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Title Page

A Chronological Classification of Periodontal Disease: A

Review.

By Drs. Stephen B. Weinmann and Philip R. Geron

Stephen B. Weinmann, D.D.S. (retired since 1994)

240 Prospect Avenue Apt # 330

Hackensack, New Jersey 07601-2552

Certifications in Radiology, Diagnosis, and Periodontics / Implantology.

Federation Dentaire Internationale (1968-1985)

American Academy of Oral Medicine (1968-1980)

Fellow of the Royal Society of Health (1970-1985)

Alpha Omega Dental Fraternity (1959- to date)

The American Academy of Periodontology (1964 to date)

Lecturing to Dental Interns at Hackensack University Medical Center

Since 2004-current date giving 18-20 lectures per year.

Philip R. Geron D.M.D. Chief of Oral and Maxillofacial Surgery Union

Hospital, Union, NJ.

Board Certifications in the American Academy of Pain Management,

American Board of Orofacial Pains, American Board of Forensic

Odontology, American Board of Forensic Dentistry, and the American

[1]
Board of Forensic Examiners.

Fellowships in the Academy of General Dentistry, Academy of Medicine of

New Jersey, American Association of Oral and Maxillofacial Surgeons,

American Association of Hospital Dentists, and the American Academy

Of Forensic Sciences.

Professor and Course Director in Forensic Dentistry and Medicine UMDNJ,

Ethics committee UMDNJ, and Athletic Team Surgeon and Trainer

Kean University in NJ.

[2]
Abstract

The subject of classification may be considered to be dull by some people,

even contentious by others but it does afford us a means to an end. The evolution

of the history allows us to see how our predecessors thought and how

Periodontal Disease has extended itself as an important entity into many aspects

of the medical field. A good classification allows us to understand the complexity

of the disease that we are attempting to treat. This is a subject that Drs. I

Glickman, I Weinmann, B Orban and the 1987 and 1999 American Academy of

Periodontology have tried to teach. In the near future some medical schools are

considering incorporating the study of Periodontal Disease into their curriculum.

[3]
A Chronological Classification of Periodontal Disease: a review.

1] Kantorowicz---1924 2] Simonton---1927

Inflammatory Disease Chemobacterial

Paradentitis Paradentitis

Dystrophic Disease with little inflammation Systemic

Presenile Atrophy Paradentitis

Dystrophy from occlusal trauma Diffuse atrophy

Dystrophy from lack of occlusion

Diffuse atrophy

3] McCall and Box---1925 4] Haupl and Lang---1927

Gingivitis Paradentitis

Acute Marginal Paradentitis (etiology

Chronic includes mechanical, thermal,

Periodontitis chemical, infectious factors,

Acute as well as, functional disturb-

Chronic ances, tooth malformation,

Periodontitis Simplex (exogenous factors). systemic disturbances, etc.

Periodontitis Complex (or rarefying pericemen- Superficial Marginal Paradentitis

titis fibrosa---endogenous factors). Epithelial changes--regressive

and progressive

[4]
5] Gottlieb---1928 Formation of the pocket

Schmutzpyorrhea. Connective tissue changes

Degenerative or Atrophic subepithelial

Diffuse Alveolar Atrophy (systemic /metabolic). supraepithelial

Paradental pyorrhea. Changes in paradental bone.

Marginal paradentitis profunda

Apical paradentitis

6] Becks---1929/1931 7] Jaccard---1930/1933

Paradentitis Inflammatory complex

Simple Pure gingivitis

Secondary Preparadontal gingivitis

Paradentosis Inflammatory paradentosis

Presenile atrophy Osteopathic dystrophic complex

Paradentosis due to trauma Dystrophic Paradentosis

Paradentosis due to lack of Occlusion Presenile atrophy

Diffuse alveolar atrophy Senile atrophy

Paradentosis secondary to Paradontitis

Paradentoma

8] Roy---1935 9] Robinson---1935

Alveolar pyorrhea, characterized by Clinical types of Paradentosis

precocious senile alveolar resorption Ortho pyorrhea (classical form)

due to upset in general constitution of Hypertrophic pyorrhea (no alveolar

the individual. [5] crest resorption and common


Pyorrhea with pockets—Common, to young people.

