104 Periodontal Disease (Pyorrhea)
The word “pyorrhea” comes from the Greek pyon (“pus”) and rhoia (“to flow”). Thus the definition is a graphic description of the disease in which there is an outflowing of pus from the gingival (gum) tissues of the oral cavity.
The term “pyorrhea” has been used in Europe since the mid-1500s and in America since the late 1800s. However, it was not until 1937 that the American Academy OfPeriodontology abandoned the term in favor of “periodontal disease.”The term “periodontal disease” is used in reference to any disease of the supporting structures of the teeth. These structures include the gingiva, periodontal ligament, and alveolar bone. In simplest terms, periodontal disease can be divided into two distinct, but not mutually exclusive, disease processes. The first involves inflammation of the gingival tissues, called “gingivitis,” and the second, a destructive loss of bone and connective tissue attachment termed “periodontitis.”
Distribution, Incidence, and Epidemiology Epidemiological research during the past 25 years indicates that periodontal disease is one of the most common diseases affecting humankind. There is a direct cause-and-effect relationship between the bacterial colonization on the surface of the tooth and the inflammation (and often consequential destruction) of the tooth’s supporting structures. The rate of destruction varies, and is dependent on the individual’s response to the bacterial irritation.
Periodontal disease is a widespread chronic disease and remains as the primary reason for the loss of teeth in the adult population throughout the world. In fact, virtually all individuals in any population exhibit manifestations of the disease. The prevalence and severity of periodontal disease increase with advancing age, tend to be greater in nonwhites than whites, and are greater for males in both races.
There appears to be a trend toward an increase in the prevalence and severity of periodontal disease in the over-35 age group. This increase is most pronounced in the lower socioeconomic groups and is highly correlated with differing levels of personal and professional oral hygiene care.Many individuals in the older population have had fewer teeth extracted as a consequence of a lower caries (cavities) incidence, which is a result of fluoride use, improvements in dental care, and better public health education. Paradoxically, this increase in the retention rate of teeth in the aging population provides an increase in the number of teeth at risk to the development of periodontitis. The only improvement that has been noted since the 1970s has been a slight reduction in the incidence and severity of gingivitis among the under-35 age group.
Etiology
Numerous studies have firmly established the primary etiologic agent in periodontal disease as “plaque.” Plaque is a colorless, soft, sticky film of bacteria that constantly forms on the teeth. Plaque is composed primarily of different and numerous types of microorganisms as well as adherent mucin (a protein and polysaccharide combination), foodstuffs, and cellular debris. One gram of dental plaque contains more than IO11 bacteria. Plaque can calcify to form a local tissue irritant - calculus (tartar) - to which new colonies of plaque can readily adhere. The microbial population of plaque is variable, and is determined by its location on the tooth surface, the intraoral environment at the time of the plaque formation, and the length of time that the colony has been present in the mouth. When plaque is removed, a new plaque may form, having different characteristics in its quantity, quality, and spatial arrangement. The microorganisms in plaque produce metabolic products and cellular constituents that affect the underlying periodontal tissues. These include exotoxins, endotoxins, antigens, and enzymes.
Any microbial plaque within the gingival crevice causes at least gingivitis. In some areas of the mouth, plaque and gingivitis lead to a destructive periodontitis. Periodontal disease is not caused by the intraoral invasion of foreign pathogens, but rather by colonization of microorganisms of the normal oral flora that exists even in the absence of disease. Certain species of this bacterial plaque play a more significant part in the development and progress of the disease because they increase in relative proportions as well as in absolute numbers. These species are also relevant in that their virulent mechanisms act to disrupt the host’s defenses.
Inadequate or improper oral hygiene techniques must be considered one of the etiologic factors in the development of periodontal disease. Other causative influences include food impaction between teeth, defective dental restorations, malposed teeth, physiological gingival stress due to high frenum attachment, effects of dry mouth, and, to a minor extent, heredity. Of course, there is a strong relationship between all of the etiologic factors and the host’s resistance. The capacity to resist or repair depends on many factors such as adequate nutrition and assimilation, antibody production, hormonal influences, white cell defenses, and formative cell capabilities.
Clinical Manifestations and Pathology
The pathogenesis of periodontal disease must be considered in four stages: colonization, invasion, destruction, and healing.
During colonization, plaque accumulates on the teeth and microbial growth ensues. If the plaque is not removed through adequate oral hygiene, the formation of calculus may begin, and the early stages of microbial invasion into the adjacent gingival tissues commence. Clinical signs may consist of gingival tissues that are tender, swollen, and red. This tissue may bleed upon probing or during brushing. However, periodontal disease usually progresses over the course of many years, and discomfort is a rarity.
