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Periodontal disease in ancient populations.

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AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY 71:173-183 (1986)
Periodontal Disease in Ancient Populations
N.G. CLARKE, S.E. CAREY, W. SRIKANDI, R.S. HIRSCH, AND
P.I. LEPPARD
Department of Dentistry, The Uniuersity of Adelaide, Adelaide,
South Australia 5000
KEY WORDS
lesions
Periodontal disease, Prehistory, Alveolar bone
ABSTRACT
Recent clinical and anthropological findings indicate that the
conventional concept of the pathogenesis of periodontal disease requires review. The periodontal lesion has been defined as a generalised horizontal loss
of crestal bone resulting from host immune and inflammatory responses triggered by the action of commensal bacteria, and the extension of gingivitis into
the deeper periodontium to become periodontitis has been assumed to occur
slowly but steadily over many years. Anthropological and clinical investigations reveal that the widespread loss of crestal tissue is relatively unusual and
that lesions of the alveolus are commonly localised and severe. Longitudinal
studies have shown that the disease progresses in bursts and is stable in both
the gingivitis and periodontal modes in between the burst activity. The findings of the present study demonstrate that generalised horizontal periodontitis
has been unusual and has not been responsible for tooth loss. Other factors
responsible for deficient alveolar margins in dry bones have been overlooked
in most studies, leading to overassessment of the incidence of periodontal
disease in postmortem materials; the same assumptions have led to overassessment of periodontal disease in clinical studies and practice.
Periodontal disease is considered to be an
ancient affliction of humans (Gold, 1985). The
traditional concept of the pathogenesis of the
disease cites the involvement of commensal
oral microbes in the initiation and progression of the disease. Bone lost from the alveolar crest by active resorption is associated
with loss of periodontal ligament integrity.
In turn, exposed cementum of the root becomes covered by extension of the gingival
epithelium to form a more apical attachment
and a periodontal pocket. It is thought that
over a period of 30-40 years bacterial products provoke the host into a damaging defensive reaction that is slowly progressive (Loe
et al, 1978). Extension of the lesion from the
gingivae into the alveolus in time was
thought to result in reduced tooth support
and eventually in tooth loss.
Page and Schroeder (1976) stated that the
natural history of the disease assumes that
some time will be spent in the gingivitis
phase of the lesion before the inflammation
extends into the deeper periodontal structures, although they later conceded that this
0 1986 ALAN R. LISS, INC
may not be the case (Page and Schroeder,
1982). Confusion occurred regarding the
interpretation of the results of clinical and
epidemiological studies because gingivitis
typically does involve wide areas of the
mouth, and the assumption was made that
the inflammation would extend to the underlying bone. The dental techniques which
have evolved over the last two centuries to
prevent or minimize the long-term consequences of periodontal disease reflect these
assumptions.
While there is no evidence to support the
assumption that gingival inflammation
would extend to the underlying bone, support can be offered for the concept that gingivitis does not usually extend into the
underlying bone (Listgarten et al., 1985), and
that periodontitis does not progress continuously (Socransky et al., 1984). The findings of
Received December 13, 1985; revision accepted May 5, 1986.
Address reprint requests to Dr. N. C . Clarke at the above
address.
174
N.G. CLARKE ET AL
TABLE 1. Location of cranial materials
Museum
Location
S. Australia Mus.
Bishop Mus.
Univ. of Arizona
N. Western Univ.
Smithsonian
Smithsonian
Smithsonian
Adelaide
Hawaii
Tucson
Evanston
Washington
Washington
Washington
Smithsonian
Harvard Univ.
Harvard Univ.
Washington
Harvard
Harvard
Am. M. Nat. Hist.
Am. M. Nat. Hist.
Am. M. Nat. Hist.
Edinburgh Univ.
Edinburgh Univ.
Brit. M. Nat. Hist.
Brit. M. Nat. Hist.
Royal Coll. Surg.
Duckworth Mus.
Duckworth Mus.
Mus. de 1’Homme
Mus. de 1’Homme
Copenhagen Univ.
Copenhagen Univ.
Copenhagen Univ.
Copenhagen Univ.
Om Monastery
Prague Mus.
Prague Mus.
Hadassah Univ.
Witwatersrand Univ.
Otago Univ.
Auckland Mus.
Aust. Nat. Univ.
New York
New York
New York
Edinburgh
Edinburgh
London
London
London
Cambridge
Cambridge
Paris
Paris
Copenhagen
Copenhagen
Copenhagen
Copenhagen
Ry (Aarhus)
Prague
Prague
Jerusalem
Johannesberg
Dunedin
Auckland
Canberra
Sagne and Olsson (1977) and Costa (1982)
show that the conventional scenario is not
true for a wide range of premodern ethnic
groups. Moreover, the causes of bone loss observed in dry skulls frequently have been
misinterpreted, resulting in overestimation
of both the incidence and severity of periodontal disease (Costa, 1982).