Hyperemic, ischemic Rubro pyorrhea--uniform redness

Pyorrhea without pockets—No of the gingiva and marked

Gingivitis, juvenile atrophy, tooth attrition seen.

Osteoporosis, deformatory Senile pyorrhea---a physiological

Pyorrhea alveolar resorption complicated

by peridental inflammation.

Classification systems vary to reflect current changes in our knowledge about periodontal

infections. In the early days Kantorowicz, Simonton, Box and McCall, Haupi and Lang, and

Gottlieb’s classification all were very simple but adequate for 1924-1928 eras. It was not

until 1929-1933 that Beck’s and Jaccard began to approach the more scientific type of

classification that we begin to see a change in thinking as far as their knowledge of the

disease process would permit.

10] Weski---1937

Paradentitis (gingivitis)—hypertrophic, simple, ulcerative

Paradentosis---partial (true form of Paradentosis), and total (alveolar atrophy).

Paradentoma—Epulis (localized form), generalized form (Elephantiasis gingivae).

Weski’s classification was a reversal to the 1924-1928 thinking by keeping it simple.

11] Isadore Weinmann---1934-1957 clinically classified periodontal disease as follows:

I] Marginal Gingivitis

a) Non-suppurative

1] Due to calculus

2] Faulty dentistry [6]


3] Pregnancy---transitory nature

4] Blood dyscrasias

5] Cardiac disease---especially the right side of the heart

6] Renal disturbance

7] Metallic poisoning

8] Diabetes

9] Scorbutus

10] Avitaminosis

11] Food allergy

b) Suppurative-----may result from long-term chronicity of and of the preceding

causes. It may occur suddenly as if the tissues are overwhelmed by pyogenic

microorganisms in debilitated individuals.

II] Gingival Recessions

a) Crescents--due to traumatic occlusion in its early stages--usually fibrous in nature.

b) Clefts ----which usually follow the crescents

a) Festoons---usually due to toothbrush trauma

b) Atrophic---psychologic due to age, or pathologic due to disease

III] Hypertrophic Gingivitis

a) Due to physical irritation

b) Due to post-nasal obstruction (mouth breathers)

c) Due to blood dyscrasias (particularly Leukemia)

d) Due to pregnancy

e) Due to Scorbutus [7]


f) Due to endocrine disturbance

g) Due to prolonged fever

h) Due to metabolic disturbance

Hypertrophies are of two types. We have hard, dense nodular masses (fibrosis) as seen

in mouth breathers; or we may have soft, spongy, jelly-like masses made up of poorly

organized granulation tissues and many faulty blood vessels as seen in pregnancy or

advanced Scorbutus.

IV] Ulcero-membranous Gingivitis

a) Vincent’s infection

b) Tuberculosis ulcers

c) Apthous ulcers

d) Noma

V] Alveolar Atrophy (true alveolaclasia)

a) Normal or psychologic due to age (senile arteriosclerosis even of slight degree)

b) Pathologic

1] Local causes

a] Faulty occlusion, food impaction, toothpicks, pipes, etc., loss of

contacts, faulty dentistry.

b] Due to involvement from inflammatory changes in the soft tissues.

2] Systemic causes

a] Diabetes

b] Syphilis

c] Dysfunction of the endocrines or any metabolic disturbance [8]


This type is referred to as chronic diffuse alveolar atrophy.

Finally in 1934, Dr. I. Weinmann’s classification began the more modern era showing the

true magnitude of Periodontal Disease. Beginning with gingival diseases such as gingivitis

both non-suppurative and suppurative; gingival recession; hypertrophic gingivitis; and ulcero-

membranous gingivitis. The category of non-suppurative gingivitis lists many medical areas

that are repeated again in hypertrophic gingivitis. This was followed by Alveolar atrophy

(Periodontitis) covering faulty occlusion, habit neuroses and systemic causes that are also

mentioned under gingivitis. The extent of Periodontitis coverage was limited to the knowledge

of the time.

12] Thoma and Goldman---1937 13] Fish---1944/1952

Inflammatory conditions Gingivitis

Gingivitis---marginal, hypertrophic, ulcerative Acute ulcerative

Marginal paradontitis Subacute marginal

Degenerative conditions Chronic marginal

Paradontosis (bone destruction affecting Traumatic

other periodontal structures).

