Nutrition and Disease

Periodontal Disease and Diet in Domestic Pets1

Cecilia Gorrel
17 Burnt House Lane, Pilley, Nr Lymington, Hants SO41 5QN, UK

ABSTRACT Periodontal disease is the most common oral condition seen in domestic pets. In addition to the
discomfort caused in the affected animal, there is strong circumstantial evidence to show that a focus of infection
in the mouth may cause disease of distant organs. Consequently, prevention of periodontal disease is of
paramount importance for the general health and well-being of pets. The presence of plaque on the tooth surfaces

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is the primary cause of periodontal disease. However, the mechanisms by which disease develops are by no means
fully understood. Dietary texture does have an effect on the accumulation of dental deposits and consequently on
disease development and progression. Daily toothbrushing remains the single most effective means of removing
plaque, thus preventing periodontal disease. On the basis of current knowledge, the best way to maintain healthy
periodontal tissues in our pets is frequent toothbrushing. The use of a dental hygiene chew and/or a diet designed
to reduce dental deposits can be useful adjunctive measures and should be recommended. J. Nutr. 128:
2712S–2714S, 1998.

KEY WORDS: ● periodontal disease ● plaque toothbrushing ● dental hygiene chew

Periodontal disease is the most common oral condition seen
in small animals. Indeed, it is probably the single most com-
mon disease in small animal practice (Gorrel and Robinson
1995). Periodontal disease is not a new problem; it has been
identified in domestic pets for at least 70 years. Also, there is
no documentation to show that the prevalence of the disease
is increasing. Suggestions that the prevalence is increasing
may well represent an increased awareness, rather than an
increased occurrence.
Periodontal disease is a collective term for a number of
plaque-associated inflammatory conditions that affect the pe-
riodontium of the tooth. Gingivitis is inflammation of the
gingiva. Periodontitis is the term used when the inflammatory
reactions also involve the periodontal ligament, root cemen-
tum and alveolar bone. The end result of periodontitis is loss
of the tooth due to progressive destruction of its attachment
apparatus.
The disease often causes discomfort to the affected animal.
Moreover, there is strong circumstancial evidence that a focus
of infection in the oral cavity may cause disease of distant
organs (DeBowes et al. 1996). Consequently, preventing peri-
odontal disease is important for the general health and well-
being of companion animals.
PLAQUE: THE PRIMARY CAUSE OF
PERIODONTAL DISEASE
The primary cause of both gingivitis and periodontitis is the
presence of plaque on the tooth surfaces. Dental plaque is
composed of aggregates of bacteria and their by-products,
1
Presented as part of the Waltham International Symposium on Pet Nutrition
and Health in the 21st Century, Orlando, FL, May 26 –29, 1997. Guest editors for
the symposium publication were Ivan Burger, Waltham Centre for Pet Nutrition,
Leicestershire, UK and D’Ann Finley, University of California, Davis.
salivary components, oral debris and occasional epithelial and
inflammatory cells. It accumulates rapidly on a clean tooth
surface. Plaque may accumulate supragingivally, i.e., on the
clinical crown of the tooth, but also below the gingival margin,
i.e., in the subgingival area of the sulcus or pocket. Differences
in the composition of the subgingival flora have been attrib-
uted in part to the local availability of blood products, pocket
depth, redox potential and p02. Therefore, the question
whether the presence of specific micro-organisms in patients or
distinct sites may be the cause or consequence of disease
continues to be a matter of dispute.
Studies in which animals were fed by intubation (Egelberg
1965b) have demonstrated that the formation of dental plaque
has very little to do with food debris. In a 4-y study using the
Beagle dog (Lindhe et al. 1975), it was shown that with no oral
hygiene, plaque accumulated rapidly along the gingival margin
with gingivitis developing within a few weeks. Dogs that were
fed an identical diet under identical conditions but were
subjected to daily toothbrushing developed no clinical signs of
gingivitis. Loss of periodontal attachment occurred at 6 mo of
undisturbed plaque accumulation and then progressed slowly.
By 4 y of study, the individual teeth of dogs had lost an average
of ;3 mm of attachment. Loss of alveolar bone as measured in
radiographs became apparent at 24 mo after the start of the
study, and at the end of the 4 y was ;2 mm. In the control
group, the dogs whose teeth were brushed daily showed no sign
of gingivitis or periodontitis, as determined at the end of the
4 y by both clinical and radiographic examination. It should be
noted that two individuals in the test group, i.e., those not
receiving daily toothbrushing, did not progress from gingivitis
to periodontitis.
In summary, undisturbed plaque accumulation will result in
gingival inflammation within a few weeks. In some, but not all
individuals, untreated gingivitis will progress to periodontitis.

0022-3166/98 $3.00 © 1998 American Society for Nutritional Sciences.

