Natural History and Clinical Signs of Periodontal Diseases
This chapter aims to explain the changing paradigm of the natural history of periodontitis and to help the reader visualise the important clinical features of periodontal health and disease.
The outcome of reading this chapter should be that the reader will understand how untreated periodontitis differs in its pattern of progression from treated disease, and will be able to recognise the salient features of gingival and periodontal diseases in their patients.
The natural history of a disease describes the pattern of behaviour of the disease process with time, in the absence of clinical intervention. Natural history studies are essential to our understanding of how a disease should behave and help to plan health care and improve clinical outcomes. In periodontal diseases, the ultimate treatment outcome is the retention of teeth in a state of comfort and function for life. This is the primary outcome measure of successful periodontal care, but is very difficult to measure, as teeth may be lost for many reasons and retrospective studies of tooth loss are often unable to determine with certainty the cause of the tooth loss. Secondary outcome measures are therefore often used. These would include:
lack of tooth mobility or mobility compatible with comfortable function
BOP at < 25% of sites
no pocketing >4mm at any sites
no suppuration from the gingival crevice at any sites
plaque scores in the range of 20%–40% or less
stable or improved CALs.
It is important to realise that decisions on ideal outcome goals must be made on an individual basis, since a target of <25% whole mouth plaque may be compatible with stability for one patient, but others may need to achieve levels <10%. Patients are likely to add to the above outcomes their own measures of success, such as:
no gingival redness
no malodour, etc.
Harold Löe and colleagues, who examined a population of Sri Lankan tea workers who had no access to dental care, performed one of the classical natural history studies. Such population studies are important in helping identify risk factors (Chapter 4) for the disease under scrutiny and are either cross-sectional (i.e. looking for comparisons between populations at one moment in time) or longitudinal (longitudinal studies help link cause to effect and allow disease progression to be assessed). The Sri Lankan tea-worker study took place over a 15-year period and found higher disease prevalence in the tea workers than a control population in Norway. Despite the fact that the tea workers had large amounts of plaque and calculus the progression rate for disease was:
8% in a rapid-progression group (high-risk group)
81% progressed at a moderate rate (medium-risk group)
11% showed no progression and were apparently disease resistant.
These figures are now regarded as being on the high side, owing to the methods used to define disease presence and progression, but, nevertheless, worldwide studies support figures of between 5% and 15% of the population being at risk from severe destruction in adult life. The statistics for early-onset (aggressive) diseases are closer to 1% of Caucasian subjects below the age of 25 years being at risk of significant destruction and up to 3% of Asian and Afro-Caribbean subjects. However, more recent studies by Clerehugh and colleagues have identified progression of attachment loss, albeit slow, in 77% of 167 adolescents aged 14–19 years at some point over a five-year observation period. The attachment loss was related to high levels of plaque and calculus. Nevertheless, whilst a minority of the population appears to be at risk of total tooth loss from periodontitis, a significant number may experience some tooth loss owing to disease that starts at a younger age than previously thought. Periodontitis is believed to account for 35% of all tooth loss.
Until the early 1980s, periodontal disease progression was thought to follow a linear pattern with time (Fig 5-1). High-risk individuals would lose attachment at a rapid rate owing to a higher level of disease activity than lower-risk individuals. However, a series of studies performed between 1982 and 1984 in Boston changed the traditional paradigm and the random burst and multiple asynchronous burst hypotheses were born (Fig 5-2). Goodson and colleagues examined 22 subjects by manual probing of six sites per tooth, every two months for a year. They estimated the errors involved in their probing and set thresholds above this error (around 2.5mm) to signify a real change in attachment level. They determined that the disease process appeared to follow a more random pattern than previously thought where periods of active disease were interspersed with periods of inactivity and repair. The number and magnitude of episodes differed both between and within individual subjects, and sometimes occurred in multiple asynchronous bursts. Some claimed that the high thresholds used in these studies favoured the finding of a more unpredictable pattern of attachment loss. In 1991, a study by a group in Alabama utilised an electronic probe which measured to a degree of accuracy of 0.1mm (i.e. smaller increments) and found linear disease progression in 76% of their 30 subjects. However, t/>