Atrophy Pyorrhea

Gingival recession Pyorrhea simplex/Profunda

Presenile atrophy Senile alveolar resorption

Disuse atrophy Neoplasia

Atrophy due to abnormal occlusal trauma Odontoclasma

Syndrome of paradentitis and Paradentosis Cementoma

[9] Fibrous epulis


14] Hine and Hine---1944 15] Orban---1942/1949

Inflammation Inflammatory conditions

Gingivitis (local calculus, faulty Gingivitis---localized to the free

Restorations, poor contact areas margins of the gingiva, swelling,

Drugs). and shallow pockets----acute or

Systemic---nutritional deficiencies, chronic according to duration----

blood dyscrasias, etc. ulcerative or purulent according

Periodontitis simplex (more severe to symptoms----local (extrinsic)

Irritation than gingivitis) infections (physical or chemical)/

Specific entities (tuberculosis, syphilis, systemic (intrinsic) ---dietary

Radiation). deficiency, endocrine disturbances.

Atrophy or degeneration Degenerative conditions

Gingival Recession Gingivosis---systemic etiology,

Trauma degeneration of connective

Senile tissue.

Disuse Periodontosis ----degeneration of

Idiopathic collagenous fibers of the

Periodontitis Complex periodontal membrane.

Periodontitis-----systemic disturbances-- Irregular bone resorption.

Degeneration of connecting fibers in Primarily systemic etiology--

periodontal membrane. inherited inferiority of the

Bone resorption. dental organ. Early no

[10]
Hypertrophy inflammation—late deep

Gingival hypertrophy may accompany pockets with Periodontitis

gingivitis. Atrophic conditions

Trauma periodontal atrophy—bone recession.

Senile precocious ageing.

Disuse Disuse—loss of normal function.

Idiopathic Trauma----toothbrush/orthodontia.

Periodontal traumatism---pressure

Necrosis and its consequences.

Primary (overstress/Bruxism)

Secondary (loss of supporting

tissues).

16] Hulin---1949 17] Held---1949

Inflammatory processes True Paradontopathia

Paradontitis Gingivitis

Exogenous gingivitis Paradontolysis

Tartar Paradontitis

Bacteria Periodontal atrophy

Endogenous gingivitis Symptomatic paradontopathia

Avitaminosis (avitaminosis, blood

Intoxication dyscrasias, etc.).

Degenerative processes Enlargement conditions

paradontosis [11] Epulis, elephantiasis gingivae.


Precocious senile atrophy or

Juvenile paradontosis

Senile paradontosis

Pyorrhetic paradontosis

Traumatic paradontolysis

Paradontomes

Epulis / gingival elephantiasis

18] Pucci---1950 19] Lyons---1951

Marginal paradentitis Inflammatory

Gingivitis

Incipient Acute

Hypertrophic simple, purulent, necrotizing

Desquamative Chronic

Localized simple, purulent, necrotizing,

Advanced hyperplastic, Desquamative,

Paradentosis pigmented

Atrophic Periodontitis

Constitutional simplex

Horizontal alveolar atrophy with complex

Marginal Paradentitis retrogressive periodontosis

Pure form atrophic periodontosis, senile,

Complicated form presenile, hyperfunctional ,

Alveolar decalcification [12] periodontosis gravis includes


Physiologic alveolar atrophy deficiency diseases, endocrine-

Horizontal-precocious senile opathies, systemic toxicities,

Accelerated passive eruption blood dyscrasias, and metabolic

diseases.

Neoplastic

Benign

Fibroma

Elephantiasis gingivae

Malignant

20] Miller---1950 21] Kerr---1951

Gingivitis---acute, subacute, etc Gingivitis---simple, infective, hormonal, atrophic,

Periodontal abscess herpetic gingivostomatitis

Parodonta, pericemental,

Periapical Periodontitis

Alveolaclasia----bone resorption Periodontosis

Nutritional deficiencies Traumatism

Endocrinopathic

Pericementoclasia-----pocket formation

Ulatrophia ----ischemic, calcic, afunctional,

Or traumatic.