2712S
 PERIODONTAL DISEASE AND DIET
However, regular removal of plaque will prevent development
of gingivitis and periodontitis.
The significance of calculus. Calculus or tartar is mineral-
ized plaque. It is not in itself thought to be an irritant; in fact, it
has been shown that under certain circumstances a normal at-
tachment may be seen between the junctional epithelium and
calculus (Fitzgerald and McDaniel 1960). It has also been shown
that autoclaved calculus may be encapsulated in connective tis-
sue without causing marked inflammation (Allen and Kerr 1965).
The primary consequence of calculus is that it acts as a retention
surface for plaque. The consensus is that supragingival calculus
per se is not directly involved in the etiology or pathogenesis of
the disease, and is mainly of cosmetic significance if plaque
removal is adequate (Lang et al. 1997).
PATHOGENESIS OF DISEASE
The pathogenesis of periodontal disease is by no means fully
elucidated. The plaque microbiota as well as the inflammatory
reactions of the host contribute to the destruction of the
periodontium.
Direct injury by plaque microorganisms. Although nu-
merous microbiological studies have been performed, the as-
sociation between specific periopathogens and periodontitis
remains to be conclusively proven, and it is as yet not possible
to state whether the microbiota found in deep pockets are the
cause or effect of periodontitis.
Plaque microorganisms produce a large variety of soluble
enzymes to digest host proteins and other molecules and
thereby produce nutrients for growth. Among the enzymes
released by the bacteria are proteases capable of digesting
collagen, elastin, fibronectin, fibrin and various other compo-
nents of the intercellular matrix of epithelial and connective
tissue. The microorganisms in dental plaque also release nu-
merous metabolic products such as ammonia, indole, hydrogen
sulphide and butyric acid. Periodontal disease is initiated and
sustained by factors produced by the subgingival microbiota.
Some of these factors can directly injure host cells and tissues.
Host response. Many microbial products have little or no
direct toxic effect on the host; instead, they possess the po-
tential to activate nonimmune and/or immune inflammatory
reactions. It is these inflammatory reactions that actually cause
the tissue damage.
The view that the tissue destruction is mediated by the host
response to plaque rather than by direct injury by the micro-
organisms is supported by the findings that anti-inflammatory
drugs do not affect the microbiota but still reduce attachment
loss (Nyman et al 1979, Williams et al 1989), and that sterile
granulation tissue degrades collagen in the absence of bacteria
(Åsman et al 1988).
The assumption of a specific host response is further sup-
ported by epidemiologic studies in humans (Hugosson et al
1992, Yoneyama et al 1986), which show that the frequency of
moderate-to-severe periodontitis is in the order of 5–10% in
most parts of the world, independent of oral hygiene measures.
In areas with little oral hygiene, higher amounts of plaque and
dental calculus and higher frequencies of gingivitis have been
reported, but the majority of the population still do not de-
velop periodontitis (Baelum et al 1986 and 1988). Moreover,
in families with a high frequency of early onset periodontitis
(Michalowicz et al 1991, van der Velden et al 1990), there is
a genetic coupling, indicating that periodontitis is a patient-
associated specific host response.
Nonimmune inflammatory responses. Lipopolysaccha-
rides (endotoxins) of gram-negative microorganisms may be
responsible for a spectrum of inflammatory events. They in-
2713S
teract with and modulate the behavior of leukocytes and
platelets and induce changes in endothelial cells.
It is also known that specific proteins or polysaccharides
produced and released from plaque bacteria activate endoge-
nous mediators of inflammation (Kinane and Lindhe 1997).
Specific factors belonging to most categories of endogenous
mediators of inflammation have been identified in gingival
exudates. It is not possible at present to assign a more impor-
tant role to one category of mediators compared with the
others. Many different mediators are present in the lesion
simultaneously and contribute to the vascular and cellular
phases of the disease process. Moreover, several mediators are
linked to one another via positive feedback systems that am-
plify their biological potentials. Indeed, most mediators have
more than one inflammatory function and many have physi-
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ologic effects unrelated to their proinflammatory effects. After
being released or activated, mediators are usually rapidly in-
activated in the local area (Kinane and Lindhe 1997). This is
an important step in the control of the inflammatory process.
It is conceivable that an abnormality in one or more of these
control mechanisms contributes to the development of disease.
Immune reactions. Most of the substances produced and
released by plaque microorganisms are antigenic and elicit
both cell-mediated and antibody-mediated immune reactions.
It has been shown that both systemic and local antibody
synthesis are activated in response to many plaque antigens.
Local antibody synthesis by lymphoid cells may well be more
relevant in gingival defense than the systemic immune re-
sponse. In support of this, it has been shown that gingival
exudates usually contain higher concentrations of antibodies
against specific plaque organisms compared with serum from
the same patient (Taichman and Lindhe 1992).
Other conditions such as physical or psychological stress
(Green et al. 1986) and malnutrition (Enwonwu 1994) may