In the present study a n attempt was made
to discriminate between alveolar modifications resulting from bacterially related crestal bone resorption (periodontal disease) and
anatomical, developmental, physiological,
and other pathological defects that may be
responsible for the increased distances between the cemento-enamel junction (CEJ)
and the alveolar crest (AC) in excess of the
“normal” 2mm. This discrimination between
the variety of causes of deficient alveolar
bone probably accounts for the low incidence
GrouD
No.
Aust. Aborigine
Mokapu, Oahu
Grasshopper Ind.
Woodland Ind.
Eskimo (Alaska)Tanunuk
Egypt (XI1 Dyn)
Peru (Chicama,
Pachacamac)
Terry (modern)
Mexico (Yucatan)
Yugoslavia (medieval)
Panik
New Britain (Ralum)
Bolivia (Sicasica)
Hungary (Keszo Hidegkut)
India (Southern Prov)
China (Hokien)
Romano-Brit. (Poundbury)
Egypt (Hawara) 2-3rd cent.
Ancient Brit. (Breedon)
Somali
India (N. W. Prov)
Romano-French (Maule)
Japan (Izumu)
Eskimo (Greenland)
Romano-Danish (300 B.C.)
‘modern’ Danish
Egypt (Nubia 350 A.D.)
Danish (800 A.D.)
Czech (Ducove middle ages)
Czech (Rajarad 9th cent.)
Jerusalem
Bantu (modern)
Maori
Maori
Aust. Aborigine
52
49
50
40
40
32
47
23
39
40
20
20
40
20
20
40
20
20
10
15
54
40
22
37
21
33
43
33
40
16
51
46
54
42
-
of bone loss attributable to periodontal disease in this study.
MATERIALS
Sku 11 selection
Cranial materials located in 20 museums
in ten countries from 34 populations were
measured for bone loss believed to be of a
periodontal origin. In total, 30,057 teeth from
1,149 skulls were documented to provide the
data shown in Tables 2-7. The jaws of two
modern populations from South Africa and
St. Louis (U.S.A.)were included for comparison with the ancient material. The sample
populations are listed in Table 1.
Skull selection was based upon maximal
development of dental pathology. In all instances, worst-case specimens were diligently sought, and the data reflect the most
severe conditions that could be found in each
175
DISEASE IN ANCIENT POPULATIONS
group. Where the collections contained a n
abundance of materials, the first 40-50 suitable skulls were used (except for the Terry
collection where only 23 samples were examined). In smaller collections, or in instances in which the incidence of alveolar
pathology was very low, all skulls were examined and the sample size reflects the total
number of suitable skulls available for that
population. It was not intended that the sample be representative of the population but
that the maximum incidence of periodontal
pathology should be measured. Most of the
skulls selected were in sufficiently good condition to provide confidence in the estimation
of bone height and the presence or absence of
disease.
METHODS
Measurement criteria
In estimating the alveolus lost as a result
of periodontal disease, the general practice of
assigning any increase over 2mm in the CEJ
to AC distance as periodontal disease was
rejected. It was recognised that there is a
need to account €or anatomical, developmental, pathological, and physiological
causes of increase over 2mm in the CEJ to
AC distance. Several reports have shown that
there is a progressive increase in the CEJ to
AC distance throughout life, and some evidence exists to indicate that this “physiologic” bone loss corresponds with the degree
of compensatory process of continuous active
eruption (Murphy, 1959; Newman and Levers, 1979; Tal, 1985; Whittaker et al., 1985).
Periodontal disease was recorded only
when the bone crest of the alveolar margins
showed either the loss of the cortical surface,
revealing porous cancellous spaces, or a n altered morphology of the alveolar crest. These
changes resulted in the appearance of a porous bony surface or a shelflike margin instead of the normal knife-edged configuration
(Fig. 1).Great care was taken with the assessment of the bony status, and when bone
was considered to have been lost as a result
of periodontal disease, measurements were
made on both the buccal and proximal surfaces. A William’s periodontal probe was used
to classify the bone loss into three categories:
0-2mm, 2-4mm, and > 4mm. While the difficulties in assessing both quality and quantity of alveolar bone may not have been
entirely overcome, the data reflect the best
effort to be accurate, objective, and consis-
tent. All materials were measured by the
same investigator (N.G.C.), with the exception of the South Australian collection, which
was measured by N.G.C. and W.S. together.
