- 1 Difference between gingivitis and periodontitis
- 2 Can periodontal disease kill my dog? Not with good prevention measures
- 3 Can periodontal disease kill my dog? Not if diagnosed early
- 4 Can periodontal disease kill my dog? Not with the appropriate treatment
- 5 Can periodontal disease kill my dog? If untreated, consequences can be major
Periodontal disease is the most common infectious disease in companion animals, with a prevalence of almost 80%, which is increasing with age and decreases with the size of the animal. It is much more common in small animals than in medium and large animals. Can periodontal disease kill my dog? Read below for the answer.
Difference between gingivitis and periodontitis
The periodontium includes the gum, the cementum, the alveolar-dental ligament and the alveolar bone, which constitute the supporting structures of the tooth. Periodontal disease is caused by dental plaque, and can be divided into two conditions: gingivitis and periodontitis.
Gingivitis is a reversible inflammation of the gums, because once its cause (bacterial plaque) is eliminated, the inflammation goes back.
Periodontitis is an irreversible inflammatory condition of the non-gingival tissue (alveolo-dental ligament, cementum and alveolar bone) and is assessed by measuring the loss of periodontal attachment (loosening) of the tooth. Periodontitis can be inactive (dormant), when there is no sign of gum inflammation (if there is a loss of tooth attachment, it must date before), or active, when destruction tissue is in progress.
Although periodontitis is classified as “infectious” diseases, and more than 700 bacterial species have been recognized as capable of colonizing the biofilm of the subgingival groove.
Gingivitis, even if left untreated, does not necessarily lead to periodontitis as the development of periodontal disease is actually determined by an imbalance between the bacterial population and the dog’s immune system. Immune capacity, stress, age, nutritional and metabolic status, race and dysendocrinies are all factors that can promote or prevent the progression of periodontal disease. If the disease progresses, bone destruction and apical migration of the supporting connective tissue will lead to the loosening and then the loss of one or more teeth.
Periodontal disease is a focal infection. This notion, introduced more than a century ago, describes a localized chronic disease, caused by sources of microorganisms, toxins, bacterial activity and tissue breakdown, capable of reaching distant organs and tissues. The area of the periodontitis zone was measured in dwarf breeds and was found to be between 3.18 and 29.8 cm, the area of affected tissue can therefore represent a considerable proportion of the total area of the dog’s body.
During the development of periodontitis, bacteria in the periodontal pockets can reach the bloodstream, causing bacteremia, and, although they are intercepted by the reticuloendothelial system in healthy individuals, prolonged continuous exposure to bacteremia may be associated with systemic disease involving distant organs and systems.
Can periodontal disease kill my dog? Not with good prevention measures
Preventing periodontal disease involves carefully removing bacterial plaque by brushing your teeth and good oral hygiene. Some industrial foods help reduce super-gingival dental plaque, but the crucial point remains the elimination of sub-gingival plaque. The objective is not to sterilize the oral cavity but to prevent the bacterial biofilm from infection.
Can periodontal disease kill my dog? Not if diagnosed early
Generally, periodontal disease begins with little or no clinical signs, and the main reason for consultation for examination of the oral cavity is halitosis. The diagnosis cannot be based solely on a visual examination of the oral cavity. General anesthesia is essential to perform a periodontal examination using a probe as well as an intraoral X-ray. There are different periodontal probes but all are designed to measure the depth of the pockets and assess a possible hyperplasia or gingival recession. The probe also makes it possible to assess the degree of mobility of the teeth and the presence of lesions at the level of radicular bifurcations / trifurcations. The probe is gently introduced into the gingival groove to ideally assess 4 to 6 points on the circumference of each tooth. Apparently, healthy teeth may have deep pockets on their palatal or lingual sides.
Can periodontal disease kill my dog? Not with the appropriate treatment
Treatment of periodontal disease should be carried out in anesthetized and intubated animals. After detailed evaluation of the dental arches and analysis of the intra-oral radiographs, a supra and sub-gingival scaling is performed, followed if necessary by more complex interventions such as dental extraction or periodontal surgery.
Severe and widespread periodontal disease in an otherwise healthy animal cannot be treated with long-term antibiotics. Good treatment consists in eliminating the cause by scaling (plaque, tartar) and any necessary extractions (periodontitis too advanced). Antibiotics should be reserved for two types of situations: the treatment of a local infection and the prevention of bacteremia.
Treatment of local infection
If periodontal disease has resulted in osteomyelitis of the maxilla or mandible, antibiotic therapy is recommended. It should be started a few days before surgery and continued for several weeks. Administration of antibiotics a few days before surgery is also helpful.