[13]
21] Goldman---1956 22] McCall---1956

Inflammation Primary (process originates in the periodontium)

Gingivitis 1. Productive processes (periodontal

Marginal periodontitis hyperplasia)

Dystrophy 2. Destructive processes (periodontitis)

Disease atrophy 3. Degenerative processes (Periodontosis)

Occlusal traumatism Secondary (process originates outside the

Gingivosis periodontium)

Periodontosis 1. Diseases and non-pathological conditions

Having specific periodontal effects

2. Diseases having non-specific periodontal

effects

3. Neoplasms

23] American Academy of 24] Robinson---1959

Periodontology---1957 Gingivitis

Inflammation Periodontitis

Gingivitis Periodontosis

Periodontitis Atrophy

Primary (simplex) Hypertrophy and hyperplasia

Secondary (complex) Traumatism

Dystrophy 25] Carranza---1959

Occlusal traumatism Inflammatory periodontal syndrome

Periodontal disuse atrophy [14] Superficial, deep


Gingivosis Traumatic periodontal syndrome

Periodontosis Compensated, uncompensated

26] Ray---1962 Combined periodontal syndrome

Inflammatory Compensated, uncompensated

Gingivitis

Periodontitis

Degenerative

Gingivosis

Periodontosis

Trauma

Atrophy

Proliferative

Gingival hyperplasia, periodontal neoplasms

From 1937-1962 The classifications took a reversal in length in an attempt to condense their

complexity. But, the classification systems of Thoma and Goldman, Fish, Hine and Hine,

Orban, Hulin, Held, Puci, Lyons, Miller, Kerr, Goldman, McCall, The American Academy of

Periodontology, Robinson, Carranza, and Ray all fall short of being thorough. Again a reversal

of by-gone eras. All the classifications for this 25 year period did not reflect any improvement.

27] Glickman---1964

Classification of Gingival Disease

I. Uncomplicated gingivitis

a) Chronic marginal gingivitis

b) Acute NUG [15]


c) Acute herpetic gingivostomatitis and other viral infections

d) Allergic gingivitis

e) Nonspecific gingivitis

f) TB and Syphilis

g) Moniliasis and other fungal infections

h) Pyostomatitis vegetans

II. Combined gingivitis

a) Dermatoses

b) Chronic Desquamative gingivitis (Gingivosis)

c) Chronic menopausal gingivostomatitis (senile atrophic gingivitis)

d) Benign mucous membrane pemphigoid

III. Conditioned gingivitis

a) Gingivitis in pregnancy and puberty

b) Gingivitis in vitamin C deficiency

c) Gingivitis in Leukemia

IV. Gingival enlargement

a) Inflammatory

b) Noninflammatory hyperplastic

c) Combined

d) Conditioned

e) Neoplastic

f) Developmental

V. Recession [16]
a) Gingival atrophy

Classification of Periodontal Disease

A. Periodontitis

1) Simple Periodontitis

2) Compound periodontitis

B. Periodontosis

1) Early

2) Advanced

C. Trauma from occlusion

D. Periodontal atrophy

1) Presenile atrophy

2) Disuse atrophy

Dr. I. Glickman’s classification was an attempt to support that of Dr. I. Weinmann in 1934

and trying to right the ship in the correct direction; but, again the classification of Periodontitis

was in my opinion far short of what it could have been. We had enough knowledge of osseous

problems to have done a more thorough classification. In many states the use of hip marrow

grafting was already common practice. And, the gingival portion of Dr.Glickman’s system had

a lot of systemic disease overlapping.

28] Drum---1975

Dr. Drum felt that “all persons afflicted by periodontal diseases exert parafunctions” that

may be classified as follows:

1] Physically motivated parafunctions---neurotic phenomina such as Bruxism,

Bruxomania, clenching/grinding of the teeth, nail biting, thumb sucking, etc. [17]
2] Stress-motivated parafunctions---non-neurotic phenomina such as athletes, truck

drivers, combat related stress, workers on high rise buildings/bridges, severe pain,

etc.

3] Habitual parafunctions---tailors, seamstresses, bootmakers, upholsterers, wind

instrument players, chewing on pens/pencils, etc.

4] Endogenous parafunctions---muscle spasms caused by diseases such as tetanus,

meningitis, epilepsy, etc.

5] Hyper-compensating parafunctions---exaggeration of normal compensating motions

triggered by occlusal interferences and other disturbances in the mouth.

