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[pyrnet] HEALTH: Periodontal disease and leucopenia (minus tables) JSAP (1995) 36, 542-546



PERIODONTAL DISEASE AND LEUCOPENIA

T Lonsdale
Riverstone Veterinary Hospital
Garfield Road
RIVERSTONE  NSW  2765
Australia

ABSTRACT

Periodontal disease is rare in nature but widespread in domestic dog and
cat populations. Unnatural diets are known to facilitate the build-up of
oral microbial communities which then interact with host-immune defences
giving rise to periodontitis. Eight of 14 animals undergoing dental
treatment and dietary change at a suburban veterinary practice were
investigated and found to have low leucocyte counts.  Follow-up testing
revealed changes averaging a 77.7 per cent increase with concomitant
'subjective good health'. These findings serve to cast doubt on the
commonly used haematological reference ranges where the subject animals may
have suffered from periodontal disease. The demonstrated reversibility of
white cell depression associated with periodontal disease should provide a
focus for further research.

INTRODUCTION

Periodontal disease is the inflammatory disease involving the supporting
structures of the teeth.  Whilst plaque organisms are known to be closely
involved in the initiation of disease, emphasis is now shifting to
investigations of the factors that influence host/plaque interaction
(Harvey, 1993b).

Removal of plaque either by physical or chemical means (Sanz & Newman,
1994) or by the abrasive forces of feeding, exerts control over the
development of periodontal disease. Various authors have commented that the
natural diet of wild carnivora has a plaque retarding effect (Page and
Schroeder 1982, Higgins 1987, Harvey 1993a, Watson 1994). The human dentist
and comparative periodontist, Sir Frank Colyer (1947) concluded:
'Paradontal disease is always associated with an alteration in the physical
or chemical character of the diet of the animal - in other words with a
departure from natural diet and conditions.'

There is accumulating evidence of systemic consequences of periodontal
disease - in its simplest view, pain, local to the lesion, is registered in
the brain with concomitant lack of appetite and evidence of malaise.
Various authors  (Beard 1991, Hamlin 1991, Lonsdale 1993a, DeBowes 1994)
cite a range of systemic conditions, eg, bacterial endocarditis,
glomerulonephritis, polyarthritis, polyvasculitis, believed to be
consequences of the chronic oral inflammation.

It is thought that systemic conditions may actively exacerbate periodontal
disease (Harvey and Emily 1993, Liebana and Castillo 1994). One theory
postulates that there is an interactive cascade of events involving a
progressive, two-way worsening of periodontal disease and body systems
giving rise to a range of degenerative diseases (Lonsdale 1993a).  Due to
the reserve capacity of the various organ systems (eg, liver,
cardiovascular system and kidneys) it is believed that the interactive
spiral decline may remain clinically undetectable until end-stage
developments. The same could be said for circulating leucocytes which may
exhibit minimal effects on circulating numbers but profound alteration in
function of the cells (Latimer and Meyer, 1989b). Due to a wide reference
range, leucocyte numbers can increase or decrease markedly whilst still
disguising underlying disease. In the event of reduced circulating numbers
this can be explained by decreased production of the leucocytes,
redistribution between circulating and marginal pool and emigration into
the tissues. (Latimer and Meyer, 1989a)

This paper details the outcome of eight cases presented to a suburban
clinic showing advanced periodontal disease and reduced leucocyte and
erythrocyte numbers. Surgical treatment of the presenting condition and
change of diet resulted in a marked increase in circulating leucocytes with
a return to 'subjective good health'.

MATERIALS AND METHODS

Eight animals presented at a suburban practice for a number of reasons were
selected. These comprised six dogs and two cats.  In each instance clinical
examination revealed advanced stage periodontal disease. Treatment
consisted of radical dentistry including removal of diseased teeth, and the
institution of a five-day course of amoxycillin (Amoxil; Smith Kline
Beecham Animal Health) or clindamycin (Antirobe; Upjohn).

From day 1 after surgery the animals were fed a raw meaty bone diet with
occasional supplemental table scraps. The small dogs and cats received
chicken wings, rabbit legs and whole raw fish whilst the larger dogs
received lamb flaps, ox brisket, kangaroo tails, etc. The size of pieces
was important as a regulator of chewing function. Pieces too small would
permit swallowing whole with the risk of obstruction. Large bones without
meat have lesser nutrient value whilst risking the wear or breakage of
teeth. At the time of dental treatment, five of the cases had full blood
counts performed; of the remaining three cases a white cell count plus
differential cell count were performed. Blood tests were repeated at the
time of the animals' check up.

RESULTS

The results of the present study are summarised in Table 1.

Cases 1 and 2, a seven-year-old male and nine-year-old female silky
terrier, were assessed first. During the previous six years the dogs had
been presented to the surgery on numerous occasions with non-specific
illness, lethargy or dermatitis. A recurrent complaint was that the male
had 'anxiety attacks'. Several theories and treatments had been propounded
by different clinicians in the practice but all to no avail. At the time of
the animals' annual vaccinations the owners were not aware of any unusual
features concerning their pets, but a  clinical examination revealed a
sparse hair coat and marked generalised periodontitis in both animals. Up
until that time dietary advice had been to feed dry dog food, table scraps
and the occasional raw bone. The raw bone component had been progressively
overlooked by the owners and their pets' halitosis had been accepted as
normal.