In the present study, periodontal granulomae with origins apical to the alveolar crest
were classified as being of pulpal origin. It
was possible to record the location of a typical dental abscess a t the root apex and identify the extension of the abscess along the
ligament to reach the crest (Fig. 2). Lesions
in this category traditionally have been erroneously called periodontal lesions, as clinically they are probed as periodontal pockets.
Lesions located in the root fork (furcation
lesions) without evidence of adjacent crestal
mesial or distal proximal periodontal disease
were also considered to be of pulpal origin
(Fig. 31, as were lateral wall lesions where
discrete granulomae formed without continuity with the crestal tissue (Fig. 4). The
present data therefore discriminated between alveolar bone loss of marginal (gingival) origin (Fig. 1)and alveolar bone loss of
pulpal origin resulting from the extension of
the lesions along the ligament to discharge
inflammatory exudate into the gingival sulcus (Figs. 2-4).
Only data for periodontal lesions of marginal (gingival) origin are presented here,
and in Tables 3, 4, 6 , and 7 the data shown
are for the right quadrants only.
Data processing
The data were processed by a Vax computer of The University of Adelaide using
the Biomedical Package (BMDP) software
package developed by Statistical Sofeware,
Inc., of the University of California, Los Angeles. Statistical tests for significance were
considered inappropriate due to the lack of
randomness which results from selecting
“worst case” skulls, and to the large sample
sizes. Data are therefore presented as percentages for comparison and interpretation.
RESULTS
The data for teeth free from periodontal
disease, and for the three categories of bone
loss by group, indicate that a marked difference existed between the premodern and
modern groups (Table 2). The incidence of
teeth free from periodontal disease in the
premodern groups ranged from 99.9% (Romano-Danish) to 76% (Mokapu), with twothirds of the groups showing more than 90%
176
N.G. CLARKE ET AL.
Fig. 1. Moderate marginal periodontal disease reveals both an altered bone morphology of
the crest and “porosity” in the surface of the bone.
Fig. 2. Severe localised vertical loss of bone. Severe attrition resulted in the exposure of the
pulp chamber and establishes the relationship between heavy tooth wear and periodontal
lesions.
DISEASE IN ANCIENT POPULATIONS
Fig. 3. Alveolar bone was destroyed in the furca of the 36. A pulpal etiology for the furcation
lesion may be deduced from the presence of an abscess on the apex of the mesial root.
Fig. 4. Lateral root abscesses are present on two adjacent teeth. The crowns show evidence
of severe tooth wear.
177
178
N.G. CLARKE ET AL.
TABLE 2. Degree ofperiodontal disease by group
Alveolar bone loss
Buccal (proximal)
Normal
Aust. Aborigine
Mokapu Indian
Grasshopper Indian
Woodland Indian
Eskimo (Alaska)
Egypt (XI1 dyn)
Peru (Chicama)
Mexico (Yucatan)
Yugoslav (medieval)
New Britain @alum)
Bolivia (Sicasica)
Hungary (Hidegkut)
India (S. Prov)
China (Hokien)
Rorn-Brit. (P'bury)
Egypt (Hawara)
British (Breedon)
Somali
India (N. W. Prov)
Rorn-French (Made)
Japan (Izumu)
Eskimo (Greenland)
Rom-Danish (300 B.C.)
Modern Danish
Egypt (Nubia 350 A.D.)
Danish (800 A.D.)
