Gum disease, also called periodontal disease when it involves the tissues supporting the teeth, is primarily caused by the accumulation of dental plaque around the teeth and along the gum margin. Dental plaque is a sticky biofilm containing large communities of microorganisms embedded in an extracellular matrix. It forms continuously on tooth surfaces and is not simply loose food debris.
When plaque is not removed effectively by brushing and cleaning between the teeth, the microbial community changes and produces substances that irritate the adjacent gum tissues. The initial inflammatory response is called gingivitis. If inflammation persists and the tissues supporting the teeth become progressively damaged, the disease can develop into periodontitis, in which periodontal attachment and supporting bone are lost. NHS guidance identifies plaque accumulation as the principal cause of gum disease.
Plaque becomes particularly important at the gum line because this is where the tooth surface meets the soft tissue and where cleaning can be more difficult. Bacterial metabolites and components of the biofilm stimulate the body's innate immune response, producing redness, swelling and bleeding. If plaque remains undisturbed, it can mineralise and become dental calculus, commonly called tartar.
Calculus is a hardened deposit that cannot normally be removed effectively with an ordinary toothbrush and provides a rough surface on which additional plaque can accumulate. Calculus itself is not the original microbial cause of gum disease, but it makes effective plaque control more difficult and can maintain local inflammation. Professional dental cleaning can remove calculus, while daily home care is necessary to prevent new plaque from accumulating.
The transition from gingivitis to periodontitis involves more than simply increasing amounts of plaque. In susceptible individuals, prolonged inflammation alters the relationship between the gum and tooth. The tissue can detach from the tooth surface, creating a periodontal pocket in which bacteria and inflammatory products can accumulate below the gum line. The inflammatory response can activate pathways that stimulate osteoclasts, cells responsible for bone resorption, resulting in destruction of the alveolar bone supporting the teeth.
Periodontitis is therefore a disease involving both microbial biofilms and an abnormal or excessive host inflammatory response. The amount and composition of plaque matter, but individual susceptibility to inflammation also helps explain why people exposed to apparently similar levels of plaque can experience different degrees of periodontal damage.
Smoking is one of the most important modifiable risk factors for periodontal disease. Tobacco smoke affects immune and inflammatory responses, changes the local environment of the mouth, impairs healing and can make periodontal treatment less successful. Smoking can also alter the appearance of gum disease because reduced blood flow may sometimes make inflamed gums bleed less visibly, potentially masking disease rather than preventing it. Other tobacco products can also increase oral health risks.
Diabetes, particularly when poorly controlled, is another important risk factor because altered immune function and metabolic changes can make periodontal inflammation more severe and harder to control. Conversely, severe periodontal inflammation can complicate diabetes management, illustrating the two-way relationship between oral and systemic health. NHS and NHS-affiliated guidance identifies smoking and diabetes among important risk factors for gum disease.
Genetic susceptibility helps explain differences in periodontal disease risk. Some people have immune or structural characteristics that make them more susceptible to destructive periodontal inflammation, and a family history of significant gum disease can be associated with increased risk. Hormonal changes can also influence gum tissues. Puberty and pregnancy can alter the inflammatory response of the gums, sometimes making them more sensitive to plaque.
Pregnancy itself does not create plaque or directly cause periodontal disease, but hormonal changes can make existing plaque-induced inflammation more pronounced. Stress, poor nutrition and some systemic conditions can further influence immune function, oral hygiene behaviours or tissue repair. These factors generally act as modifiers of risk rather than replacing plaque as the fundamental local trigger.
Oral hygiene practices strongly influence whether plaque remains at levels compatible with healthy gums. Brushing removes plaque from accessible tooth surfaces, while interdental brushes or dental floss address areas that a toothbrush cannot clean effectively. Failure to clean between teeth is particularly important because plaque can remain undisturbed in interdental spaces and around the gum margin. Incorrect technique can also contribute to problems: brushing too aggressively may injure gums, while brushing inadequately may leave plaque behind. Dental appliances, crowded teeth, braces, poorly fitting dentures and rough dental restorations can create areas where plaque is more difficult to remove. Regular dental examinations allow early inflammation, calculus and periodontal pockets to be identified before substantial supporting tissue has been lost.
Gum disease can also be influenced by conditions or circumstances that alter the oral environment or immune response. Certain medications can affect saliva production or gum tissues, and reduced saliva can make plaque control more difficult. Poorly fitting dental appliances and local trauma can irritate tissues, although irritation alone should not be confused with the bacterial biofilm-driven process of periodontal disease.
Diet can influence general oral and metabolic health, while obesity is associated with increased periodontal risk through metabolic and inflammatory pathways. Stress may influence immune function and oral hygiene behaviour. Some people also have periodontal disease despite apparently good oral hygiene because genetic susceptibility, smoking, diabetes or other risk factors modify the inflammatory response. The disease should therefore be understood as multifactorial: plaque initiates the local problem, while host, behavioural, systemic and environmental factors influence whether inflammation remains superficial or progresses to tissue destruction.
A common misconception is that gum disease is caused simply by brushing too little or by ageing. Age increases the cumulative opportunity for periodontal disease to develop, but healthy older gums are not inevitably diseased. Another misconception is that bleeding gums should be treated by avoiding brushing the bleeding areas; persistent bleeding generally indicates inflammation and makes effective plaque removal more important, although unusually severe bleeding requires professional assessment.
Periodontal disease can also be relatively painless, meaning that the absence of pain does not indicate healthy gums. As disease progresses, gums may recede, teeth can become sensitive or mobile, periodontal pockets can deepen and supporting bone can be destroyed. In advanced cases teeth may become loose and eventually fall out. Early detection is therefore important because gingivitis can generally be reversed with effective plaque control, whereas bone destroyed by established periodontitis cannot simply be restored by ordinary brushing.