All of these depend upon the following factors:

1] Force of the parafunctions

2] Directions of that force

3] Duration of the parafunctions

4] Intervals between periods of parafunctions

5] Configuration of the roots

6] Configurations of the alveolar bone

7] Position of teeth

Dr. Drum was attempting to revitalize some older theories that most if not all periodontal

problems could be corrected by occlusal equilibration. A better explanation of the

aforementioned may be better understood through the review and the application of Frost’s

Laws of Bone Formation and reference to Dr. Sidney Sorrin’s classification of habitual

contributions to periodontal disease and its revision by Dr. S. Weinmann.

[18]
29] American Academy of Periodontology---1987

I] Gingival Disease

A] Gingivitis

1) Nonspecific (plaque, bacteria, and their products)

2) Acute Necrotizing Ulcerative Gingivitis (ANUG)

B] Manifestations of Systemic Diseases and Hormonal Disturbances

1) Acute Herpetic Gingivostomatitis

2) Blood dyscrasias

3) Leukemias

4) Autoimmune Diseases (Pemphigus)

5) Diabetes

6) Sex Hormones

C] Drug Associated---Gingival inflammation and/or enlargement (dilantin

Hyperplasia).

D] Miscellaneous gingival changes associated with various etiologies

1) Atrophy

2) Cyst formation

3) Hyperplasia

4) Neoplasia

5) Infection

6) Irritation

7) Trauma

II] Mucogingival conditions [19]


A] Recession

B] Frena

C] Muscle attachments

D] Minimal attached gingivae

III] Periodontitis

A] Adult Periodontitis

1) Slight

2) Moderate

3) Advanced

4) Refractory

B] Juvenile periodontitis (JP)

1) Prepubertal (generalized or local)

2) Generalized (GJP---circumpubertal or postpubertal)

3) Localized (LJP) thought to be associated with

a) Actinobacillus Actinomycetemcomitans

b) Heredity

c) Abnormalities in white blood cell functions (predilection for central

incisors and first molars)

C] Periodontal Abscess

IV] Pathology associated with occlusion (associated with TMJ disorders)

A] Trauma from occlusion

B] Bruxism

[20]
V] Other conditions of the attachment apparatus---all pathologic processes of the

periodontium including:

A] Infection

B] Abrasion

C] Trauma

D] Cystic changes

E] Degenerative changes

F] Neoplastic changes

The 1987 Academy of Periodontology Classification refined and better organized the systems

expressed by Dr. I. Weinmann (1934) and Dr. I. Glickman (1964). This was the first time that

Drug-associated gingival disease was recognized; but, it was still far short on the subject.

This holds true for their systemic disease and endocrine involvement. The Periodontitis

Section was broader in depth of coverage than all of its predecessors. This classification did

not compare as well to the 1999 classification on Periodontal Disease.

30) American Academy of Periodontology---1999

I. Gingival Diseases 3. Gingival diseases of fungal origin

A. Dental plaque-induced gingival diseases a. Candida-species infection

1. Gingivitis associated with dental plaque only 1. generalized gingival candidiosis

a. without other local contributing factors b. linear gingival erythema

b. with local contributing factors (see VIII A) c. histoplasmosis

2. Gingival diseases modified by systemic factors d. other

a. associated with the endocrine system 4. Gingival lesions of genetic origin

1] puberty-associated gingivitis a. hereditary gingival fibromatosis

2] menstrual cycle-associated gingivitis b. other

[21]
3] pregnancy-associated 5. Gingival manifestations of systemic conditions

a] gingivitis a. mucocutaneous disorders

b] Pyogenic Granuloma 1] lichen planus

4] diabetes mellitus-associated gingivitis 2] pemphigoid

b. associated with blood Dyscrasias 3] Pemphigus vulgaris

1] leukemia-associated gingivitis 4] Erythema multiforme

2] other 5] lupus erythematosis

6] drug-induced 7] other

3. Gingival diseases modified by medications b. allergic reactions

a. drug-influenced gingival diseases 1] dental restorative materials

1] drug-influenced gingival enlargements a] mercury

2] drug-influenced gingivitis b] nickel

a] oral contraceptive-associated gingivitis c] acrylic

b] other d. other

4. Gingival diseases modified by malnutrition 2] reactions attributable to

1] ascorbic acid-deficiency gingivitis a] toothpastes/dentifrices

2] other b] mouthrinses/mouthwashes

B. Non-plaque-induced gingival lesions c] chewing gum additives

1. Gingival diseases of specific bacterial origin d] foods and additives

a. Nesseria gonorrhea-associated lesions 3] other

b. Treponema pallidum-associated lesions 6. Traumatic lesions (factitious, iatrogenic,