Czech (Ducove)
Czech (Rajarad)
Jerusalem
Maori
Maori
Aust. Aborigine
% Total teeth
Terry (modern)
Bantu (modern)
% Total teeth
94.9 (92.1)
70.5 (81.3)
80.7 (82.2)
75.6 (83.6)
88.8 (91.0)
89.2 (90.6)
98.3 (95.4)
90.8 (89.0)
78.7 (79.5)
86.1 (82.7)
93.3 (92.6)
81.3 (80.7)
84.6 (86.4)
84.8 (77.6)
94.6 (95.9)
94.0 (94.4)
97.6 (97.1)
97.7 (95.5)
89.9 (79.3)
99.1 (98.7)
95.2 (90.0)
99.2 (99.0)
100.0 (99.8)
89.9 (86.7)
99.8 (98.3)
94.7 (91.8)
97.5 (97.0)
96.4 (93.2)
86.8 (79.5)
99.1 (98.9)
98.1 (98.0)
97.4 (93.2)
90.8 (90.3)
66.2 (64.4)
78.2 (70.8)
74.7 (68.9)
% Mild
4.2
13.5
11.8
16.3
5.8
7.4
1.6
5.9
10.1
9.2
5.4
11.6
10.2
12.2
4.5
3.9
2.0
1.5
5.9
0.4
3.6
0.5
0.0
8.1
0.2
2.9
1.5
2.7
6.3
0.9
0.9
1.8
5.7
13.0
14.1
13.8
(5.6)
(6.6)
(9.0)
(9.6)
(5.4)
(6.1)
(3.8)
(6.6)
(9.0)
(10.3)
(5.4)
(12.2)
(9.1)
(18.3)
(2.9)
(3.6)
(2.2)
(3.8)
(10.1)
(0.8)
(8.5)
(0.2)
(0.2)
(10.2)
(0.8)
(5.1)
(2.7)
(5.3)
(11.2)
(1.1)
(0.0)
(3.9)
(5.8)
(15.6)
(21.0)
(19.4)
% Moderate
0.8 (1.7)
11.6 (8.5)
3.9 (5.7)
7.7 (6.5)
5.1 (2.7)
3.3 (3.1)
0.1 (0.7)
3.1 (3.9)
9.6 (9.8)
4.5 (6.2)
1.3 (1.7)
6.2 (6.3)
3.8 (3.6)
2.0 (3.0)
0.7 (1.1)
2.1 (1.9)
0.2 (0.6)
0.8 (0.4)
3.9 (8.9)
0.5 (0.5)
1.3 (1.5)
0.3 (0.5)
0.0 (0.0)
1.8 (2.6)
0.0 (0.8)
2.1 (2.9)
1.0 (0.2)
0.9 (1.5)
5.2 (7.7)
0.0 (0.0)
0.5 (0.7)
0.8 (2.7)
2.9 (3.1)
14.4 (12.8)
6.8 (7.1)
9.0 (8.8)
9% Severe
0.1 (0.5)
4.4 (3.6)
3.5 (3.1)
0.3 (0.4)
0.3 (0.8)
0.1 (0.1)
0.0 (0.1)
0.1 (0.5)
1.6 (1.6)
0.2 (0.8)
0.0 (0.3)
0.8 (0.8)
1.3 (0.0)
1.0 (1.2)
0.2 (0.1)
0.0 (0.2)
0.2 (0.2)
0.0 (0.4)
0.2 (1.7)
0.0 (0.0)
0.0 (0.0)
0.0 (0.3)
0.0 (0.0)
0.2 (0.5)
0.0 (0.0)
0.3 (0.2)
0.0 (0.0)
0.0 (0.0)
1.6 (1.6)
0.0 (0.0)
0.5 (0.5)
0.0 (0.3)
0.6 (0.7)
6.5 (7.2)
0.8 (1.1)
2.5 (2.9)
n
1,487
1,371
1,106
1,097
1,093
733
690
1,038
1,098
595
299
,056
,125
597
,085
534
543
264
406
777
,094
603
999
607
836
,263
881
,152
365
1,008
1,032
1,245
26,079
585
1,393
1.978
n, number of teeth in each group; mild, 0-2mm; moderate, 2-4mm; severe, > 4mm.
of teeth to be disease free and nearly one
third to be disease free at the 79-90% level.
Only one group (Mokapu) showed less than
79% of teeth to be disease free.
In the two modern groups, 74.5% (South
Africa) and 65.3% (Terry) of teeth were free
of periodontal disease. The only sample from
the premodern groups that showed a level of
periodontal disease comparable to that of the
modern groups was Mokapu, and there was
doubt concerning whether that group may in
fact be relatively modern.
to periodontal disease. The incidence of buccal periodontal disease was greater in the
mandible than in the maxilla for all categories of severity (Table 3). Mild bone loss
was observed adjacent to 5.6% of teeth, moderately involved teeth constituted 2.9% of the
total. There was a very low incidence of severely involved teeth (0.6%), and this category was found in only four of the 32
premodern groups examined. In no case was
the loss of alveolar tissue which was due to
periodontal disease of sufficient severity to
jeopardise tooth retention.
