A full mouth examination and recording is required to document and track periodontal disease including:

Pocket Depth (PD)
Clinical Attachment Loss (CAL)
Bleeding On Probing (BOP)
Plaque index/score
Furcation involvement
Suppuration
Mobility
RadiographsMeasuring disease progression is carried out by measuring probing pocket depth (PPD) and bleeding indices using a periodontal probe. Pockets greater than 3mm in depth are considered to be unhealthy. True pocket formation of 4 mm or more are specifically related to chronic periodontitis. Bleeding on probing is considered to be a sign of active disease. Discharge of pus, involvement of the root furcation area and deeper pocketing may all indicate reduced prognosis for an individual tooth. Evidence of alveolar bone loss is also required to differentiate between true bone loss and not attributions of gingival oedema. Usually, a horizontal pattern of bone loss would be found however, vertical (infrabony) bone loss may also be present on specific sites. A Basic Periodontal Examination (BPE) or Periodontal Screening and Recording (PSR) should give a score of 3 or 4. A correct diagnosis is vital to allow the formation of a specific treatment plan for the patient and to arrest the disease progression. Chronic periodontitis can be further classified into:

Extent (can be either localised affecting < 30% of sites; or generalised if > 30% of sites are affected)
Severity (slight = 1–2 mm CAL; moderate = 3–4 mm CAL; severe ≥5 mm CAL)

2017 classification
Chronic periodontitis is not included within the newer 2017 World Workshop classification.
The anterior dentition occasionally have recession and maxillary anterior and palatal surfaces are more adversely affected. Pathophysiology
Chronic periodontitis is initiated by Gram-negative tooth-associated microbial biofilms that elicit a host response, which results in bone and soft tissue destruction. In response to endotoxin derived from periodontal pathogens, several osteoclast-related mediators target the destruction of alveolar bone and supporting connective tissue such as the periodontal ligament. Major drivers of this aggressive tissue destruction are matrix metalloproteinases (MMPs), cathepsins, and other osteoclast-derived enzymes. Plaque hypothesis
At least two mechanisms of the microbiology of periodontitis have been described: the specific plaque hypothesis and the non-specific plaque hypothesis. Consensus is that neither view is entirely correct, but via a middle path, that damage is due to a shift in the relative populations of more and less dangerous bacteria in the plaque. This is called the ecological plaque hypothesis. The disease is associated with a variable microbial pattern.Anaerobic species of bacteria Porphyromonas gingivalis, Bacteroides forsythus, Treponema denticola, Prevotella intermedia, Fusobacterium nucleatum, Eubacterium sp. have all been implicated in chronic periodontitis.Microaerophile bacteria Actinomyces actinomycetemcomitans, Campylobacter rectus, and Eikenella corrodens also may play a role in chronic periodontitis. Signs and symptoms
In the early stages, chronic periodontitis has few symptoms and in many individuals the disease has progressed significantly before they seek treatment. Symptoms may include the following:

Redness or bleeding of gums while brushing teeth, using dental floss or biting into hard food (e.g.