etiology of periodontal

Lec : 6 Periodontology DR .Hussein Al Dabbagh

PREDISPOSING FACTORS OF OERIODONTAL DISEASES:
In recent years, it has become apparent that the pathogenesis of periodontal diseases is more complex than the presence of virulent microorganisms. In fact, periodontitis is defined as an inflammatory disease of bacterial origin begin with the accumulation of biofilms on the tooth surface which is called dental plaque, in addition to dental plaque, some of the host factors has been considered as risk factors that associated with increased severity of periodontal diseases.
Gingivitis: it is inflammation of the gingiva in which the junctional epithelium remains attached to the tooth at its original level. It is a reversible condition and has been extensively studied in a model system referred to as experimental gingivitis in man by Loe et al (1965). Gingivitis is inflammation of the gingiva tissue. It is characterized by areas of redness and swelling, and there is tendency for the gingiva to bleed easily. Gingivitis is limited to the epithelium and gingival connective tissues. It is important to note that there is no tissue recession or loss of connective tissue or bone.
Periodontitis: it is inflammation of the supporting tissue of the teeth leading to permanent destruction of these tissues. It is characterized by clinical attachment loss, periodontal pocketing and alveolar bone loss (these features not found in gingivitis). Periodontitis is irreversible disease can cause a breakdown of the periodontium resulting in loss of tissue attachment and destruction of alveolar bone. It means inflammation of the supporting tissues of the teeth.
Periodontitis is the extension of inflammatory process from the gingiva into the connective tissue and alveolar bone that support the teeth. The progression of periodontitis involves the destruction of connective tissue attachment at the most apical portion of a periodontal pocket.
Gingivitis may progress to periodontitis when it is left untreated and with the presence of other contributing factors beside the essential factor (dental plaque), but when treatment is conducted, the gingiva will return back to healthy situation.
In some individuals gingivitis may not progress to periodontitis for a long period of time even if it is not treated and this condition is called contained gingivitis and this is depending on host response and pathogenicity of bacteria.
Risk: probability that an individual will develop a specific disease in a given period.
A risk factor: can be defined as an occurrence or characteristic that has been associated with the increased rate of a subsequently occurring disease. It is important to make the distinction that risk factors are associated with a disease but do not necessarily cause the disease.

Systemic risk factor may be modifiable or non-modifiable.

Modifiable risk factors
Dental plaque and oral hygiene
The primary etiological factor in the development and initiation of periodontal disease is dental plaque. Dental plaque is a bacterial aggregation on the teeth or other solid structures in the oral cavity.
Dental calculus which mineralized dental plaque is consider as secondary etiological factor of periodontal disease and it is covered with dental plaque so it serve as reservoir for bacterial plaque (retentive factor).
The oral bacterial microbiome includes over 700 different phylotypes, with approximately 400 species found in sub-gingival plaque. The sub-gingival microflora in periodontitis can harbor hundreds of bacterial species but only a small number has been associated with a progression of disease and considered etiologically important. Oral hygiene can favorably influence the ecology of the microbial flora in shallow to moderate pockets, but it does not affect host response. Oral hygiene alone has little effect on sub-gingival microflora in deep pockets and personal oral hygiene practices among professional have been shown to be unrelated to periodontitis in these individuals.
Comprehensive oral hygiene programs are effective in preventing or reducing the level of gingival inflammation in children and adults. These programs, however, may not be viable in preventing aggressive periodontitis and it may be difficult achieve a satisfactory level of oral hygiene in the general population to prevent chronic periodontitis and periodontal tissue loss effectively.
Specific microorganisms
Although there is sufficient evidence that accumulation and maturation of a plaque biofilm is necessary for the initiation and progression of periodontal disease. Studies show that bacterial species colonizing the gingival pocket play variable roles in the pathogenesis of these disease and may therefore possess difficult levels of risk of periodontal tissue loss.
Of all of the various microorganisms that colonize the mouth, there are
Aggregatibacter actinomycetemcomitans (A.a)
Porphyromonas gingivalis (P. gingivalis)
Prevotella intermedia (P. intermedia)
Tannerella forsythia (T. forsythia)
These microorganisms produce endotoxins that will cause severe periodontal destruction.