BUCCAL ALVEOLAR BONE LOSS
When buccal bone loss by tooth type was
Premodern groups
considered in the maxilla, the first and secThe majority of teeth examined (90.8%) ond molars were the most frequently inwere free from buccal alveolar bone loss due volved in all categories of periodontal disease
179
DISEASE IN ANCIENT POPULATIONS
TABLE 3. Alveolar bone loss due to periodontal disease in 32 premodern and two
modern groups’ buccal surfaces
Premodern
Modern
Maxilla
No disease
Mild disease
(0-2mm)
Moderate disease
(2-4mm)
Severe disease
(> 4mm)
Total teeth
Mandible
Maxilla
Mandible
n
(%)
n
(%)
n
(%I
n
(%)
13,525
713
192.2)
(4.9)
11,972
875
(89.21
(6.5)
759
121
(77.3)
(12.3)
718
152
(72.0)
(15.3)
352
(2.4)
466
(3.5)
87
(8.9)
92
(9.2)
76
(0.6)
100
(0.7)
15
(1.5)
34
(3.4)
14,666
13,413
982
996
TABLE 4. Alveolar bone loss due to periodontal disease in 32 premodern
groups’ buccal surfaces of individual teeth
Tooth
18
17
16
15
14
13
12
11
Total
No. of teeth
758
878
860
929
972
1,002
973
950
7,322
Upper right quadrant
Severe (%)
0.7
Moderate (%)
3.7
Mild (%)
7.1
Normal (%)
88.5
0.9
4.4
10.0
84.6
1.4
5.0
7.7
85.9
0.2
2.0
5.1
92.8
0.2
2.2
4.3
93.3
0.2
1.2
2.9
95.7
0.2
0.9
2.5
96.4
0.0
1.1
1.6
97.2
0.4
2.5
5.0
92.1
47
46
45
43
42
41
Total
Tooth
48
44
No. of teeth
725
773
722
867
914
929
908
873
6,711
Lower right quadrant
Normal 1%)
91.4
5.4
Mild (%I
Moderate (%a)
2.8
Severe (%)
0.4
84.9
9.8
4.7
0.6
80.0
13.3
5.3
1.5
93.0
4.4
2.2
0.5
93.4
3.5
2.4
0.7
93.3
3.7
1.7
1.3
89.4
6.4
3.4
0.8
89.2
6.5
3.7
0.6
89.6
6.4
3.2
0.8
Mild, 0-2mm; moderate, 2-4mm; severe, >4mm.
severity, with involvement approximately
twice as frequent as in the central incisors.
Mandibular first molars were more vulnerable than any other unit in the mandible or
maxilla for all categories (Table 4).
Modern groups
The most notable finding from the combined results of the two twentieth century
groups was that, while the incidence of periodontal disease was greater than in that of
the premodern specimens, the incidence of
severe alveolar bone loss resulting from periodontal disease was still very low. Seventyfive percent of teeth were free from periodontal disease (Table 3); mild periodontal disease
was observed in 13.8% of the buccal surfaces;
and moderate periodontal loss was estimated
to have occurred in 9.0% of the surfaces. This
compares with 90.8, 5.6, and 2.9%, respectively, in the combined premodern groups.
The pattern of bone loss by tooth type was
less regular than in the premodern groups of
skulls, and the severity of the periodontal
loss was greater. The areas of greatest damage in the maxilla were in the molar regions
in all categories of disease (Table 4). In contrast, the mandibular patterns of bone loss
were the most severe in the incisior region
for all categories, but in the posterior quadrant the first molar was the more severely
involved. The overall percentages of involve-
180
N.G. CLARKE ET AL.
TABLE 5. Alveolar bone loss due to periodontal disease in two modern groups’ (American and South African)
buccal surfaces of individual teeth
Tooth
18
17
53
Upper right quadrant
Severe (%)
0.0
Moderate (%I
15.1
18.9
Mild (%I
Normal (%)
66.0
16
15
14
13
12
11
Total
69
62
61
498
65
61
63
No. of teeth
64
1.5
13.8
12.3
72.3
6.5
13.1
13.1
67.2
1.6
3.2
17.4
77.8
1.6
7.8
15.6
75.0
0.0
4.4
11.6
84.1
0.0
4.8
11.3
83.9
0.0
3.8
9.8
86.9
1.4
8.1
13.7
76.9
47
46
45
44
Tooth
48
50
Lower right quadrant
Normal (%)
84.0
Mild (%)
8.0
Moderate (%)
6.0
Severe (%)
2.0
55
57
67
No. of teeth
69
72.7
14.5
12.7
0.0
68.4
15.8
14.0
1.8
82.1
13.4
3.0
1.5
82.6
11.6
4.3
2.9
43
42
41
Total
70
68
60
496
75.7
15.7
5.7
5.9
55.8
20.6
17.6
5.9
55.0
21.7
16.6
6.7
72.0
15.3
9.9
2.8
Mild, 0-2mm; moderate, 2-4mm; severe, >4mm.
