plaque index to indicate to the patient areas of plaque they are not removing on their own. this can be removed through the procedure of a dental prophylaxis. aetiology the primary aetiological factor for periodontal disease is plaque biofilm of dental biofilm. a dental biofilm is a community of microorganisms attached to a hard, non-shedding surface. in the oral cavity, hard non-shedding surfaces include teeth, dental restorative materials and fixed or removable dental appliance such dentures. it is this adherence to non-shedding surfaces that allows bacteria in a dental biofilm to have unique characteristics of clinical significance. the stages of biofilm formation: formation of an acquired pellicle: involves selective absorption of salivary and gcf molecules through an electrostatic affinity with hydroxyapatite. bacterial transportation: bacteria will readily adhere to the acquired pellicle through adhesins, proteins and enzymes within one to two hours. reversible interaction: there is electrostatic attraction or hydrophobic interaction between microorganisms and the tooth surface. irreversible interaction: bacterial adhesins recognise specific host receptors such as pili and outer membrane proteins. the different species of bacteria bind together and require specific receptors to interact with the pellicle. co-adhesion: there is a natural affinity for oral microorganisms to adhere to one another which is termed co‐adhesion. co-adhesion involves the adherence of planktonic or single culture cells to already attached organisms on a surface. the organisms which make first contact with the surface and allow the platform for later co-adhesion of bacteria are called early colonisers; they facilitate the formation of complex multispecies dental biofilms. multiplication: through continued growth and maturation of existing plaque micro-organisms and the further recruitment of later colonisers. climax community (homeostasis): after a prolonged period of stability, the bacterial community has sufficient nutrients and protection to survive. these complex biofilms are usually found in hard to cleanse areas. nutrition is provided from dietary consumption of the host for supra-gingival biofilm organisms and from blood and gcf for the sub gingival biofilm organisms. detachment: from one surface to another or within biofilm allows colonization at remote sites. bacteria contained within the biofilm are protected by a slimy extracellular polysaccharide matrix which helps to protect them from the outside environment and chemotherapeutics agents. an example of a chemotherapeutic agent is an antiseptic such as chlorhexidine mouth-rinse or antibiotics. thus, antibiotics are not generally used in the treatment of periodontal disease, unlike other bacterial infections around the body. the most effective way to control the plaque biofilm is via mechanical removal such as toothbrushing, interdental cleaning or periodontal debridement performed by a dental professional. pathogenesis an individual's host response plays an important role in the pathogenesis of periodontal disease. even in a mouth where the gingiva appear healthy, there is constant low-level inflammatory response facilitated by the host to manage the constant bacterial load of plaque micro-organisms. leukocytes and neutrophils are the main cells that phagocytose bacteria found in the gingival crevice or pocket. they migrate from the tissues in a specialized exudate called gingival crevicular fluid also known as gcf. neutrophils are recruited to the gingival crevice area as they are signalled to by molecules released by plaque microorganisms. damage to epithelial cells releases cytokines which attract leukocytes to assist with the inflammatory response. the balance between normal cell responses and the beginning of gingival disease is when there is too much plaque bacteria for the neutrophils to phagocytose and they degranulate, releasing toxic enzymes that cause tissue damage. this appears in the mouth as red, swollen and inflamed gingiva which may bleed when probed clinically or during tooth brushing. these changes are due to increased capillary permeability and an influx of inflammatory cells into the gingival tissues. when gingival disease remains established and the aetiology is not removed, there is further recruitment of cells such as macrophages, which assist with the phagocytic digestion of bacteria, and lymphocytes, which begin to initiate an immune response. pro-inflammatory cytokines are produced inside the gingival tissues and further escalate inflammation, which impacts the progression of chronic systemic inflammation and disease. the result is collagen breakdown, infiltrate accumulation as well as collagen breakdown in the periodontal ligament and alveolar bone resorption. at this stage, the disease has progressed from gingivitis to periodontitis and the loss of supporting periodontium structure is irreversible. risk factors a risk factor is a variable that in health can be defined as "a characteristic associated with an increased rate of a subsequently occurring disease". risk factors are variables that contribute to disease, rather than being factors that induce disease. risk factors may be seen as modifiable and non-modifiable. modifiable risk factors are often behavioural in nature and can be changed by the individual or environmental circumstances, whereas non-modifiable factors are usually intrinsic to an individual's genetics and cannot be changed. to determine risk factors for a disease, evidence-based research and studies are needed for evidence, with longitudinal studies giving the most statistically significant outcomes and the best reliability for determining risk factors. risk factors often coexist with other variables, rarely acting alone to contribute to a disease. risk factors can be genetic, environmental, behavioural, psychological, and demographic in nature. there are many risk factors that contribute to placing an individual at higher risk for developing gingival and periodontal diseases. however, the only aetiological factor for periodontal disease is bacterial plaque, or biofilm. identification of one's risk factors plays an important role in the diagnosis, treatment and management of periodontal diseases. it was previously believed that each human being had the same risk of developing periodontal diseases, but through the identification and classification of risk factors, it has become well understood that each individual will have a differing array of risk factors that generate susceptibility and contribute to severity of periodontal disease. individual, modifiable risk factors include: tobacco smoking: tobacco smoking is firmly established as a major risk factor for periodontal disease, with the relationship between smoking exposure and periodontal tissue destruction being supported strongly by various research papers. smoking decreases the healing abilities of the oral tissues by destroying blood vessels and supply and preventing essential immune-defence organisms from penetrating the tissues. therefore, pathogenic