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| SHORT COMMUNICATION |
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| Year : 2016 | Volume
: 8
| Issue : 2 | Page : 137-141 |
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Congenital heart disease and its journey from dental plaque to arterial plaque
Vinathi Reddy Kankara1, Nagireddy Ravindra Reddy2
1 Department of Periodontology, Sri Sai College of Dental Surgery, Vikarabad, Telangana, India
2 Department of Periodontology, C. K. S. Teja Institute of Dental Sciences, Tirupati, Andhra Pradesh, India
| Date of Web Publication | 15-Jul-2016 |
Correspondence Address:
Dr. Vinathi Reddy Kankara
Plot No. 60, Srinagar Colony, Hyderabad, Telangana - 73
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2231-0754.186424
 Abstract | | |
Congenital heart disease is mostly found in children, approximately around 7–10% from overall heart diseases. The etiology is multifactorial but reported associations include untreated maternal diabetes, phenylketonuria, intake of retinoic acid last but not least is oral pathogens present in periodontopathic bacteria. The main objective of this article is to explain about different mechanisms by which it is associated with dental, periodontal manifestations. It also explains about two patients who reported to our hospital with congenital heart disease and their dental and periodontal management. Keywords: Congenital heart disease, Fallot's tetraology, periodontitis
How to cite this article:
Kankara VR, Reddy NR. Congenital heart disease and its journey from dental plaque to arterial plaque. J Int Clin Dent Res Organ 2016;8:137-41 |
How to cite this URL:
Kankara VR, Reddy NR. Congenital heart disease and its journey from dental plaque to arterial plaque. J Int Clin Dent Res Organ [serial online] 2016 [cited 2022 Jul 3];8:137-41. Available from: https://www.jicdro.org/text.asp?2016/8/2/137/186424 |
| Introduction | |  |
From more than a decade, around 19th and 20th centuries, the theory of focal infection was promulgated, this stated that foci of sepsis were responsible for initiation and progression of a variety of inflammatory diseases.[1] The hypothesis, named the focal theory, suggested that there is a casual association between common oral diseases like caries, periodontitis with other systemic diseases such as cardiovascular disease, diabetes, and lung diseases. Earlier having this focal theory in mind, therapeutic edentulation was done. Since many teeth were extracted without evidence of infection, thereby providing no relief of symptoms, as a result this theory was ignored for many years.[2]
Recently, the progress in classification and identification of oral microorganisms and realization that certain microorganisms found in the oral cavity have opened a pathway for realistic assessment of the importance of oral focal infection.[1],[2] A number of epidemiological studies, microbiological, and immunological studies have suggested that oral infection, especially marginal and apical periodontitis are at higher risk factors for systemic diseases. A number of epidemiological studies documented that bacteremia is caused following different dental procedures. Bacteremia was observed in 100% of patients after dental extraction, in 70% after dental scaling and periodontal procedures, in 55% after third molar surgery, in 20% after endodontic treatment, and 55% after bilateral tonsillectomy. Dissemination of oral microorganisms into the bloodstream is common and it takes <1 min after an oral procedure, organisms enter the bloodstream and reach the heart. More than 1013 microbes on all surfaces of the body including the oral cavity.[1],[2],[3]
The article mainly focuses on the relation between periodontal disease and congenital heart defects, where till now there is little knowledge known regarding this.
| Pathways Linking Periodontal Infection to Systemic Disease | | |
[4]
There are three mechanisms or pathways linking oral infection to secondary systemic effects. These are metastatic infection, transient bacteria, and metastatic injury.[2]
Metastatic infection
The periodontal procedures cause transient bacteria. The microorganisms gain entrance to the blood, cross the barriers and circulate throughout the body. Usually, these are eliminated by reticuloendothelial system within minutes. If disseminated microorganisms find favorable conditions, they may settle down in arteries and capillaries forming arterial plaque, which on further accumulation can increase and cause blockage of blood vessels.[2],[5]
Metastatic injury
Some Gram-positive and Gram-negative bacteria have the ability to produce diffusible proteins or exotoxins which include cytolytic enzymes and dimeric toxins. These pharmacological actions produce lethal poisons which cause pathological manifestations.[4]
Metastatic inflammation
Soluble antigen may enter the bloodstream, react with circulating specific antibody and form a macromolecular complex. These immune complexes give rise to a variety of acute and inflammatory reactions which help in the destruction of periodontium leading to periodontitis.[2]
Clinical report 1
A 34-year-old man reported to our hospital with the complaint of bad breath and bleeding gums while brushing, through medical history was obtained from the patient which revealed that he is known congenital heart disease patient with medical records. On physical examination, he was thin, weak, exertional dyspnea and orthopnea were present. His blood pressure was about 110/60 mm of hg and pulse rate was 79 beats/min. Mild cyanosis was present on upper and lower lips [Figure 1]. C lubbing of fingers was well observed [Figure 2]. On intraoral examination, cyanosis was observed on marginal and attached gingival of all the teeth [Figure 3]. Plaque and calculus were well demarcated, marked cyanosis is seen on the hard and soft palate [Figure 4]. According to his medical records echocardiography showed bilateral dilatation, normal left ventricular dimensions, functions, and thickening of left ventricular walls [Figure 5]. He was diagnosed as having congenital disease with tetralogy of Fallot.