c. Streptococcal species-associted lesions accidental)

d. other a. chemical injury

2. Gingival diseases of viral origin b. physical injury

a. herpesvirus infections c. thermal injury

1] primary herpetic gingivostomatitis 7. Foreign body reactions

2] recurrent oral herpes 8. Not otherwise specified (NOS)


3] varicella-zoster infections [22]

b. other

II. Chronic Periodontitis VII. Periodontitis associated with Endodontic Lesions

A. Localized A. combined periodontic-endodontic lesions

B. Generalized VIII. Developmental or Acquired Deformities and conditions

III. Aggressive Periodontitis A. Localized tooth-related factors that modify or

A. Localized predispose to plaque-induced gingival diseases/

B. Generalized Periodontitis.

IV. Periodontitis as a manifestation of 1. Tooth anatomic factors

Systemic Diseases 2. Dental restorations/appliances

A. Associated with hematological disorders 3. Root fractures

1. Acquired Neutropenia 4. Cervical root resorption and cemental tears

2. Leukemias B. Mucogingival deformities and conditions around teeth

3. Other 1. Gingival/soft tissue recession

B. Associated with genetic disorders a. facial or lingual surfaces

1. Familial and Cyclic Neutropenia b. interproximal (papillary)

2. Down syndrome 2. Lack of keratinized tissue

3. Leukocyte adhesion deficiency syndromes 3. Decreased vestibular depth

4. Papillon-Lefėvre syndrome 4. Aberrant frenum/muscle position

5. Chediak-Higashi syndrome 5. Gingival excess

6. Histocytosis syndromes a. pseudopocket

7. Glycogen storage disease b. inconsistent gingival margin

8. Infantile genetic Agranulocytosis c. excessive gingival display

9. Cohen syndrome d. gingival enlargement (see 1.A.3 and 1.B.4

10. Ehlers-Danlos syndrome (Types IV and V) 6. Abnormal color

11. Hypophosphatasia C. Mucogingival deformities and conditions on

12. Other edentulous ridges

C. Not otherwise specified (NOS) 1. Vertical and horizontal ridge deficiency


[23]

V. Necrotizing Periodontal Diseases 2. Lack of gingival/keratinized tissue

A. Necrotizing ulcerative gingivitis (NUG) 3. Gingival/soft tissue enlargement

B. Necrotizing ulcerative Periodontitis (NUP) 4. Aberrant frenum/muscle position

VI. Abscesses of the Periodontium 5. Decreased vestibular depth

A. Gingival abscess 6. Abnormal color

B. Periodontal abscess D. Occlusal trauma

C. Pericoronal abscess 1. Primary occlusal trauma

2. Secondary occlusal trauma

It appears that throughout history we went from short to lengthy to moderate to longer

classifications as we realized the multiple complications of pure periodontitis to the role of

medical factors in the periodontal disease process and the role of periodontal disease in

contributing to medical problems. Now we are considering the enormity of periodontal

disease as it relates to the patients’ overall health. While most of the classifications listed

are for pure historical comparison the only classifications that are of significant importance

are those of Dr. I. Weinmann (1934-1957), Dr. I. Glickman (1964), and The American

Academy of Periodontology (1987 and 1999). These all show the value of a good and

thorough classification.