impair protective responses such as production of antioxidants
and acute phase proteins; as such, they can aggravate peri-
odontitis but not cause destructive tissue inflammation per se.
Disease progression. In many instances, disease progres-
sion may be an episodic occurrence rather than a continuous
process. Tissue destruction occurs as acute bursts of disease
activity followed by relatively quiescent periods. The acute
burst is characterized by rapid deepening of the periodontal
pocket, detachment of periodontal fibers from root cementum
and loss of alveolar bone. The quiescent phase is not associ-
ated with clinical or radiographic evidence of further disease
progression. The inactive or quiescent phase often lasts for
extended periods of time.
The pathogenic basis of these active and inactive phases of
periodontal tissue destruction are, as yet, unexplained. Theo-
retically, the burst may represent a transient impairment of the
inflammatory response. Lowered resistance may also allow
“new” organisms to infect the pocket. By contrast, it is possible
that the host’s inflammatory response is activated in such a
way that it damages rather than protects the affected site.
In summary, it is not yet possible to give an entire account
of the pathogenesis of periodontal disease. The dog has been
used for the last 30 years as the experimental model for human
periodontal disease. Despite this, we still do not fully under-
stand the mechanisms involved in disease development in
either species. It is now well accepted, however, that it is the
host’s response to the organisms rather than microbial viru-
lence per se that actually causes the tissue damage. Further
studies in dogs to gain information about the host response are
required.
Effect of diet. Gross nutritional imbalances will affect the
individual9s ability to mount a protective inflammatory re-
2714S SUPPLEMENT
sponse. At present, when most animals are fed nutritionally
complete commercially prepared pet foods, such gross imbal-
ances are uncommon. The main effect of diet on the initiation
and progression of periodontal disease can thus be attributed to
the texture of the diet, which affects accumulation of plaque.
Several studies have evaluated mechanical methods of re-
ducing plaque accumulation via dietary texture. A coarse diet
may reduce plaque accumulation on some teeth and on some
tooth surfaces (Egelberg 1965a). A recent study (Logan 1996)
performed over a 6-mo period that investigated oral cleansing
by dietary means showed that dogs consuming a test diet
(Canine t/d, Hill’s Pet Nutrition, Topeka, KS) specifically
designed to promote dental hygiene accumulated significantly
less plaque and calculus and developed less gingival inflam-
mation than the control group. Similarly, the daily use of a
specifically designed dental hygiene chew (Pedigree Rask/
Dentabone, Mars, McLean, VA) has been shown to reduce
accumulation of dental deposits (plaque and calculus) and
gingivitis in both short- and longer-term studies (Gorrel and
Rawlings 1996a and 1996b, Gorrel and Bierer 1997). A study
comparing the effect of feeding the test diet with that achieved
by feeding a nutritionally complete dry meal supplemented
with the daily addition of the dental hygiene chew, showed
the two regimens to be equivalent (Rawlings and Gorrel
1997). Both regimens reduced the accumulation of dental
deposits and the severity of gingivitis.
Control of periodontal disease. It has been shown by
several studies that the single most effective way of remov-
ing plaque and thus preventing periodontal disease is reg-
ular, usually daily, toothbrushing (Lindhe et al 1975, Gorrel
and Rawlings 1996b, Tromp et al 1986a and 1986b). As
noted, other studies have evaluated mechanical methods of
reducing plaque accumulation via dietary texture. However,
it has yet to be demonstrated whether reducing the amount
of dental plaque on a tooth via dietary texture, compared
with regular removal by means of toothbrushing, will actu-
ally achieve the goal of controlling disease.
Antiplaque agents delivered from toothpastes, gels or
mouthrinses can augment mechanical oral hygiene to control
the formation of supragingival plaque and the development of
early periodontal disease. Clinically effective antiplaque
agents are characterized by a combination of intrinsic antibac-
terial activity and good oral retention properties. Agents that
have been evaluated include chlorhexidine, essential oils, tri-
closan, sanguinarine, fluorides, oxygenating agents, quaternary
ammonium compounds, substituted amino alcohols and en-
zymes. Of the above, the greatest effect on the reduction of
plaque and gingivitis can be expected from chlorhexidine,
essential oils, triclosan and substituted amino alcohols. It must
be emphasized that none of these agents will prevent gingivitis
on their own. Long-term studies with chlorhexidine (Hamp et
al. 1973) have shown that although plaque accumulation is
reduced, gingivitis, albeit at a reduced frequency, does still
develop. Moreover, all of these agents are associated with
adverse effects. These effects vary according to the chemical
agent and include poor taste, burning sensation of oral mucous
membranes, staining of teeth and soft tissues, and allergic
reactions. The use of chemical antiplaque agents should be
seen as adjunctive to the mechanical removal of plaque by
means of toothbrushing.
SUMMARY
There is as yet no magic bullet that we can feed pets to
prevent periodontal disease. Daily toothbrushing remains
the single most effective way of maintaining clinically
healthy gingivae. However, reduction of plaque by dietary
texture is a useful adjunctive measure and should be rec-
ommended.
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