Smoking:
tobacco smoking is the major risk factor for increasing the prevalence and severity of periodontal destruction. Smoking suggest an imbalance between bacterial challenge and host response which may due to changes in the composition of sub-gingival plaque with increase in the number and/or virulence of pathogenic organisms, so the microbiological effect of smoking in the etiology of periodontal disease include increase colonization of shallow periodontal pocket by periodontal pathogens and increase levels of periodontal pathogens in deep periodontal pocket. In a study on subjects with different smoking histories, it was found that smokers had significantly higher levels of Tannerella forsythia(2.3 times) more likely than nonsmokers and former smokers. Of particular interest was the observation that smokers do not respond to mechanical therapy as well as nonsmokers; this is associated with increased levels of T. forsythia, A. actinomycetemcomitans, and P. gingivalis remaining in the pockets after therapy in the smoking group with greater post treatment probing depth and less gain in clinical attachment levels when compared with nonsmokers
While immunological effect of smoking on the etiology of periodontal disease include mainly impairment of chemotaxis and phagocytosis activity of neutrophils which is an important component of the host response to bacterial infection, also there will be reduction in the production of antibodies essential for killing the bacteria specially IgG2.
Finally, the physiological effect of smoking on the etiology of periodontal disease include of following:
Decrease of gingival blood vessels and reduce bleeding on probing with increase severity of inflammation (vasoconstriction).
Decrease gingival crevicular fluid flow.
The risk of periodontal disease increase with the number of cigarettes smoked per day. Smoking cigars and pipes carries the same risk as smoking cigarettes. Exposure to secondhand smoke may also be associated with an increased risk for developing periodontal disease. Fortunately, when smoker quit, their periodontal health gradually recovers to a state comparable to that of nonsmokers.
Diabetes mellitus:
Diabetes is a clear risk factor for periodontitis Epidemiologic data demonstrate that the prevalence and severity of periodontitis is significantly higher in patients with type I and type II diabetes than in those without diabetes and that the level of diabetic control is an important variable in relationship with the pathogenesis.
Diabetes is a modifiable factor in the sense that through it cannot be cured, it can be controlled. Studies have been done which suggest that poorly controlled diabetics respond less successfully to periodontal therapy relative to well-controlled and non-diabetics. It is an important disease from periodontal standpoint. It is an complex metabolic disease characterized by chronic hyperglycemia. Uncontrolled diabetes (chronic hyperglycemia) is associated with many problems as reduction in the defense mechanism (neutrophil dysfunction, impairment of chemotaxis and phagocytosis), atherosclerosis and reduce normal gingival blood flow, increased susceptibility to infections including periodontitis and poor wound healing. Diabetes mellitus does not cause gingivitis or periodontal pocket, but it alters the response of periodontal tissue to local factor. Diabetic patients with poor oral hygiene may have very sever gingival inflammation, deep periodontal pocket, rapid bone loss and frequent periodontal abscesses, which is an important feature of periodontal disease in diabetic patients.

Psychological factors

The incidence of necrotizing ulcerative gingivitis increases during periods of emotional and physiologic stress, suggesting a link Between them.
Emotional stress may :
1) interfere with normal immune function.
2) result in increased levels of circulating hormones that can have an impact on the periodontium.
Individuals with financial strain, distress, depression, or inadequate coping mechanisms have more severe loss of attachment.
Obesity
Obesity is one of the most significant risks of modern society, and is now recognized as a major health concern in both developed and developing countries.
Conditions associated with obesity, e.g. "the metabolic syndrome", a clustering of dyslipidemia and insulin resistance may exacerbate periodontitis. Obesity has been postulated to reduce blood flow to the periodontal tissue, promoting the development of periodontal disease. Furthermore, obesity may enhance immunological or inflammatory disorders, which might be the reason obese subjects tend to exhibit escalating poor periodontal status relative to non-obese individuals.
Socioeconomic status (SES)
Multitudes of disease conditions are associated with socioeconomic status, and cause/effect is possible. Generally, those who are better educated, wealthier, and live in more desirable circumstances enjoy better health status than the less educated and poorer segments of society. Periodontal disease are on different and have been related to lower SES. The effect of living in deprived circumstances can started early in life. Gingivitis and poor oral hygiene are clearly related to lower SES. But the relationship between periodontitis and SES is less direct.
Pregnancy, puberty and menopause (hormonal)
Pregnancy associated gingivitis is inflammation of the gingival tissues associated with pregnancy. This condition is accompanied by increase in steroid hormones in crevicular fluid and increase in levels of (Prevotella intermedia microorganism) which use the steroids as growth factors. The increase in sex hormones may exaggerate the inflammatory response to dental plaque which means small amount of plaque may lead to gingivitis. Puberty is also accompanied by an exaggerated response of gingiva to local irritation. As adulthood is approached, the severty of the gingival inflammation diminishes even when local factors persist. During menopause, estrogen deficiency will reduse bone mineral density. Some women may develop menopausal gingivostomatitis , Burning mouth.
HIV \ AIDS :
It has been stated that the immune dysfunction ( immune suppression) associated with human immunodeficiency virus( HIV) infection and acquired immunodeficiency syndrome increase susceptibility to periodontal disease . those patients often had severe periodontal destruction characterized by necrotizing ulcerative periodontitis .