The owners were persuaded that radical dentistry involving tooth
extractions followed by a change of diet to raw meaty bones would benefit
their pets. In an attempt to obtain objective information about the
animals, a haemogram was performed. The dogs were discharged
postoperatively with a five-day course of amoxycillin and instructions for
the feeding of raw meaty bones.

After 10 months the owners reported how delighted they were with the change
in health and wellbeing of their animals. The initial change of diet had
created some difficulties but a regimen had become well established.
Clinical assessment revealed a much-reduced halitosis, although there was
evidence of calculus on those teeth which lacked an opposing member in the
opposite jaw. The hair coat of both animals was generally more lustrous and
the non-specific dermatitis of past years was absent. Comparison blood
tests were commissioned and are recorded in Table 1.

The percentage change in cell counts in these two cases prompted further
investigation in other cases. Blood tests were undertaken in the next 12
cases presenting at the clinic for radical dentistry. In six cases the cell
counts were considered to be low or at the low end of 'normal' and in these
cases the owners were asked to bring their pets in for follow-up screening
at a later date. In each instance treatment involved radical dentistry with
teeth scaling and, or, extractions as appropriate together with a
post-operative course of antibiotics and a change in diet.

Owner assessment of all the test animals was of a markedly increased
vitality and well-being; four of the cases (1, 2, 3 and 4) were only
considered to be healthier in hindsight. These cases had been presented for
routine vaccination by their owners who were unaware that their animals
were unwell.

Fuller clinical findings were recorded in case 8, a 12-year-old female
Maltese terrier. The owner's presenting complaint was of a sudden onset
lameness of the right hind leg. Clinical examination revealed a generalised
dermatitis, bilateral otitis, flea infestation, pansystolic murmur, mammary
lump, marked dehydration and severe oral disease. The weight was recorded
as 3.8 kg.  Post-operative clindamycin was prescribed together with
eardrops and a splint applied to the presumed sprained hock. The owners
were asked to institute a raw chicken wing diet immediately with the
addition of a few table scraps from time to time commencing one week later.
Although the majority of teeth had been removed from the maxilla and
pre-maxilla, case 8's bodyweight had increased to 4.55 kg within 50 days.

Case 8's red cell count was found to have decreased by 3 per cent. However,
it should be borne in mind that the initial reading was taken from a
markedly underweight, dehydrated animal. By the second reading the animal's
bodyweight had increased by 20 per cent and as such it can be assumed that
the total circulating erythrocytes would have increased significantly.

DISCUSSION

The eight cases studied provided a strong subjective correlation between
increase in health and increase in cell counts - this result being
demonstrated by a simple percentage change. Whilst correlation does not
imply causation, the fact that all cell counts moved in the same direction
(with one small exception) provides persuasive evidence that either the
periodontal disease or diet or both were continuing to influence the
overall health of the patients.

Dental treatment and dietary change represent generic concepts that
incorporate numerous elements in numerous interrelationships. In the light
of the known presence of endotoxins and exotoxins and the immune
interaction at the gingival sulcus (Liebana and Castillo 1994), these
factors might be considered in the lowering of white cell counts. Cooked,
macerated processed food has no cleansing effect on the teeth and gingiva,
so can be expected to potentiate periodontal disease.  Page and Schroeder
(1982) state that in order to produce periodontal disease 'somewhat extreme
measures such as placement of ligatures in subgingival position,
mono-infection of the oral cavity, or feeding of grossly abnormal diets are
required'. Adverse reactions to ingesta are well known and can affect many
systems (Wills and Harvey, 1994) which, in turn, can be expected to
directly or indirectly affect white cell counts.

This study made no attempt to provide qualitative assessment of the
circulating red and white cells.  It should not be overlooked that the
health of an immune system involves a balance of number and function of
immune components. Valid concerns arise that dogs and cats suffering from
severe periodontal disease can show cell counts within the standard
reference range. In our study, four animals were alleged to be normal by
their owners but then showed average red blood cell increases of 35 per
cent and white blood cell increases of 55 per cent following dentistry.
Since these increases coincided with an increase in the apparent wellbeing
of the animals then it would be reasonable to assume that the higher values
were closer to the true 'normals' for the subject animals.