TABLE 6. Alveolar bone loss due to periodontal disease in 32 premodern and two
modern groups’ proximal surfaces
Pre-modern
Maxilla
No disease
Mild disease
0-2mm)
Moderate disease
(2-4mm)
Severe disease
(> 4mm)
Total teeth
Modern
Mandible
Maxilla
Mandible
n
(%)
n
(%I
n
(%)
n
(%)
13,459
753
(91.8)
(5.1)
11,904
884
(88.7)
(6.6)
668
197
(68.0)
(20.1)
695
187
(69.8)
(18.8)
375
(2.5)
507
(3.8)
96
(9.8)
78
(7.8)
75
(0.6)
120
(0.7)
21
(2.1)
36
(3.6)
14,666
13,413
982
996
The proximal surfaces most frequently inment for mandibular teeth were higher than
for the maxillary units, especially in the in- volved were found in the molar regions for
all disease categories (Table 7). The maxilcisor region (Table 5).
lary molars were notably more involved than
PROXIMAL ALVEOLAR BONE LOSS
any other maxillary teeth. The pattern of
Premodern groups
bone loss was more regular in the mandible
Less than 10% of total teeth showed evi- than in the maxilla and slightly more severe.
dence of proximal bone loss due to periodonModern groups
tal disease (Table 6). The incidence of
proximal periodontal disease was higher in
The frequency of proximal alveolar bone
the mandible than the maxilla for all cate- loss for periodontal reasons was approxigories of disease but the differences were mi- mately three times greater in the modern
nor. Mild disease accounted for 5.8% of the groups than in the premodern groups; howtotal of marginally damaged sites, moder- ever, the overall incidence was still relaately involved locations comprised 3.1% of tively low, with 68.9% of teeth free from the
the total, while severely involved sites were evidence of periodontal disease (90.3% in the
less than 1%of the total (Table 6).
premodern groups). The severity of proximal
DISEASE IN ANCIENT POPULATIONS
181
TABLE 7. Alveolar bone loss due to periodontal disease in 32 premodern groups’ proximal
surfaces of individual teeth
Tooth
18
17
16
15
14
13
12
11
Total
No. of teeth
758
878
860
929
972
1,002
973
950
7,322
Upper right quadrant
Severe (%)
0.8
Moderate (%)
5.1
Mild (%)
7.3
Normal (%)
86.8
1.3
6.3
8.7
83.8
0.8
4.7
7.3
87.2
0.0
2.2
4.6
93.2
0.1
2.3
4.2
93.5
0.1
1.2
3.2
95.4
0.1
1.0
3.0
96.0
0.0
0.6
2.6
96.7
0.4
2.6
5.0
91.9
47
46
45
43
42
41
Total
Tooth
48
44
No. of teeth
725
773
722
867
9 14
929
908
873
6,711
Lower right quadrant
Normal (%j
87.6
Mild (%)
7.3
Moderate (%)
4.4
Severe (%j
0.7
84.7
9.2
4.9
1.2
85.7
8.7
4.2
1.4
91.8
5.2
2.5
0.5
92.8
3.7
2.8
0.6
91.4
5.2
2.5
1.0
88.0
7.0
4.0
0.9
88.7
6.6
3.8
0.9
88.9
6.5
3.6
0.9
Mild, 0-2mm; moderate, 2-4mm; severe, >4mm.
TABLE 8. Alveolar bone loss due to periodontal disease in two modern groups’ (American and South African)
proximal surfaces of individual teeth
Tooth
18
17
16
15
53
65
61
63
1.5
13.8
12.3
72.3
6.5
13.1
13.1
67.2
1.6
3.2
17.4
77.8
48
47
46
45
50
55
57
67
72.7
14.5
12.7
0.0
68.4
15.8
14.0
1.8
82.1
13.4
3.0
1.5
13
12
11
Total
64
69
62
61
498
1.6
7.8
15.6
75.0
0.0
4.4
11.6
84.1
0.0
4.8
11.3
83.9
0.0
3.8
9.8
86.9
2 .o
8.2
21.9
67.9
44
43
42
41
Total
69
70
68
60
496
82.6
11.6
4.3
2.9
75.7
15.7
5.7
5.9
55.8
20.6
17.6
5.9
55.0
21.7
16.6
6.7
71.0
17.5
8.1
3.4
14
No. of teeth
Upper right quadrant
Severe (%)
0.0
15.1
Moderate (%)
18.9
Mild (%)
66.0
Normal (%I
Tooth
No. of teeth
Lower right quadrant
84.0
Normal (%I
8.0
Mild (%)
6.0
Moderate (%I
2.0
Severe (%j
Mild, 0-2mm; moderate, 2-4mm; severe, 24mm.
alveolar bone loss was also notably greater
than in the premodern groups, with 19.4%
mildly involved teeth in the modern groups
compared with 5.8% in the premodern
groups; 8.8%moderately affected teeth in the
modern groups compared with 3.1% in the
premodern groups; and 2.9% severe bone loss
in the modern groups compared to 0.7% of
the premodern groups (Table 6).