The systemic consequences of periodontal disease, however, are not limited to the bacterial load. Inflammatory chemical mediators, bacterial endotoxins and toxins from tissue breakdown can also come into play, either through direct or indirect harmful effects by causing immune reactions in organs distant from the oral cavity.
Can periodontal disease kill my dog? If untreated, consequences can be major
More than 50 studies have been published on the link between periodontal disease and cardiovascular disease (CVD) in humans, and most of them indicate a direct correlation between the two. For example, components of periodontal disease-causing bacteria have been detected in atherosclerotic plaques and two recent meta-analyzes have concluded that there is a significant correlation between periodontal disease and MCV9.
The same is true in animals in general and in dogs in particular, where studies have also shown a positive correlation between the presence of periodontal disease and the observation of histopathological changes in the heart and other internal organs. However, international scientific opinion is not unanimous on the importance of oral infections in the genesis of systemic diseases. There is indeed today no compelling evidence of a direct link between periodontal disease and other diseases.
Pregnant women with periodontitis have been shown to be up to 7.5 times more likely to give birth prematurely to a under-average weight baby. This risk is correlated with the increase in production of pro-inflammatory cytokines triggered by circulating bacterial lipoproteins. In some cases, periodontal disease-causing bacteria have been directly detected in the amniotic fluid.
An increase in the levels of inflammatory chemical mediators, such as interleukin 6 (IL-6), TNF (“tumor necrosis factor”) and reactive protein C (CRP), could increase insulin resistance and therefore prevent good control of blood sugar in diabetic patients. According to an article, having treated periodontal disease in a diabetic dog had made it possible to control his blood sugar by insulin therapy.
Degenerations, fatty liver and intrahepatic abscesses have been described and associated with periodontitis in humans as well as in dogs. A recent publication has observed that the parameters of the liver function improve after periodontal treatment in male, and that bacterial infection with Porphyromonas gingivalis could be a risk factor for the development and progression of fatty liver and steatohepatitis.
Since the mechanisms connecting oral diseases to systemic diseases are particularly difficult to identify, various hypotheses have been put forward to explain this link: direct infection, systemic inflammation with endothelial damage, and molecular mimicry between bacterial antigens and autoantigens.
Hypothesis of direct infection
Streptococcus, Staphylococcus, gingivalis bacteria and their breakdown products can cross the vascular barrier and enter the general blood circulation system. Transient bacteremia has been demonstrated after chewing and brushing teeth as well as during prophylaxis and dental surgery but this bacteremia is generally not clinically significant in healthy subjects. However, it has been shown experimentally that gingivalis bacteremia leads to the development of atherosclerosis in pigs and mice. Several periodontopathogenic agents were then isolated, either directly or indirectly by PCR, in organs and tissues distant from the oral cavity. A recent study has shown that gingivalis is present in 100% of cases of atherosclerotic plaques in humans.
Systemic inflammation hypothesis
According to this hypothesis, periodontitis causes an increase in circulating cytokines which can directly damage the endothelium of blood vessels, leading to the formation of lesions in the heart and other internal organs. Pro-inflammatory cytokines such as TNF and IL-6 have been shown to cause anabolic myocyte mutations by activating intracellular signals, resulting in myocardial hypertrophy. Several studies have found elevated levels of CRP in cases of chronic periodontitis, while a recent study has shown that, in patients having undergone intensive periodontal treatment (scaling and root planning), the elasticity of the brachial artery 24 hours after treatment was significantly lower to that of the control group. This was linked to increased CRP and IL-6 levels during periodontal therapy. However, 60 and 180 days after dental treatment, vascular elasticity was significantly increased in the treated group compared to the control group. This increase has been attributed to the beneficial effects of periodontal therapy.
According to this hypothesis, the systemic disease is the result of an immune reaction induced by bacterial heat shock proteins (HSP). All cells (including endothelial cells) that are under some form of stress express HSP proteins, and bacterial HSPs add additional antigenic stimulation upon infection. The immune system is not always able to tell the difference between bacterial HSP and autologous HSP so that, during infectious periodontitis, there is activation of T lymphocytes and production of antibodies which can provoke an autoimmune reaction towards host tissues which have an antigenic similarity. In the case of atherosclerosis, endothelial cells have been shown to express human HSP called hHSP60. However, several bacterial periodontopathogenic species have also been shown to produce their own HSP60, very similar to autologous stress protein.
Bacterial HSPs induce the synthesis of specific antibodies capable of attacking host cells. Several studies have shown that periodontal infection may contribute to atherosclerosis and cardiovascular disease through cross-reaction mechanisms.