree of injury (Harvey & Emily, 1993). Some authors do not report the presence of moderate periodontitis, considering only the severe periodontitis after the initial process of aggression to the support tissues of the teeth (De

Fig. 4. Dog with gingivitis: A) red line on the cervical region of the tooth indicating gingival

Initial periodontitis (Figure 3) is a sequel of the untreated gingivitis. It is the phase that begins with loss of the junctional epithelium insertion considered the first irreversible phase of the disease, and from this point it becomes only possible to stabilise it (De Marco & Gioso, 1997; Gioso, 2007; Roza, 2004). This phase is the extension of the inflammatory process toward the supporting periodontium (periodontal ligament, cementum and alveolar bone) and leads to progressive destruction of the reported tissues (Harvey & Emily, 1993; Hennet, 2002). The gingiva is still in its normal topography and may have slight gingival recession in some breeds, but when it is very sore it may bleed when touched. There is mild inflammation in the periodontal ligament and little evidence of bone loss (Harvey & Emily, 1993). Intensive halitosis is presented (De Marco & Gioso, 1997). There is also the formation of dental calculus, commonly called tartar, which is nothing more than the mineralisation of dental plaque by salts of the saliva that makes it easier for the adherence of new microorganisms with more pathogenic features, subsequently increasing the severity of injuries caused to the periodontal tissues. The amount of calculus should not be used for the classification of the disease, since it is not the aetiologic agent, but the bacterial plaque. Large amounts of calculus are not indicative of the stage of the disease, and the diagnosis must be established in the gingival poll to assess the loss of adhesion of the epithelium

Moderate (Figure 5) and severe (Figure 6) periodontitis are the most advanced stages of periodontal disease and differ only in the degree of injury (Harvey & Emily, 1993). Some authors do not report the presence of moderate periodontitis, considering only the severe periodontitis after the initial process of aggression to the support tissues of the teeth (De

inflammation in a two years old poodle

(Gioso, 2007; Roza, 2004).

Fig. 5. Into de red circle: root exposure in the upper left central incisor, indicating moderate periodontitis in a poodle with five years.

Marco & Gioso, 1997). In these stages the microbiota of dental plaque is completely different from the initial one, having only a small amount of non-motile gram-positive cocci and large percentages of motile gram-negative spirochetes, virtually absent in healthy individuals (Niezengard et al., 1997). This phase shows severe inflammation, eventually cyanotic (Figure 3), with bleeding in response to the minimum stimulus, greater accumulation of bacterial plaque, intense halitosis (De Marco & Gioso, 1997), mild (in moderate) or large (in severe) tooth mobility (Harvey & Emily, 1993 ), and in most cases, there is also receding gingiva and a large accumulation of dental calculus. The bacteria enter the bloodstream and cause damage to the heart, liver, kidneys, joints and other organs (De Marco & Gioso, 1997; Gioso, 2007). In moderate periodontitis, there is between a 25 and 50% loss of supporting periodontium (which can be masked by large gingival hyperplasia in some animals), creating the need for treatment and care for the maintenance of the teeth in the socket. In severe periodontitis there is a loss of more than 50% of the supporting periodontal tissue and furcation may be exposed in multirooted teeth and in many cases leading to exfoliation of teeth (Harvey & Emily, 1993).