Case report 2
A 24-year-old man reported to our hospital with the chief complaint of bad breath, bleeding gums, and mobile teeth [Figure 6]. A thorough medical history revealed that patient is known critical congenital heart disease (CCHD) patient under medical supervision. On physical examination, he was weak and thin. Patient was having dyspnea while talking. His blood pressure was about 100/70 mm of Hg. Patient was unable to walk and talk for longer time. Skin was pale and bluish, clubbing of fingers and toes was present [Figure 7]. Intraoral examination showed poor oral hygiene, generalized plaque, calculus, reddish marginal, and attached gingiva was present. Bleeding on slight probing was present [Figure 8]. Generalized recession, periodontal pockets, mobility were present. 11, 12, 13, 14, 15, 16, 21, 22, 24, 31, 32, 33, 35, 41, 42, 44 were missing due to periodontal loss of attachment. Furcation involvement was present in 46 [Figure 8]. He was diagnosed as generalized periodontitis [Figure 9]. According to orthopantomogram the periodontal findings were confirmed [Figure 10]. According to medical reports obtained from the patient he was diagnosed as CCHD, tetralogy of Fallot. Large sub aortic ventricular septal defect with bidirectional shunt. Electrocardiogram, ultrasound reports revealed, pulmonary valve was thickening, whereas mitral valve, aortic valve, and tricuspid valve were normal. Right atrium and ventricle were dilated and hypertrophied [Figure 11]. Blood tests were normal. Urine tests revealed uric acid levels were about 8.9 mg/dl, which was abnormal finding. Doppler study revealed difference in the ventricular septum.
| Discussion | | |
TU reported an evidence or association between tooth loss and increased mortality from cardiovascular disease patients in Glasgow alumni cohort. The research design and methodology adopted in this investigation are unique and well-chosen for several reasons. From his study, he concluded that there is positive association between poor oral health defined by tooth loss and patterns of mortality later in life.[2] An oral and periodontal treatment in congenital heart disease patients is very important. The main point to be noticed is the disorder with which patient is suffering, by which susceptibility to bacterial endocarditis can be predicted.[6] In the first case, the plaque and calculus were minimal and history of bacterial endocarditis was not present. Chronic cyanosis club like deformation of fingers and toes was induced.[7],[8],[9] The anatomic and histological structure of the ungula phalanx displays a striking similarity to that of the gingiva. In that terminal arteries are found in both devoid of subcutaneous layers. For this reason, the gingiva may be recorded as one of the acra. For this reason, the gingival lesions are common in burger's disease, raynaund's gangrene, endangiitis obliterans, scleroderma, and vascular disturbances of childhood atrophy of the periodontium is a constant symptom.[4]
According to study conducted by Sallay, the clinical findings recorded that gingiva was livid in color, more cyanotic than inflamed. Atrophy of gingiva and the alveolus occur synchronously. No deep pockets are formed. In the majority of patients, atrophy was not complicated by intercurrent gingival inflammation and it started in the region of lower first incisors and remained most marked in this region. Gingival atrophy is aggravated by intercurrent gingivitis or occusal trauma. With progress of age and of cardiac disease, the severity and extension of periodontal atrophy increases which lead insufficient supply of oxygen to periodontium leading to atrophy and periodontitis. These findings coexist with findings of the first case.[4]
But in second case, there was poor oral hygiene; severe periodontal destruction was present. He was more susceptible to bacterial endocarditis. This coexists with findings of Guntheroth. According to American Association for Periodontology 1 out of 4 infective endocarditis is caused by periodontal germs like Eikenella corrodens. Simple scaling resulting in bleeding can produce transient bacteremia. This was evidenced with the findings of Hunter KM, TU.[10]
In hypoxemia, the organism attempts to improve function by establishing adaptative mechanisms. In hemopoietic, system formation of erythrocytes and hemoglobin is accelerated, and tissue oxygen is better utilized, the capillary bed is dilated, and the permeability of the capillary endothelium is increased, by these processes, increase of the hemoglobin, on one hand, and decrease of O2 saturation in the circulating blood, on the other hand is observed, as a result cyanosis becomes manifested first in the mucous membranes.[4]
| Conclusion | | |
Dental and periodontal treatments are very important steps to be carried out in congenital heart disease patients for every 3 months. Important aspects about relation between congenital heart disease and periodontitis are not well known to patients as well doctors. Dental health education relating to its association, treatment of periodontal disease has to be delivered to patients. Early dental health education and patient motivation can minimize oral and periodontal disease which may risk the existence of bacterial endocarditis and prevent mortality. The main focus of this article is on the medical as well dental condition of patient. Still further studies are needed to come to conclusion of journey from dental plaque to arterial plaque.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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| 10. | Choussat P. Prophlaxis of dental infectious endocarditis. Odontostomatol Trop; 1997. p. 6-12. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11]
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