Medications:
Gingival enlargement is a well-known consequence of the administration of some drugs as anticonvulsants ( phenytoin or Dilantin) , immunosuppressants ( cyclosporine) ,and Ca channel blockers (nifedipine) .in general the over growth of the gingiva start as painless enlargement of the interdental papilla and extend to the marginal gingiva , then as the condition progress , the marginal and papillary enlargement unite together and may cover the clinical crown and may interfere with the occlusion . it has been shown that the presence of dental plaque will increase the chance of development of the enlargement and plaque removal may limit the severity the lesion, but it does not prevent the overgrowth. Also thee gingival enlargement may be dose-related mean if the physician reduce the dose of the drug without affecting the systemic condition of the patient, this may reduce the enlargement or use an alternative medication that does not cause gingival enlargement as a side effect. Other factors that may influence the gingival enlargement is the continuous use the drug for a long period of time (the duration) which may result in recurrence of the lesion even if it is treated surgically.
The first drug induced gingival enlargement is Phenytoin (Dilantin Na) which is anticonvulsant drug used in the treatment of epilepsy. Gingival enlargement occur in 50-65% of patients receiving the drug.
The other drug is Cyclosporine A which is immunosuppressive agent used to prevent organ transplant rejection. The enlargement occurs in 30% of patients receiving this drug.
Ca channel blockers are drug used for the treatment of cardio-vascular conditions such as hypertension and angina pectoris. Some of these drugs can induce gingival enlargement. Nifedipine is one of most commonly used drug that induced the enlargement in about 20% of the patients. More recent are Amlodipine and Verapamil which also induced enlargement.
Non-modifiable risk factors:
Osteoporosis
Many of the studies conducted to date suggest there is a relationship between skeletal osteoporosis and bone loss to the extent that postmenopausal osteoporosis may result in dental osteopenia involving the jaws, and particularly the mandible. Osteoporosis was significantly associated with severe alveolar crestal bone loss and the prevalence of periodontitis cases in postmenopausal women.

Hematological disorders

Hemorrhagic gingival overgrowth with or without necrosis is a common early manifestation of acute leukemia. Patients with chronic leukemia may experience similar but less severe periodontal changes. Chemotherapy or therapy associated with bone marrow transplantation may also adversely affect the gingival health.
Genetic factors
There is evidence that genetic differences between individuals may explain why some patients develop periodontal disease and other do not. Genetic factors may play an important role in determining the nature of the host response and may affect the function of phagocytic immune cells or the structure of the epithelia or connective tissue. One of these disease is papillon-lefevre syndrome which is a rare hereditary disease characterized by hyperkeratotic skin lesion in the palms, soles, knees and elbows and sever destruction to the periodontium with early loss of primary and permanent teeth. Other disease is aggressive periodontitis which has familial aggregation (which mean seen in one family). Some immunological defected are associated with aggressive periodontitis.
Aging
Ageing is associated with an increased incidence of periodontal disease. However it has been suggested that the increased level of periodontal destruction observed with aging is the result of cumulative destruction rather than a result of increased rates of destruction. With aging a number of changes take place in the periodontal tissues.
Arteriosclerosis (reduction in arterial blood supply).
The gingiva become more fibrotic and less keratinized.
The periodontal fiber bundles become thicker with decrease in cellularity.
Osteoporosis of alveolar bone.

Sex
) males have more loss of attachment than Females.
(2) males have poorer oral hygiene than females.
So higher levels of plaque and calculus lead to gender differences in prevalence and severity of periodontitis that related to preventive practices rather than any genetic factor.
Ethnicity
The level of attachment loss is also influenced by race/ethnicity, although the exact role of this factor is not fully understood. Certain racial/ethnic groups, particularly subjects of African and Latin American background, have a higher risk of developing periodontal tissue loss than other groups.
There are local contributing risk factors to the etiology of periodontal diseases including Anatomic and Iatrogenic factors, these factors may facilitate bacterial plaque accumulation and retention or they interfere with plaque removal. (Relative factors).


The local anatomic risk factors:
Furcation anatomy: the entrance of bifurcations or trifurcations is restricted enough to limit the access for mechanical root instrumentation. Also the presence of concavities in the furcal aspects of molar will limit instrumentation as well.
Cervical enamel projections (CEP): these are tooth developmental deformities of the CEJ found on molars. The enamel is projected toward the entrance of the furcation and this projection may responsible for furcation invasion and localized severe bone loss around the teeth.
Palatoginival grooves (PGG): These are tooth developmental deformities of maxillary central and lateral incisors. They begin in lingual pits and extend vertically onto root surfaces and may extend to the root apex and are associated with increased gingival inflammation and plaque accumulation.
Root morphology: the mesial root surface of the maxillary first premolar presents with a pronounced concavity which may not be accessible to oral hygiene procedures or professional instrumentation.
The iatrogenic risk factors (faulty dentistry) include many examples as:
Overhang margins of proximal restorations.
Open or loose contract of crowns and fillings.
Poorly designed or fitted prosthesis…ex. Lingual bar is better than full coverage to keep the cleansing action of saliva and massage from tongue.