But, in the 1999 classification the following are points of disagreement; (1) the word “other”

too freely used; (2) under “drug-influenced gingival diseases” it does not mention the effects

of alcohol, cocaine, heroin, crack, and heart medications (Alpha & Beta blockers, Mevacor,

and Lipitor) that are well documented in the literature as causing increased plaque formation

and stimulating gingival overgrowth; (3) there is no discussion of TMJ and stress as an

aggravating factor in periodontal disease; (4) there is no mention of the biochemical

mediators of the gingival crevicular fluid and their affects upon the periodontal tissues
[24]

(such as the cytokines IL-1α, IL-1β, IL-6, IL-8, IL-10, TNF-α, MMP 3, PGE2, etc.); (5)

the section on occlusal trauma does not in our opinion adequately cover the magnitude of

the pathology associated with occlusion, malocclusion, and the habit neuroses that alter

occlusion and contribute to TMJ malfunction; (6) we still believe in the breakdown of

“adult Periodontitis” over “chronic Periodontitis” (especially to the lay person to whom

chronic means non-curable and because it is non-curable the patient(s) would wonder

why they should bother to undergo treatment); and (7) with Juvenile (early onset)

Periodontitis which is age-related instead of “Aggressive Periodontitis” which means

Rapidly Progressing Periodontitis (RPP) independent of age despite totally adequate

periodontal therapy. These are two separate entities and should be recognized as such; (8)

there is still considerable overlap in disease categories. For example, in aggressive

Periodontitis we have two categories that involve. Localized Juvenile Periodontitis (LAP)

and Generalized Juvenile Periodontitis (GAP). Both forms share the following features---

rapid loss of attachment and bone; patients are clinically healthy except for the presence

of Periodontitis; and familial aggregation. LAP patients have a big serum antibody response;

whereas, GAP patients have a poor antibody response to the infecting agents; and (9)

NUP involves a great deal of alveolar bone and attachment loss; whereas, in NUG loss of

clinical attachment is generally absent. It is with our sincere hope that this paper be

received by the professional community as a desire to enliven a rather mundane but

necessary subject; as well as attempting to make the classification of periodontal disease

a more realistic, current concept as we become aware of more medical problems that are

influenced by periodontal diseases and the more periodontal problems that are affected
[25]

by medical diseases. The classification of Periodontal Disease should be kept as simple

and thorough as possible. This classification can be added to more simply than past

attempts without semantics becoming a major stumbling block.

A recommendation for the next classification is that wherever possible the insertion of the

periodontal codes, the ADA codes, and the International codes be included. For some

reason since the 1960’s the addition of the code numbers has never been attempted.

This will help to facilitate insurance claims and office procedures as well as not allowing

the insurance companies a back door to denying claims. Perhaps we should add a

section devoted entirely on Implantology and surgeries connected to improving implant

procedures since so many periodontal practices are now doing 80% Implantology and

20% pure Periodontics.

The comments I hear from general practitioners is that when the dentist refers a patient

for straight forward periodontal therapy they end up as implant cases. I fear that we are

driving more general practitioners into doing both periodontal surgery as well as implants

since most Periodontists are riding the “implant express”. We should be more cognizant

of what our referring general practitioners want from us. This is some additional food for

thought.
[26]

REFERENCES

American Academy of Periodontology in Current Procedural Terminology, 1957.

American Academy of Periodontology in Current Procedural Terminology, 1987, 1-3.

Armitage GC: Development of a Classification System for Periodontal Diseases and

Conditions. Annals of Periodontology 1999 4(1): 1-6.

Becks H: “General Aspects in Pyorrhea Research.” Paciffic Dental Gazette 1929, 37: 259-

282.

Carranza FA; Carranza FA Jr: A suggested classification of common periodontal

disease. The Journal of Periodontology 1959: 30: 140-147.

Carranza FA Jr: Glickman I: Glickman’s Clinical Periodontology. Philadelphia, Saunders:

1990; 202-209

Drum W: A new concept of periodontal diseases. The Journal of Periodontology, 1975:

46(8); 504-510.

Fish EW: Classification, Clinical Course and Diagnosis of Parodontal Disease. In Parodontal

disease: a manual of treatment and atlas pf pathology. Philadelphia, Lippincott 1952

(original 1944) ; 52-72.

Goldman: Schluger; Fox: Periodontal Therapy. St Louis, Mosby 1956, pg15-52.

Gottlieb B: Parodontal Pyorrhea and Alveolar Atrophy. Journal American Dental Assoc-

iation 1928 15: 2196.

Haupi K; Lang FJ: Marginal Paradontitis. Zeitschrift fur Stomatologie, 1927, 25: 1110-1123.

Held AJ: Nomenclature and Classification of Diseases of the Dental Structures.

Paradontologie 1949 3: 85.


[27]

Hine MK; Hine CL: Classification of Periodontal Disturbances. Journal American

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