Maxillary molars and mandibular incisors
were more frequently affected than other
units (Table 8).
DISCUSSION
The findings of the present study suggest
that several important dental concepts require careful review. One important finding
was the very low incidence of periodontal
182
N.G. CLARKE ET AL.
disease which could be attributed to a spread
of gingival inflammation. The jaws examined in the premodern groups had not been
influenced by sophisticated oral hygiene
practices and yet, despite the presence of
massive calculus deposits in many instances,
there was no discernible loss of bone from a
periodontal origin in over 90% of the teeth.
The data for periodontal disease was similar for both buccal and proximal surfaces in
most groups, although some variation was
present. While the concept of a bacterial
etiology for the disease would suggest that
the proximal surfaces should be more heavily involved, the present data do not show
the expected bias toward the disease at proximal sites.
Another important finding was the marked
difference between the premodern and modern groups in the incidence of periodontal
disease. In the premodern groups, approximately 10% of subjects were found to have
experienced loss of crestal bone as a n extension of a gingival lesion, while approximately 30% of the modern groups demonstrated some evidence of crestal resorption.
The present findings also suggest that
where progression of a superficial lesion was
evident in the bone crest, the attack was not
aggressive and usually resulted in only minor degrees of lost tissue. None of the teeth
examined had experienced a degree of bone
loss that could have resulted in eventual
tooth loss. The resistance to the extension of
gingivitis in the population groups examined
may have been due to the level of efficiency
of the host defence systems that operate in
the gingival crevice and the gingivae (Clarke
and Carey, 1985). In modern society these
defence mechanisms may be compromised by
prolonged or combined environmental factors such as stress, smoking, and diet. In
prehistory, the seasonal availability of food
may have resulted in periodic nutritional inadequacies (Gilbert and Mielke, 1985), but
the periodontal structures appear to be unaltered.
Ruffer (1920) found, in a study of ancient
Egyptian skulls, that severe suppurative periodontitis was often associated with marked
attrition of the teeth. The question was posed,
is periodontal disease caused or made worse
by very heavy tooth wear? It is unfortunate
that this early observation has not been investigated further, since heavy tooth attrition has the capacity to injure the dental
pulp. Subsequent diffusion of inflammatory
mediators from the dental pulp to the periodontal ligament via the dentinal tubules and
cementum may result in inflammation of the
periodontal ligament (Torobinejad and Bakland, 1980).
Larato (1970) also found that abscesses
were commonly seen in relation to teeth with
severe caries or tooth wear in dry skulls.
There is no correlation between attrition and
gingivitis, but a strong correlation does exist
between attrition and pathology of the pulp,
culminating in the most severe condition
with exposure of the organ. There is also a
strong correlation between pulp pathology
and the formation of ligamental granulation
tissue (Simon, 1983). Where the bone is thin
on buccal or lingual surfaces, total destruction of the process results in a suprabony
lesion. Such lesions occurring in the periodontium as a result of pulpal pathology are
generally deep, destructive of alveolar bone,
and can seriously compromise tooth support
(Simring and Goldberg, 1964).
In teeth with sound crowns, pulpal disease
may result from disturbed vascular supply to
the most peripheral aspect of the pulpal microcirculation. Causes of such a disturbance
are conjectural but could correlate with age
changes or any one of the environmental factors involved in peripheral vascular disease.
Periodontal lesions of pulpal origin (furcation, hemiseptal, vertical, and deep, isolated
bony defects) eventually discharge into the
gingival crevice and may be probed, thereby
mimicking a periodontal pocket. In the present study such dental abscesses were frequently observed to cause alveolar bone loss.
Nevertheless, periodontal lesions of pulpal
origin other than those at the apex of the
root are not generally recognised in either
the dental literature (Schafer et al., 1983)or
the anthropological literature (Molnar and
Molnar, 1985).
The low incidence of periodontal disease
found in the present study is consistent with
the findings of a number of recent studies.
One epidemiological survey of a n adult Dutch
population found that periodontal disease did
not generally occur in the older age group
and only a few cases of severe periodontal
destruction were found, these being in many
cases limited to single teeth (Pilot and
Schaub, 1985). A comprehensive longitudinal survey of periodontally involved patients
found that most periodontal lesions are stable (Socransky et al., 1984). Similarly, a longitudinal study of patients with gingivitis
DISEASE IN ANCIENT POPULATIONS
(Listgarten et al., 1985) found that little, if
any, periodontal breakdown occurred in the
study population over a 3-year period. Another study found that the most apical point
of bony craters in 148 skulls was located adjacent to the tooth rather than in the interdental supporting bone, and clinical
observations of angular bony defects were
found to be consistent with the skeletal materials (Saari et al., 1968).