It is because of this asymptomatic evolution that persistent bacterial invasion and local irritation can progress into the destructive phase of the disease in which loss of connective tissue and loss of alveolar bone take place. Signs and symptoms of the destructive stage can include pocketing around the tooth within the gingival crevice, gingival recession, suppurative exudate (pus) from the gingiva, and looseness or separation of the permanent teeth.An examination of the teeth may entail numerous tests and measurements for the evaluation of the presence and severity of periodontal disease. These may include visual signs of inflammation, probing pockets’ depths around teeth, evaluation of bleeding on probing, assessment of plaque or calculus accumulation above and below the gingival margin, phasecontrast microscopic analysis of the bacteria recovered from the crevice, assaying the crevicular fluid flow, and interpretation of dental radiographs.
The healing phase is the least understood of the four stages of the disease. However, studies reveal that periodontal disease is episodic, and undergoes periods of remission and exacerbation. Although colonization, invasion, and destruction are interrelated and overlapping, this fourth stage, healing, is clearly distinct in that it is characterized by reduction of inflammation, the repair of gingival tissues, and the sclerosis and remodeling of the alveolar bone.
History and Geography
Antiquity Through the Seventeenth Century Although periodontology has been practiced as a specialty only during this century, the recognition of periodontal disease in various forms has persisted for millennia. The condition of the dental structures of teeth and bone of our ancestors has been revealed through examination and radiographs of skulls discovered in archaeological excavations. There is evidence that periodontal disease existed in some of the earliest members of humankind.
Egyptian mummies show signs of dental caries and periodontal disease as well as primitive, yet valiant, attempts at repairing these dental pathoses.
Indeed, it is believed that the Papyrus of Ebers, which was written around 1550 B.C. by Egyptians, and describes various conditions of the oral cavity, is the earliest written record of dentistry as a distinctive branch of the healing arts. The Greek historian Herodotus described Egypt as being the home of medical specialties, including dentistry.About 1300 B.C., Aesculapius, the mythical physician, supposedly recognized the importance of dental hygiene by recommending cleaning of the mouth and teeth. The physician to the King of Babylon, Arad-Nana, in the sixth century B.C., suggested removing the “film” and “deposits” from the teeth with a cloth-covered index finger. More aggressive periodontal therapy appears about 25 B.C., when Celsus, a Roman physician, treated gums and loose teeth with gold wire and seared the gingiva with red-hot iron. Oral hygiene techniques can also be traced to the Mayan culture and to those living around Central America between 200 B.C. and A.D. 800.
Pliny, a Roman, published his book Natural History in the first century A.D.; in it he describes the prevalence of periodontal disease among the Romans as well as various remedies for its prevention and care. The most notable prescriptions were the use of dentifrices, mouthwashes, and toothpicks; the first mention of “toothbrushing” seems to have been made by the Roman poet Ovid in his Art of Lovemaking, in the first century A.D. The siwak, a fibrous wood product which preceded the toothbrush, was used by the Arabians since the ninth century, and can still be found in use in some areas today. The modern-day toothbrush, however, was invented in China only in 1498.
In 1530, Zene Artzney wrote a book dealing with dental therapeutics in which he discusses the formation and modes of prevention of calculus. He also noted in his writing that loose teeth and their premature loss were a result of “carelessness, weakness, or... disease.” In 1575 Ambroise Pare coined the term “pyorrhea alveolaris,” and describes the teeth attaching to the jaw via “a ligament which goes from the root of the tooth.”
Eighteenth Century to the Present
Pierre Fauchard, the founder of modem dentistry, in his now famous 1728 publication Le Chirurgien Den- tiste, or Traite des Dents, stated that the “relation between the gums and teeth is such that the diseases of one may easily extend to the other.” In 1820, Eleazar Parmly recommended that for the “constant security of the teeth,” all deposits on the teeth must be removed.
He later became known as the “Apostle of Dental Hygiene.” In the latter half of the nineteenth century, John Riggs, who was to become “the father of periodontology,” described periodontal disease as a “progressive process from marginal gingivitis to the final exfoliation of the teeth.” He developed preventive as well as surgical treatments for what he called “scurvy of the gums.” For decades, any such condition was called “Rigg’s disease.”Our understanding of periodontal disease, including its etiology and pathogenesis, grew enormously during the 1900s. Periodontal disease is currently under attack on several fronts, through preventive care, improvements in oral hygiene techniques, mechanical and chemical plaque inhibitors, nutrition, surgical intervention, drugs, and immunology. Much work, however, remains ahead, especially in the relationship of the disease to the host’s immune system.
Jeffrey Levin
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