bacteria are able to destruct the periodontal tissues more rapidly and escalate the severity of disease. although the clinical signs of inflammation are less pronounced, smokers have a larger portion of sites with deep pocketing depths and loss of clinical attachment when compared with nonsmokers. smoking cessation and counselling is an integral part of a dental professional's work with periodontal disease patients. smoking cessation has been proven to prevent progression of periodontal disease and to return the oral microflora to a less pathogenic microbial state. alcohol consumption: more research needs to be conducted in the form of longitudinal studies on the effects of alcohol on the periodontal tissues. however, current studies suggest that alcohol consumption moderately increases one's risk for progression of periodontal disease. diabetes mellitus: diabetes falls under the category of modifiable risk factors as although it cannot be cured, it can be controlled, which greatly helps periodontal disease control. a clear two-way relationship has been established with blood glucose control directly affecting periodontal disease severity and progression, and vice versa. periodontal disease patients with diabetes mellitus also have poorer healing abilities than those without diabetes, and hence are at an increased risk for more severe diseases if blood glucose control is poor and when healing abilities are affected by systemic disease. obesity and vitamin d deficiency are both risk factors for periodontal disease that go hand in hand. obesity is generally associated with a decreased consumption of fruits and vegetables, with an increase in foods high in fat, salt and sugar. having a poor diet not only contributes to obesity but also results in a lack of essential nutrients, including vitamin c, d, and calcium, which all play important roles in ensuring a healthy immune system and healthy oral tissues and bone. poor oral hygiene: as plaque is the only aetiological factor for periodontal disease, poor oral hygiene is the most prominent risk factor in initiating, progressing and determining severity of disease. performing brushing and interdental cleaning is perhaps one of the most effective ways at removing dental plaque biofilm and prevention of periodontal diseases. cardiovascular disease: not only does poor oral hygiene have a clear relationship with an increased risk of developing cardiovascular disease, high concentrations of cholesterol and the mechanisms of oral bacteria in the process of atherosclerosis may increase in individuals with chronic periodontitis. stress: various studies have demonstrated that individuals under psychological, ongoing chronic stress are more likely to have clinical attachment loss and decreased levels of alveolar bone due to periodontal destruction. this is due to the increased production of certain immune cells and interleukins, which decrease the defensive mechanisms against pathogenic bacteria, therefore increasing chances of developing periodontal disease. pregnancy: studies have shown that the oral tissues are affected and altered during pregnancy due to a decreased immune response and increased vascular blood supply and volume systemically. it is important to note that pregnancy does not cause gingival and periodontal diseases but may exacerbate the inflammatory response to a pre-existing disease. it is also important to note that pregnancy does not detract minerals from the oral tissues or teeth as previously thought and heard in old wives' tales. existing disease often presents during pregnancy due to an altered oral environment, and not merely due to pregnancy causing disease. these effects can be prevented by good oral hygiene through toothbrushing and interdental cleaning. non-modifiable risk factors include: genetics and the host response have been shown to play an important role in periodontal disease development in studies on identical twins and isolated indigenous populations. periodontal disease also may result due to an abnormal or decreased immune response, rather than aggressive properties of bacterial pathogens. osteoporosis: in individuals with osteoporosis, studies have shown that alveolar bone is less dense than in a healthy adult. however, this does not demonstrate a relationship with periodontal pathogens or clinical attachment loss, therefore more research is needed to investigate if osteoporosis is a true risk factor for periodontal disease. drug-induced disorders: many drugs and medications can have an adverse effect on the periodontal tissues, through contributing to various oral conditions such as dry mouth and gingival enlargement (gingival hyperplasia). it is crucial that dental professionals ensure that poly-pharmacy patients have medical history reviewed at each visit to correctly evaluate the patient's risk and determine appropriate course of action for dental treatment. haematological disorders: important cells and nutrients carried in the blood to the periodontal tissues are crucial for the tissues' defence mechanisms and response to toxins and pathogens, gas exchange and efficient hemostasis. therefore, red blood cells have a pivotal role in maintaining the health of the periodontium, meaning haematological disorders can have profound detriment to the periodontal tissues and the onset of disease. risk characteristics must be considered in conjunction with risk factors as variables that may also contribute to increasing or decreasing one's chances of developing periodontal disease. numerous studies show that age, gender, race, socioeconomic status, education and genetics also have strong relationships on influencing periodontal disease. periodontal disease is multifactorial, requiring dental and oral health professionals to have a clear and thorough understanding of the risk factors and their mechanisms in order to implement effective disease management in clinical practice. diagnosis periodontitis and associated conditions are recognised as a wide range of inflammatory diseases that have unique symptoms and varying consequences. in order to identify disease, classification systems have been used to categorize periodontal and gingival diseases based on their severity, aetiology and treatments. having a system of classification is necessary to enable dental professionals to give a label to a patient's condition and make a periodontal diagnosis. a diagnosis is reached by firstly undertaking thorough examination of the patient's medical, dental and social histories, to note any predisposing risk factors (see above) or underlying systemic conditions. then, this is combined with findings from a thorough intra and extra oral examination. indices such as the periodontal screening record (psr) and the community periodontal index of treatment needs (cpitn) are also used in making a diagnosis and to order or classify the severity of disease. if disease is identified through this process, then a full periodontal analysis is performed, often by dental hygienists, oral health therapists, or specialist periodontists. this