It is recognised that the use of reference values is in itself a
controversial topic (Lumsden and Mullen 1978). Previously, debate has
centred on the statistical treatment of results and the method of
population selection for the gathering of data. To the author's knowledge
consideration as to the periodontal health and diet of subject groups has
not been well considered. Details were obtained of three published
reference ranges from two large commercial pathology laboratories operating
in NSW, Australia. Their data was obtained from animals presented to
suburban veterinary clinics and variously assumed to be healthy by their
owners and or veterinarians. (Macquarie Vetnostics  Services 1986, and
Veterinary Pathology Services 1989 to 1991). Questions regarding unnatural
artificial diets were seldom raised and the appreciation of periodontal
disease problems of domestic pets was at that time in its infancy. The
reference ranges published by Jacobs and others were derived from the
University of Guelph between 1989 and 1991. These were colony dogs and cats
fed a named commercial diet, it is widely reported that colony dogs and
cats suffer from periodontal disease  (Brown and Park 1968). It is for
these reasons that the reference ranges of laboratories may be suffering
distortion.

In a broader context, reference ranges represent an establishment of values
from a 'normal control group'. If these values can be so sharply affected,
then one must have concerns for the validity of any control group where the
subject animals can suffer periodontal disease and at the same time be fed
processed food  (AAFCO  1993). This sentiment was expressed in another way
by the authors of the diet and periodontal disease literature search in the
Australian Veterinary Association News:  'Those investigating small animal
health problems should also take diet and diet consistency into account
when researching systemic diseases - possible confounding effects of diet
and poor oral health must be considered in such studies.' (Australian
Veterinary Association News 1994)

In our general practice, no further comparative blood testing is performed
due to the inconvenience suffered by clients and the costs involved.
Standard care does involve, regardless of presenting conditions, the
provision of dental care and advice to return to a natural diet. (Lonsdale
1993b).  The results more than justify our confidence with the rapid
resolution and reduction in recurrence of medical complaints.

The research potential of this area remains enormous. Extensive trials can
be performed to examine the importance of periodontal disease and diet in
both the initiation and maintenance of ill health.  The standard range of
laboratory parameters can be re-examined as can other less familiar
haematological and biochemical systems. The apparent reversibility of
immune cell depression in carnivores by correcting periodontal disease and
diet suggests a potential model in which to explore immune deficiency
syndromes.

ACKNOWLEDGMENTS

This study depended on long-suffering patients, understanding owners and
supportive colleagues.  Drs Bruce Duff and David Snow of Macquarie
Vetnostics, Sydney, kindly donated the laboratory testing. Susan Rutter
processed the various drafts.

REFERENCES

AAFCO (1993) Official Publication, Association of American Feed Control
Officials, Atlanta, pp 280-302

Australian Veterinary Association News (1994) Diet and Disease Link.
February. Pages 1 and 6

Beard, G. B. (1991) Dental Seminar, Proceedings of the  Post Graduate
Committee in Veterinary Science, University of Sydney, Sydney 169,15

Brown, M. G. & Park, J. F. (1968) Control of Dental Calculus in Experimental
Beagles. Laboratory Animal Care 18, 527-535

Colyer, F. (1947) Dental Disease in Animals. British Dental Journal, 82,
31-35

DeBowes, L. J. (1994) Systemic Effects of Periodontal Disease, Proceedings
of the12th American College of Veterinary Internal Medicine Forum, San
Francisco. pp 441-445

Hamlin, R. L (1991) A theory for the genesis of certain chronic
degenerative diseases of the aged dog. Veterinary Scope International
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Harvey C.E. (1993a) Optimizing oral health: diet and periodontal disease.
Vet Forum September, 52-53

Harvey C.E. (1993b) Periodontal disease. In: Veterinary Dentistry.
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Harvey, C. E. & Emily P.P. (1993) Periodontal Disease. In: Small Animal
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Higgins, P. (1987) Preventative Dentistry. Teeth-Open Wide. Proceedings of
the Post Graduate Committee in Veterinary Science, University of Sydney,
Sydney 100, 181-184

Jacobs, R. M., Lumsden, J. H. & Vernau W. (1992) Canine and feline
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Latimer, K.S. & Meyer, D.J. (1989a) Leukocytes in heath and disease, In:
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Latimer, K.S. & Meyer, D.J. (1989b) Leukocytes in heath and disease. In:
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Liebana, J. & Castillo, A. (1994) Physiopathology of primary periodontitis
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Lonsdale, T. (1993a) Cybernetic hypothesis of periodontal disease in
mammalian carnivores, Journal of Veterinary Dentistry 11, 5-8

Lonsdale, T. (1993b) Preventative  Dentistry, Veterinary Dentistry,
Proceedings of the Post Graduate Committee in Veterinary Science,
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Lumsden, J.H. & Mullen, K. (1978) On Establishing Reference Values.
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Page, R.C. & Schroeder, H.E. (1982) Implications for clinical management
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Sanz, M. and Newman, M. G. (1994) Dental plaque and calculus. In: Oral
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Watson, A.D.J. (1994) Diet and periodontal disease in dogs and cats.
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Wills, J. & Harvey, R. (1994) Diagnosis and management of food allergy and
intolerance in dogs and cats. Australian Veterinary Journal 7, 322-326

Important Notice of Copyright

This paper was first published, complete with tables of laboratory values,
in the Journal of Small Animal Practice (1995) 36, 542-546. The copyright
holder is the Journal of Small Animal Practice. If you utilise any of this
information it is necessary to quote the source and the copyright holder's
particulars.