These findings are consistent with the concept of a tooth-derived lesion arising in the
periodontal ligament, rather than the commonly postulated site-specific bacteria attacking a localised sector of the periodontium. It would appear that severe isolated periodontal lesions have a pulpal etiology and should not be confused with more
moderate and generalised periodontal lesions resulting from host interaction with
microbes.
The dental literature asserts that periodontal disease is responsible for the majority of
tooth loss after the age of thirty. Costa (1982)
disagrees with this concept and stated that
periodontal disease was not a major cause of
tooth loss in Eskimoes at any age. The findings of the present study strongly support
those of Costa (1982) since no skulls were
examined that demonstrated a degree of bone
loss of marginal (periodontal) origin that
could be considered capable of causing tooth
loss. Periodontal disease appears to be minimally destructive, predominantly located in
molar and mandibular incisor regions, and
present in only a very small proportion of the
populations examined.
The findings of the present study, coupled
with other paleopathological and clinical
studies, contradict the traditional view of the
incidence and severity of periodontal disease,
and they suggest that the traditional concept
of the etiology of severe periodontal lesions
requires a reorientation toward a pulpal
origin.
183
110:689-691.
Costa, RL (1982) Periodontal disease in the prehistoric
Ipiutak and Tigara remains from Point Hope, Alaska.
Am. J. Phys. Anthropol. 59:97-110.
Gilbert, RI, and Mielke, JH (1985)The analysis of prehistoric diets. Orlando: Academic Press, Inc., p. 164.
Gold, SI (1985) Periodontics. The past. J. Clin. Periodont.
12:79-97.
Larato, DC (1970) Intrabony defects in the dry human
skull. J. Periodont. 41:496-498.
Listgarten, MA, Schifter, CC, and Laster, L (1985)3 year
longitudinal study of the periodontal status of an adult
population with gingivitis. J. Clin. Periodont. 12:225238.
Loe, H, Anerud, A, Boysen, H, and Smith, M (1978) The
natural history of periodontal disease in man. J. Periodont. 49:607-620.
Molnar, S, and Molnar, I(1985) Observations of dental
diseases among prehistoric populations of Hungary.
Am. J. Phys. Anthropol. 67.51-63.
Muruhv, T (1959) Comuensatorv mechanisms in facial
heigdt adjustment to'functionh tooth attrition. Aust.
Dent. J. 41312-323.
Newman, HN, and Levers, BGH (1979) Tooth eruption
and function in early Anglo-Saxon population J. Roy.
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Page, RC, and Schroeder, H (1976) Pathogenesis of inflammatory periodontal disease. A summary of current work. Lab. Invest. 33:235-249.
Page, RC, and Schroeder, H (1982) Periodontal Disease
in Man and Other Animals. Basel: Karger, pp. 5-17.
Pilot, T, and Schaub, RMH (1985) Reappraisal of periodontal treatment needs. IADWAADR Abstracts No.
770. J. Dent. Res. 64:260.
Ruffer, A (1920)Study of abnormalities and pathology of
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Saari, JT,Hurt, WC, and Biggs, NL (1968) Periodontal
defects on the dry skull. J. Periodont. 39:278-283.
Sagne, S, and Olsson, G (1977)Studies of the periodontal
status of a medieval population. Dentomaxillofac. Radiol. 6:46-52.
Simon, JH (1983) Pathology. In B Cohen and RC Burns
(ed): The Pathways of the Pulp. St. Louis: Mosby,
p. 390.
Simring, M, and Goldberg, M (1964) The pulpal pocket
approach: retrograde periodontitis. J. Periodont. 352248.
Schafer, WG, Hine, MK, and Levy, BM (1983)A textbook
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ACKNOWLEDGMENTS
South African blacks: a biometric study. J. Dent. Res.
The hospitality and the access t o the skel- 64:925-929.
etal materials offered by the curatorial au- Torobinejad, M, and Bakland, LK (1980)Prostaglandins:
their possible role in the pathogenesis of pulpal and
thorities a t all locations is gratefully re- periapical
diseases. J. Endo. 6:733-739.
corded.
Whittaker, DK, Molleson, T, Daniel, AT, Williams, JT,
Rose, P, Resteghini, R (1985) Quantitative assessment
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Clarke, NG, and Carey, SE (1985) The aetiology of ginBiol. 30:493-501.
givitis: a n alternative explanation. J. Am. Dent. Assn.
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